Key result
Variability in platelet response to aspirin is genetically determined and associated with cardiovascular risk, though specific gene variants remain unknown.
Understanding the genetic basis of variable platelet response to aspirin may enable personalized antiplatelet therapy to maximize antithrombotic benefit and minimize bleeding risk.
Pharmacogenomic testing may refine aspirin dosing for CV prevention; RCT data extends genetic insights into platelet response variability.
Aspirin is the most widely used drug in the world for cardiovascular protection. Aspirin's ability to suppress platelet function varies widely among individuals and lesser suppression of platelet function is associated with increased risk of myocardial infarction, stroke and cardiovascular death. Platelet response to aspirin is a complex phenotype involving multiple genes and molecular pathways. Aspirin response phenotypes can be categorized as directly or indirectly related to cyclooxygenase-1 (COX-1) activity, with phenotypic variation indirectly related to COX-1 being much more prominent. Recent data indicate that variability in platelet response to aspirin is genetically determined, but the specific gene variants that contribute to phenotypic variation are not known. An understanding of the relationship between genotype, aspirin response phenotype and clinical outcome will help to bring about a personalized approach to antiplatelet therapy that maximizes antithrombotic benefit whilst minimizing bleeding risk for individual patients.
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Faraday et al. (2007) conducted a review in Cardiovascular disease. Aspirin was evaluated. Variability in platelet response to aspirin is genetically determined and associated with cardiovascular risk, though specific gene variants remain unknown.
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