By failing to address the most common causes of aspirin ineffectiveness, a small clinical study recently published online in the journal Circulation highlights the importance of clinically validated, FDA-cleared testing for aspirin effect with the AspirinWorks ® Test to help prevent heart attack and stroke. In the Grosser, et al. study, University of Pennsylvania researchers looking at 400 healthy volunteers and the impact of enteric coated versus uncoated aspirin, narrowly focused on a rare, genetic resistance to the effect of taking aspirin and ignored the far more common causes limiting the effectiveness of aspirin. Millions of Americans take a daily aspirin to reduce or prevent cardiovascular events. Aspirin works on blood platelets to decrease levels of thromboxane, the chemical in the body that makes platelets sticky. Lower thromboxane levels and decreased platelet stickiness means less chance of developing a blood clot and therefore, less chance of a heart attack or stroke. The AspirinWorks Test from Corgenix Medical Corp (OTC BB: CONX), which was not included in the study, is not intended to measure or diagnose what the study refers to as “genetic aspirin resistance,” and is in fact the only U.S. FDA-cleared test that measures the urinary biomarker 11-dehydro thromboxane B2 (11dTxB2) to determine aspirin effect. “The study’s severe limitations, including the fact that it had absolutely nothing to do with our company’s AspirinWorks Test for aspirin effect, actually highlights the importance of screening patients who are taking aspirin,” said Corgenix President and CEO Douglass Simpson. “Doctors test patients because despite taking aspirin, their levels of the inflammatory chemical thromboxane could still be dangerously high, not just because they might have some rare genetic disorder.” Despite the confusing reports about the Grosser et al trial, Simpson said the bottom line is that people taking a daily aspirin with continued high levels of thromboxane are at a clinically proven increased risk of heart attack or stroke compared to patients without elevated levels.
“While we strongly believe ignoring non-genetic causes of aspirin ineffectiveness is misleading, this study gives us the opportunity to further educate the medical community and the public they serve about the critical importance of testing for aspirin effect and understanding how it impacts risk,” continued Simpson.Simpson emphasized that while so-called “genetic aspirin resistance” as defined in the study is rare, failure of patients to respond to the intended beneficial effect of aspirin is absolutely not rare. There are many roads that lead to aspirin effect or the lack thereof, putting patients at increased risk of heart attack and stroke. Reasons for the inability of aspirin to do its job include:
- Diseases and other inflammatory processes that produce chemicals (thromboxane) that can reduce aspirin’s beneficial effect
- Other medications that interfere with the intended anti-clotting effect of aspirin
- Unusually high levels of stress
- Genetically poor responders to aspirin therapy