Key result
Substantial interpatient variability exists in the level of platelet inhibition achieved by antiplatelet agents, which may have clinical consequences requiring further evaluation.
There is substantial interindividual variability in response to common antiplatelet therapies, which may explain recurrent thrombotic events and requires further clinical evaluation.
Antiplatelet response variability may underlie breakthrough events despite standard therapy; leaves open whether personalized regimens improve outcomes.
Many patients suffer thrombotic events such as myocardial infarction, stroke and peripheral embolism despite therapy with recommended doses of all currently approved antiplatelet agents. Researchers have suggested that a subset of patients may be resistant to the antiplatelet effects of aspirin, and have developed substantial evidence to support this theory. The thienopyridines ticlopidine and clopidogrel and the glycoprotein IIb/IIIa inhibitors also exhibit substantial interpatient variability in the level of platelet inhibition they achieve. There are several biochemical factors that may contribute to the etiology of individual resistance to antiplatelet medications. Some studies suggest that the variability in patient responsiveness to these drugs may have clinical consequences, and data from trials evaluating clinical end points are needed to further elucidate this correlation.
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Graaff et al. (2001) conducted a review in Thrombotic events despite antiplatelet therapy. Antiplatelet therapies (aspirin, ticlopidine, clopidogrel, glycoprotein IIb/IIIa inhibitors) was evaluated. Substantial interpatient variability exists in the level of platelet inhibition achieved by antiplatelet agents, which may have clinical consequences requiring further evaluation.
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