It may not be necessary to withhold tissue plasminogen activator from patients with acute ischemic stroke who are already taking antiplatelet therapy, researchers reported.
The antiplatelet therapy does put these patients at increased risk of developing symptomatic intracerebral hemorrhage when they receive tissue plasminogen activator (TPA). But despite this risk, “prior antiplatelet therapy increased the odds of a favorable outcome” in a single-center observational study involving 301 patients.
The question of whether TPA treatment is safe in patients taking antiplatelet therapy is important because many people who develop acute ischemic stroke have a history of vascular events and are taking the drugs as preventative therapy when a stroke occurs. Many previous studies of the issue have yielded conflicting results, according to Dr. Maarten Uyttenboogaart and his associates at the University of Groningen, the Netherlands.
Dr. Uyttenboogaart and his colleagues studied 301 consecutive patients with acute ischemic stroke given TPA at the university medical center during 2002–2006. Eighty-nine (30%) were already taking aspirin, dipyridamole, combined aspirin plus dipyridamole, or clopidogrel as preventatives.
Symptomatic intracerebral hemorrhage occurred in 18 patients (6%), of whom 12 were receiving antiplatelet drugs, and 6 were not. “The absolute risk difference of approximately 10% translates into 1 additional [hemorrhage] in every tenth patient receiving thrombolysis and prior antiplatelet therapy,” the investigators said.
Half of the patients on prior antiplatelet therapy had a favorable outcome after TPA administration, compared with 45% of those who were not taking antiplatelet drugs (Arch. Neurol. 2008 March 10 [Epub doi:10.1001/archneur.65.5.noc70077]).
Since patients taking antiplatelet therapy were more likely to be older, to have a higher prevalence of vascular risk factors, and to have more previous vascular events than those not taking the agents, the data were adjusted to account for these differences and then reanalyzed. Prior antiplatelet therapy continued to be associated with a favorable outcome after TPA treatment.
“A possible mechanism behind this beneficial effect is that aspirin remains biologically active for 4–6 days and might prevent early reocclusion after TPA treatment,” the investigators noted.
Patients in this study were offered TPA for up to 4.5 hours following stroke onset, even though the treatment is approved for use only up to 3 hours after the event. A subgroup analysis of the 188 patients treated within this 3-hour window showed the same results as that for the entire cohort.