Plavix reduces the risk of heart attack, unstable angina, stroke, and cardiovascular death in patients with cardiovascular disease by making platelets less likely to form blood clots. Plavix does not have its anti-platelet effects until it is metabolized into its active form by the liver enzyme, CYP2C19. People who have reduced functioning of their CYP2C19 liver enzyme cannot effectively convert Plavix to its active form. As a result, Plavix may be less effective in altering platelet activity in those people. These “poor metabolizers” may not receive the full benefit of Plavix treatment and may remain at risk for heart attack, stroke, and cardiovascular death.
FDA recommends that health-care professionals should:
- Be aware that some patients may be poor metabolizers of Plavix. They do not effectively convert Plavix to its active form because of low CYP 2C19 activity. The effectiveness of Plavix as a preventive therapy is reduced in these patients.
- Be aware that tests are available to determine patients’ CYP2C19 status.
- Consider use of other anti-platelet medications or alternative dosing strategies for Plavix in patients who have been identified as poor metabolizers.
- Be aware that although a higher dose regimen (600 mg loading dose followed by 150 mg once daily) in poor metabolizers increases antiplatelet response, an appropriate dose regimen for poor metabolizers has not been established in a clinical outcome trial.
- Review the newly approved Plavix drug label for complete information on the use of Plavix
For additional information about the warning visit the FDA Drug Safety Communication Web site.