Summary:
Aspirin is the widely used cheap antiplatelet agent in
coronary diseases and ischemic stroke patients.
Unfortunately for the last two decades the term ‘’Aspirin
resistance’’ (AR) has been evolved due to its’ failure to
protect the aspirin users against major cardiovascular
events. This is a clinical syndrome which can be defined
operationally as the failure of aspirin to inhibit platelet
aggregation, platelet activation, or ThromboxaneA2 (TXA2)
production. Although the nonmodifiable factors like the
PlA1/A2 polymorphism in the GPIIIa platelet receptor have
been identified as responsible for AR , bioavailability of
aspirin affected by patient noncompliance, insufficient