Letter by Kronish et al 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”

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HomeCirculationVol. 115, No. 3Letter by Kronish et al 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/EPUBLetter by Kronish et al 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” Ian M. Kronish, MD and Nina Rieckmann, PhD Daichi Shimbo, MD and Karina W. Davidson, PhD Ian M. KronishIan M. Kronish Department of Medicine, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY Search for more papers by this author and Nina RieckmannNina Rieckmann Department of Medicine, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY Search for more papers by this author Daichi ShimboDaichi Shimbo Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY Search for more papers by this author and Karina W. DavidsonKarina W. Davidson Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY Search for more papers by this author Originally published23 Jan 2007https://doi.org/10.1161/CIRCULATIONAHA.106.652628Circulation. 2007;115:e45To the Editor:Frelinger et al1 conclude that nonadherence is associated with aspirin resistance in a small minority (≈2%) of aspirin-treated patients and that a cyclooxygenase-independent pathway may mediate aspirin resistance in the remainder of patients. Although we agree that there may be a cyclooxygenase-independent pathway that allows platelets to remain active in some aspirin-treated patients, we believe that the authors underestimate the role nonadherence plays in aspirin resistance, because of their restricted sample of acute coronary syndrome patients.Other studies have found much higher rates of nonadherence. For example, in the study of aspirin resistance by Cotter et al,2 at least 16% of the patients were nonadherent as measured by a combination of adherence interview and platelet thromboxane response to aspirin. In our own study of aspirin adherence,3 nonadherence was defined as aspirin being taken correctly ≤75% of the time and was monitored via an electronic device stored in the cap of a pill bottle. We found that 10% of nondepressed patients were nonadherent to aspirin for the 3 months after hospitalization for acute coronary syndrome; among patients who were persistently depressed after acute coronary syndrome hospitalization, 42% did not adhere to their aspirin regimen.The discrepancy in rates of adherence between the study by Frelinger et al1 and those of other authors may have been caused by the studies’ different methods of patient recruitment. Frelinger et al1 enrolled patients who presented for daytime diagnostic catheterizations, and only patients who reported aspirin adherence for more than 3 days were eligible. This method of enrollment may have excluded patients who were prescribed aspirin but were not taking it. Furthermore, the adherence of this group of patients at the time of the study may not have been representative of these patients’ typical adherence because the patients were presenting for cardiac diagnostic procedures. Some of these procedures were likely scheduled in advance, and patients may have been motivated to adhere more closely to their cardiac medication regimen at a time closer to the procedure.With future studies, it will be important to accurately determine the relative role that patient behavior plays in resistance to aspirin by using methods of enrollment that capture representative adherence behaviors. Whereas a cyclooxygenase-independent mechanism of aspirin resistance suggests a pharmacological solution for aspirin resistance, poor patient adherence requires behavioral interventions.DisclosuresNone.1 Frelinger AL 3rd, 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 J Med. 2004; 147: 293–300.Google Scholar3 Rieckmann N, Kronish I, Haas DC, Gerin W, Chaplin W, Burg MM, Vorchheimer D, Davidson KW. Persistent depressive symptoms lower aspirin adherence following acute coronary syndromes. Am Heart J. 2006; 152: 922–927.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Gurbel P and Tantry U (2011) Resistance to Antiplatelet Therapy Pharmaceutical Sciences Encyclopedia, 10.1002/9780470571224.pse441 January 23, 2007Vol 115, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.106.652628PMID: 17242290 Originally publishedJanuary 23, 2007 PDF download Advertisement SubjectsAcute Coronary SyndromesCompliance/AdherencePlatelets