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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”

Originally publishedhttps://doi.org/10.1161/CIRCULATIONAHA.106.652628Circulation. 2007;115:e45

    To 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.

    Disclosures

    None.

    • 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 Scholar
    • 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 J Med. 2004; 147: 293–300.Google Scholar
    • 3 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

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