Laboratory detection of 'aspirin resistance': what test should we use (if any)?

Aspirin is widely used to decrease the risk of occlusive arterial events in patients at risk. It irreversibly inhibits the cyclooxygenase-1 (COX-1)-dependent synthesis of thromboxane A2 (TxA2), which is essential for the full aggregation response of platelets. In the last years, the issue of ‘aspirin resistance’ has been emphasized in the medical literature.1–4 Despite several studies published on this subject, its definition, diagnosis, prevalence, causes, and clinical consequences are still uncertain.1 The term ‘resistance’ to a drug should be used when a drug is unable to hit its pharmacological target, due to inability to reach it (as a consequence of reduced bioavailability, in vivo inactivation, negative interaction with other substances) or to alterations of the target.1 Based on this definition, the term ‘resistance’ to aspirin should be limited to situations in which aspirin is unable to inhibit COX-1-dependent TxA2 production (and, consequently, TxA2-dependent platelet functions).