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Up to 20 percent of patients taking aspirin to lower the risk of suffering a second cerebrovascular event do not have an antiplatelet response from aspirin, the effect thought to produce the protective effect, UB researchers have shown.
“Millions of people use low-dose aspirin either for prevention of a second stroke, second heart attack or second episode of peripheral artery disease,” says Francis M. Gengo, professor of neurology, professor of pharmacy practice and lead researcher on the study.
“In those three indications, it’s crystal clear that aspirin reduces the risk of a second heart attack or stroke in most patients,” he says. “But we have known for years that in some stroke and heart attack patients, aspirin has no preventive effect.”
In a related study, UB researchers have shown that stroke patients who use ibuprofen for arthritis pain or other conditions—while taking aspirin to reduce the risk of a second stroke—undermine aspirin’s ability to act as an antiplatelet agent.
In a cohort of patients seen by physicians at the Dent Neurologic Institute in Amherst, NY, 28 patients were identified as taking both aspirin and ibuprofen (a nonsteroidal anti-inflammatory drug, or NSAID) daily and all were found to have no antiplatelet effect from their daily aspirin. However, when 18 of the 28 patients returned for a second neurological visit after discontinuing NSAID use and were retested, all had regained their aspirin sensitivity and its ability to prevent blood platelets from aggregating and blocking arteries.