Prevalences widely differ between studies reporting on aspirin resistance .
BACKGROUND The absolute risk of recurrences among patients using aspirin for prevention of cardiovascular events remains high .
Persistent platelet reactivity despite aspirin therapy might explain this in part .
Reported prevalences of this so-called aspirin resistance vary widely , between 0 % and 57 % .
OBJECTIVES The aim of the study was to systematic ally review all available evidence on prevalence of aspirin resistance and to study determinants of reported prevalence .
Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction.
The hypothesis that aspirin resistance is often due to noncompliance was investigated . One hundred ninety patients with a history of myocardial infa rct ion were evaluated using arachidonic acid-stimulated light aggregometry at 3 different time points : while receiving their usual daily aspirin , after not receiving aspirin for 7 days , and 2 hours after the observed ingestion of aspirin 325 mg . At the first time point , 17 patients ( 9 % ) failed to show  aspirin inhibition of platelet aggregation , but 2 hours after observed aspirin ingestion ,  aspirin inhibition was observed in all but 1 patient
Prevalences widely differ between studies reporting on aspirin resistance .
BACKGROUND The absolute risk of recurrences among patients using aspirin for prevention of cardiovascular events remains high .
Persistent platelet reactivity despite aspirin therapy might explain this in part .
Reported prevalences of this so-called aspirin resistance vary widely , between 0 % and 57 % .
OBJECTIVES The aim of the study was to systematic ally review all available evidence on prevalence of aspirin resistance and to study determinants of reported prevalence .