Q. What does the ASA Effect test measure?
A. When an individual’s blood platelets become activated, they release a chemical called thromboxane A2 (TxA2) into the circulation that activates additional platelets and causes them to stick together, eventually forming a blood clot under the right conditions. The TxA2 breaks down to the biomarker called 11-dehydro thromboxane B2 (11dhTxB2) and is excreted in the urine. The ASA Effect test measures the level of 11dhTxB2 in urine thus reflecting the amount of thromboxane production in the blood. Urine 11dhTxB2 levels are lowered in individuals who respond to ASA therapy.
Q. What does the CHARISMA trial mean for the ASA Effect test?
A. This clinically validated medical research could potentially change how millions of people worldwide are tested for the effectiveness of ASA and treated to prevent heart attacks and strokes. Findings from the CHARISMA trial, published in the October 21st, 2008 issue of the peer-reviewed medical journal Circulation, directly link the level of the 11dhTxB2 biomarker to an individual’s risk of heart attack and stroke. The ASA Effect test is the world’s only non-blood-based test available to doctors who want to test for the effect of ASA.
Q. Is the ASA Effect test Health Canada cleared?
A. Yes, the ASA Effect test was Health Canada cleared in May 2007 and can be run routinely in a hospital or reference laboratory.
Q. Why is the ASA Effect test important?
A. Medical studies indicate that not everyone benefits equally from low dose ASA. In fact some people have been reported to be resistant to the effect of ASA, but new studies indicate that it may be a question of ASA therapy “failure”. Because ASA is known to reduce the risk of heart attack and stroke by helping to prevent platelets from sticking together, the ASA Effect test allows the doctor to determine if the patient is benefiting optimally from his or her ASA regimen.
Q. What are the chances that a person’s platelets are not responding to ASA?
A. According to reports in the medical literature, 10% to 40% of patients taking ASA may not achieve the desired result. In fact, even if ASA is working on platelets, there are other factors that may interfere with the benefits of ASA. Traditional platelet function assays cannot detect these factors.
ASA is the abbreviation for Acetylsalicylic Acid
*In Canada, Aspirin is a trademark of Bayer AG, used under license.
*Entrophen is a Registered trademark of PendoPharm.
*ASA Effect and its logo are trademarks of Bescot Healthcare Canada Inc.
Q. What are the dangers if the patient is not benefiting from ASA?
A. Numerous outcomes studies, including new findings from the prestigious CHARISMA trial, have demonstrated that patients with a poor response to ASA therapy have a higher incidence of second heart attacks, strokes or even death than patients with a good response.
Q. Why shouldn’t a patient just take more ASA?
A. Increasing ASA dose may cause an increase in unwanted side effects, such as stomach discomfort or gastrointestinal bleeding. More important, the ASA may be doing its job, but some other factor may outweigh the beneficial effects, which could require a change in therapy. Only a physician should decide if it is safe to change ASA dosage.
Q. How long should a patient wait to be tested after beginning ASA therapy?
A. According to the literature it takes up to five days for low-dose ASA therapy to achieve maximum reduction in urinary 11dhTxB2 levels.
Q. How often should a patient be tested?
A. The optimum frequency of testing has not been established. Clinical studies indicate that certain individuals lose the benefit of ASA therapy over time due to atherosclerotic disease or increases in cholesterol.
Q. What should a physician do if a patient’s result indicates a poor ASA response?
A. Any change in treatment is at the discretion of the physician. However, the recently published CHARISMA trial results indicate that;
- Not all patients receive the same protective benefits from low-dose ASA therapy
- The thromboxane metabolite 11-dehydro-thromboxane B2 (11dhTxB2) is an independent, modifiable predictor of risk for stroke, heart attack and cardiac death
- Higher levels of urinary 11dhTxB2 are associated with as much as a four fold increased risk for adverse cardiovascular events or death
- Statin treatment is associated with lower concentrations of 11dhTxB2
It is important that the physician and the patient recognize that an increased level of 11dhTxB2 may be an indication of increased risk of atherosclerotic disease or secondary cardiovascular events.