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Aspirin or clopidogrel in chronic coronary syndromes: the saga continues
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DOI：10.1093/eurheartj/ehag523.png)
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Abstract
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Mechanistic and clinical comparison of aspirin and clopidogrel as single antiplatelet therapy (SAPT) in patients with chronic coronary syndromes (CCS). Aspirin irreversibly acetylates platelet cyclooxygenase-1 (COX-1), thereby suppressing thromboxane A2 (TXA2) biosynthesis and TXA2-dependent platelet activation with highly predictable pharmacokinetics and pharmacodynamics. Clopidogrel, a prodrug requiring a 2-step, hepatic cytochrome P450 (CYP450)-dependent bioactivation, inhibits adenosine diphosphate (ADP)-mediated platelet activation through irreversible inactivation of the platelet P2Y12 receptor, with substantial interindividual variability in the antiplatelet effect. The use of aspirin is supported by extensive placebo-controlled, randomized evidence across the spectrum of atherosclerotic cardiovascular disease (ASCVD), whereas evidence supporting clopidogrel monotherapy is more limited and geographically heterogeneous, with superiority versus aspirin largely deriving from trials in East Asian populations. Unlike aspirin, clopidogrel has no established chemopreventive efficacy.
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