Abstract
The thienopyridine clopidogrel, which irreversibly blocks the adenosine diphosphate (ADP) receptor P2Y12 on platelets, has become an essential component of therapy in patients with acute coronary syndromes, because it significantly improves the outcomes.1 However, clopidogrel has at least three drawbacks: delayed onset of action, large interindividual variability in platelet response, and irreversibility of its inhibitory effect on platelets (Figure 1). The two-step activation process, involving a series of cytochrome P-450 (CYP) isoenzymes, is susceptible to the interference of genetic polymorphisms2 and drug–drug interactions.3 Patients with a poor response to clopidogrel have an increased risk of coronary thrombosis.4 The increased risk . . .
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