Abstract

Aspirin protects from cardiovascular events because of its antiaggregant effect. The occurrence of new events in patients who take aspirin has been called clinical aspirin resistance. Many authors believe that aspirin resistance must be detected by biochemical tests, although there is no agreement on which is the best. Nor is there agreement on the term aspirin resistance. Tests used in research laboratories are aggregometry (turbidometric and impedance), tests based on activation- dependent changes in platelet surface, and tests based on activation-dependent release from platelets. Point-ofcare tests are PFA-100, IMPACT and VerifyNow, which can detect platelet dysfunction that may be due to aspirin effect, but their use for this purpose is not yet recommended. Aspirin response may be modified by different factors: patients compliance, dose, smoking, hyperlipidemia, hyperglucemia, acute coronary syndrome, percutaneous revascularization, recent stroke, extracorporeal circulation, heart failure, exercise, circadian rhythm, absorption, concomitant medications, polymorphisms. Patients with aspirin resistance may have an increased risk of cardiovascular events, and possible therapeutic options are to increase the dosage, to replace aspirin with another antiaggregant drug or to add another drug. In conclusion, there are many reasons that explain the variability in individual responsiveness to aspirin. The term resistance is probably not exact in describing this phenomenon.

Keywords: Aspirin, cyclooxigenase, thromboxane A2, drug resistance