The well established importance of regular aspirin administration stands on firm grounds, as large meta-analyses have shown this therapy to significantly reduce the risk of death. However, not all patients benefit of aspirin administration to the same extent, thus high-lighting a sub-population of patients with inadequate platelet response to ASA. The mechanisms underlying reduced ASA efficacy remain elusive. A recent report has suggested that platelets, long believed to be incapable of de novo protein synthesis, may retain their ability to form the cyclooxygenase enzyme, once it has been inactivated by aspirin. This may explain the inefficacy of the drug to induce sustained platelet inhibition in certain patients. The current study aims to evaluate, in patients suffering from stable coronary artery disease, the stability of platelet inhibition by aspirin during the normal once daily dosing regimen.
Study Type
OBSERVATIONAL
Enrollment
10
Platelet aggregation TxA2 formation
Hôpital du Sacré-Coeur de Montréal
Montreal, Quebec, Canada
Platelet aggregation TxA2 formation
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