Pharmacogenomics of platelet responsiveness to aspirin.
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.
Faraday
Nauder
N
Johns Hopkins University School of Medicine, Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care, 298 Meyer Bldg, 600 N Wolfe St, Baltimore, MD 21287, USA. nfaraday@jhmi.edu
Becker
Diane M
DM
Becker
Lewis C
LC
D000328:Adult; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D003327:Coronary Disease / Q000517:prevention & control; D051545:Cyclooxygenase 1 / Q000187:drug effects / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D006801:Humans; D009203:Myocardial Infarction / Q000235:genetics; D010597:Pharmacogenetics; D015539:Platelet Activation / Q000187:drug effects*
D016861:Cyclooxygenase Inhibitors; D051545:Cyclooxygenase 1; D001241:Aspirin