Summary
Aspirin reduces major atherothrombotic events across a wide spectrum of patients with
atherosclerotic disease. The occurrence of ischemic events despite of aspirin treatment
is a failure of therapy, often denoted ‘clinical aspirin resistance’. This is distinguished
from laboratory assays showing an insufficient inhibition of platelet function, which
indicate ‘laboratory aspirin resistance’. Laboratory aspirin resistance has been reported
in up to 60% of patients after stroke or peripheral arterial disease, up to 70% in
stable coronary heart disease and even up to 80% in acute myocardial infarction. However,
this data must be interpreted carefully because of small sample sizes and potential
confounding factors such as compliance, co-morbidities and large differences between
the laboratory methods used for detection. During the past years, evidence has accumulated
that laboratory aspirin resistance is associated with an increased incidence of major
atherothrombotic events, with an up to 13-fold increased risk of events in patients
with cardiovascular disease. Thus, an individualized antiplatelet therapy will have
to consider the possibility of aspirin resistance, and the identification of aspirin
non-responders may improve antiplatelet therapy in future. Whether an increased dose
of aspirin or another antiplatelet drug (e.g. clopidogrel) instead or in addition
to aspirin should be given is unclear. Prospective trials are underway which address
this issue. This review gives an overview on the various clinical studies that have
investigated the prevalence and clinical importance of laboratory aspirin resistance.
Moreover, therapeutic options, as well as future perspectives are discussed.
Keywords
Aspirin resistance - atherosclerosis - platelet function - prevalence - clinical outcome
