When Aspirin Protection Falls Short
Study finds some people with heart disease don't benefit from drug's effects
MONDAY, March 25, 2002 (HealthDayNews) -- Aspirin may not offer the desired protection against heart disease for some people because their body doesn't respond to the drug as it should.
But this new finding doesn't mean people at high risk of heart disease should stop taking aspirin, says Dr. John W. Eikelboom, a clinical lecturer at the University of Western Australia, and lead author of the study that appears in tomorrow's issue of the journal Circulation.
It does mean that "some patients may need more protection than aspirin alone can offer," he adds.
The new study doesn't say how many people might need that extra protection, Eikelboom says. It uses data from the HOPE (Heart Outcomes Prevention Evaluation) study, which was designed to tell whether the drug ramipril could protect against heart attack and stroke. Because the study was so large, researchers have been mining its data for other purposes.
Eikelboom's study used information about 5,529 people with heart disease who were enrolled in HOPE at 129 Canadian medical centers. Because all the participants gave urine samples, he was able to determine each body's levels of a close chemical relative of thromboxane, a molecule that makes blood platelets sticky and likely to form clots that block arteries in the heart or brain.
Aspirin protects against those conditions because it reduces production of thromboxane by the platelets. The American Heart Association recommends aspirin for all people with artery disease, with a second anti-platelet drug added for those with the uncontrolled chest pain called unstable angina.
All the people in Eikelboom's study had been taking aspirin. He found that the five-year incidence of heart attacks in those with the highest levels of the thromboxane-related molecule was double that of those with the lowest levels. As thromboxane levels went up, so did the risk of heart attacks, and of death. The risk of any cardiovascular event was 1.8 times higher for those with the highest levels compared to those with the lowest levels, and the risk of death was 3.8 times higher.
"This study shows that there is such a phenomenon as aspirin resistance," Eikelboom says. "It shows the need to develop new therapeutic strategies in such a case."
And studies over the past decade have shown that "thromboxane is not made exclusively by platelets," he says. "It can be made by other cells."
More studies are needed, he says, first to seek out those people who may have aspirin resistance, then to "explore more carefully the benefit of new combinations of anti-platelet drugs."
"The last thing we want to do is to stop using aspirin," Eikelboom says. "There is overwhelming evidence that it works for most people.