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Platelet function-guided approach worsens outcomes after stroke or TIA

NEW YORK (Reuters Health) – Using platelet function to guide antiplatelet therapy after an ischemic stroke or transient ischemic attack (TIA) may worsen clinical outcomes, researchers warn.

They had hoped for the opposite result.

“We had hoped that a strategy of testing platelet function and altering therapy based on the results would lead to improved outcomes,” Dr. Deepak L. Bhatt from Harvard Medical School in Boston told Reuters Health by email. “At the same time, we did have some reservations about this approach, as there are no great data to date supporting it. That is why we did the study.”

His group’s retrospective study of 324 patients was published online June 19 in Stroke.

At the time of platelet function testing, the prevalence of nonresponse was 43% for aspirin (128 of the 296 patients who were currently taking aspirin) and 35% for clopidogrel (54/156).

Antiplatelet therapy was increased after platelet function testing in 42 (33%) of aspirin nonresponders and 23 (43%) clopidogrel nonresponders, either by increasing the aspirin and/or clopidogrel dose or by adding clopidogrel.

The composite rate of death, bleeding, or ischemic event was significantly higher in patients who underwent antiplatelet therapy modification than in patients without modification (40% vs 21%; p=0.001).

Antiplatelet therapy modification was also associated with a higher risk for bleeding or ischemic events (34% vs 19%, p=0.006).

Rates of bleeding were highest when clopidogrel was added or increased or when both aspirin and clopidogrel doses were increased.

Among patients whose platelet function was retested after therapy modification, there were no significant differences in clinical outcomes between patients who became responsive compared with those who remained nonresponsive.

Rates of death, bleeding, or ischemic events remained significantly higher in the antiplatelet therapy modification group after propensity score adjustment, whereas there remained only a trend toward increased bleeding or ischemic events.

“In patients with cerebrovascular disease, it does not appear that antiplatelet therapy guided by platelet function testing is warranted,” Dr. Bhatt concluded. “There is no reduction in future ischemic events and bleeding may be increased by intensifying antiplatelet therapy in patients who are deemed aspirin or clopidogrel non-responders. Unless future randomized clinical trials find merit in tailoring antiplatelet therapy based on platelet function testing, it should not generally be utilized in patients with stroke.”

He added, “While this study was specific to patients with cerebrovascular disease, the results may also apply to coronary artery disease. There as well, randomized clinical trials of platelet function testing are needed before adopting these tests for routine use.”

Several ongoing trials in cardiology are trying to address related questions, Dr. Bhatt said, adding, “It is a bit trickier in cerebrovascular disease because of the additional risk of intracranial hemorrhage, which is higher in patients with a history of prior cerebrovascular disease and tends to be an issue with more potent antiplatelet therapy.”


Stroke 2012.