In their meta-analysis, Snoep et al1 found that “laboratory-defined aspirin resistance” was associated with an increased risk of recurrent cardiovascular events in aspirin-treated patients. However, this conclusion is undermined by a significant heterogeneity test result, even when using a random effects model. The authors included studies with very different designs and particularly different definitions of “aspirin resistance.” Indeed, the biological tests used in the selected studies were either specific for aspirin inhibition of thromboxane (Tx)A2 synthesis (measurement of TxB2 levels or of arachidonic acid–induced platelet aggregation) or nonspecific (eg, template bleeding time or the Platelet Function Analyzer100 [Dade Behring, Deerfield, Illinois]).
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