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Effects of Ibuprofen on the Magnitude and Duration of Aspirin's Inhibition of Platelet Aggregation: Clinical Consequences in Stroke Prophylaxis

From the Departments of Neurology (Dr F. M. Gengo, Dr Bates), Pharmacy (Dr F. M. Gengo, Dr Rubin), and Pharmaceutical Sciences (Dr Mager), University at Buffalo, Buffalo, New York and Dent Neurologic Institute, Buffalo, New York (Dr F. M. Gengo, Mr Robson, Dr Rainka, Mr M. F. Gengo, Dr Bates). Preliminary data presented at the 35th annual meeting of the American College of Clinical Pharmacology Cambridge Massachusetts.

This study was designed to measure the magnitude and duration of inhibition of platelet aggregation following doses of aspirin or ibuprofen alone or taken in combination in a group of healthy volunteers. Ten normal volunteer subjects underwent 3 randomized treatment sessions: aspirin 325 mg alone, ibuprofen 400 mg alone, and ibuprofen 400 mg, followed by dosing with aspirin 325 mg 2 hours thereafter. In addition, a confirmatory study was performed in patients. Over 27 months, a cohort of patients treated with aspirin for secondary stroke prophylaxis while concomitantly taking a nonsteroidal anti-inflammatory drug (NSAID) was identified. A significant reduction was found in both the magnitude and duration of aspirin's inhibitory effect on platelet aggregation when ibuprofen was given prior to aspirin administration in normal volunteer subjects. During a 27-month period, a cohort of 28 patients took regular daily doses of ibuprofen or naproxen. Of these 28 patients, 18 returned for follow-up testing in the absence of this pharmacodynamic interaction. None of these 18 patients demonstrated inhibition of platelet aggregation while on both NSAID and aspirin; however, all showed inhibition of aggregation following discontinuation of the NSAID. Notably, 13 of these 18 patients (72%) had experienced a recurrent ischemic episode while taking aspirin and NSAIDs concomitantly. These data suggest that ibuprofen prevents the irreversible inhibition of platelet aggregation produced by aspirin needed for secondary stroke prophylaxis, and this interaction can have clinical consequences for patients taking aspirin.

Key Words: Platelet aggregation • aspirin • ibuprofen • nonsteroidal anti-inflammatory drug • stroke

Address for reprints: Fran Gengo, PharmD, FCP, Dent Neurologic Institute, 3980 Sheridan Drive, Suite 200, Amherst, NY 14226; e-mail: fgengo{at}buffalo.edu.

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