Summary

Incomplete P2Y12-inhibition during clopidogrel treatment is associated with increased cardiovascular events and mortality after coronary intervention. We investigated the incidence of impaired individual clopidogrel-responsiveness using a P2Y12-specific and pre-treatment-independent assay in a real world situation. One hundred consecutive patients with coronary artery disease (CAD) on combined acetylsalicylic acid and clopidogrel treatment (75 mg/d) and 33 patients on aspirin only were screened for platelet ADP-induced signalling by conventional aggregometry, platelet P-selectin expression and the platelet reactivity index (PRI). Impaired P2Y12-specific inhibition by clopidogrel was defined as a PRI>50%. Functional platelet reactivity was significantly lower in clopidogrel-treated patients compared to controls. Impaired individual response to treatment was diagnosed in 69% of clopidogrel-treated patients. Conventional assessment of maximumADP-induced platelet aggregation failed to detect impaired P2Y12 inhibition in 36% of patients identified by PRI to have an impaired clopidogrel response. Impaired clopidogrel response was associated with lower HDL levels and a history of hyperlipidaemia.In conclusion, PRI as a P2Y12-specific assay to evaluate the treatment effect of clopidogrel in patients with CAD revealed insufficient P2Y12-inhibition in two thirds of patients in a real-world scenario indicating a markedly higher incidence than previously assumed.PRI detected significantly more patients with impaired response than conventional platelet aggregation.