Abstract
The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?
Highlights
Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH2
Platelet thromboxane falls below 95% only after several days
This study suggests that aspirin non-responders might obtain less benefit with respect to cardiovascular events
Summary
Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH2. As was suggested by Bertele et al [36], our study indicated no correlation between platelet function and thromboxane level, implying that aspirin does not prevent an agonist potentiation effect when low doses or a daily high dose are administered These results are in line with those obtained by Cerletti et al [37]. Aspirin resistance is a poorly defined term It can imply a clinical inability of aspirin to protect individuals from arterial thrombotic events; or laboratory indications of the failure of aspirin to inhibit platelet activity, mainly platelet aggregation; or a close-to-normal urinary concentration of thromboxane metabolites. We support the view that aspirin resistance cannot be defined by the level of serum thromboxane or its urinary metabolites, because these measurements do not correlate with the reduction of inhibition of platelet aggregation in response to multiple stimuli, and because: 1. The underlying endothelial and/or atheroma inflammation in coronary syndromes could explain why the antiplatelet effect of aspirin fails, irrespective of its anti-aggregating capacity or the urinary levels of thromboxane metabolites
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