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Low-dose aspirin (acetylsalicylic acid (ASA)) treatment is a cornerstone in cardiovascular prevention, and is well documented in several patient categories.1–3 It inhibits platelet-dependent thromboxane (Tx) formation from arachidonic acid (AA) via irreversible inhibition of cyclo-oxygenase-1 (COX-1) in platelets in the portal circulation, with minimal systemic effects owing to efficient clearance in the liver when low doses are ingested. The dosage of ASA must be sufficient to block platelet COX-1 by >95% in order to effectively counteract Tx-mediated platelet aggregation.4 However, platelets also interact with other blood cells, and ASA may have non-platelet-dependent antithrombotic effects.5 Thus, the clinical efficacy of ASA may not depend entirely upon its ability to block the COX-1-mediated formation of Tx from AA in platelets. The optimal balance between protection against atherothrombotic events and risks for side effects appears to be obtained with an ASA dosage of 75–150 mg daily.1–3
In recent years it has become clear that all patients do not benefit fully from ASA treatment, and the concept of “aspirin resistance” has emerged.4–6 However, the routine use of antiplatelet efficacy testing has been questioned, since there is no agreed definition of “aspirin resistance” (as detected by a standardised and well-documented test), and no well-documented strategy for the treatment of “aspirin-resistant” patients.1 5 6 The paper by Muir et al7 is interesting in this context, since it questions the validity of testing for the antiplatelet efficacy of ASA in individual patients (see page 1225).
Muir et al7 compared four different tests on two occasions—that is, after ⩾7 days on ASA 150 mg/day and again 2 weeks later, in 172 patients with stable coronary artery disease. They studied “residual platelet activity” rather than true “aspirin resistance” (failure of the drug to influence …
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