Post-stroke clot-busting therapy beneficial for patients on aspirin

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Patients given a clot-busting drug following stroke appear to have better outcomes if they were already taking anti-platelet medications, despite an apparent increased risk for bleeding in the brain, according to an article posted online today that will appear in the May 2008 print issue of Archives of Neurology, one of the JAMA/Archives journals.

Dissolving blood clots by administering the drug tissue plasminogen activator (tPA) appears to improve outcomes in some patients with stroke, according to background information in the article. However, the medication is associated with a 10-fold increased risk of symptomatic brain hemorrhage (bleeding). Antiplatelet medications, such as aspirin, might further increase the risk for bleeding because these drugs impair the function of cells critical in forming blood clots.

Maarten Uyttenboogaart, M.D., and colleagues at the University of Groningen, Groningen, the Netherlands, studied 301 patients who received tPA following stroke between 2002 and 2006. Of those, 89 had used antiplatelet drugs prior to receiving tPA.

Symptomatic brain hemorrhages occurred in 12 patients who had received antiplatelet therapy (13.5 percent) and six patients who had not (2.8 percent). Patients who had been taking antiplatelet therapy had a higher risk for symptomatic brain hemorrhages. “Despite this increased risk, prior antiplatelet therapy increased the odds of a favorable outcome,” defined as the ability to independently carry out activities of daily living after three months, the authors write. “Therefore, our study suggests that tPA treatment should not be withheld from patients receiving antiplatelet therapy.”

Aspirin remains active for four to six days and might prevent an additional blood vessel blockage from occurring following tPA therapy, leading to the observed improved outcomes, the authors note. “Larger prospective studies are warranted to further investigate the influence of antiplatelet therapy on outcome after thrombolytic therapy for acute ischemic stroke,” they conclude.

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(Arch Neurol. 2008;65[5]:(doi:10.1001/archneur.65.5.noc70077). Available pre-embargo to the media at www. jamamedia.org.)

Editor’s Note: This study was supported by a grant from the Catharina Heerdt Foundation. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Contact: Maarten Uyttenboogaart,

JAMA and Archives Journals

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