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To the Editor:
We were intrigued by the recent article and editorial regarding antiplatelet medication and outcome after ICH.1,2
The analysis presumes that a history of aspirin use obtained from the patient or surrogate is a reliable indicator of platelet activity but this may be inaccurate. We have found that a substantial number of patients not known to take aspirin have reduced platelet activity on admission when tested.3 Because the presumed mechanism of aspirin's effect on outcome after ICH would be reduced platelet activity, the important question is not whether reported aspirin use is related to ICH volume growth and outcomes, but whether platelet activity is.
Reduced measured platelet activity on admission—usually but not always related to clinically verifiable aspirin use—is associated with ICH volume growth and worse outcomes.4 Aspirin use alone is not. This may be due to the significant number of patients with reduced platelet activity without known aspirin use, the variable effect of aspirin on platelet activity, and the potential unreliability of the medication history. Why would patients have reduced platelet activity without aspirin use? We suspect this is because patients often take an antiplatelet agent at the onset of headache but are unable to relate this history because of aphasia or depressed mental status.
We have since identified one patient admitted with an ICH who was alert and able to relate she took ibuprofen for headache, but not aspirin, and had …
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