[Platelet response to aspirin and clopidogrel. Biochemical evaluation, clinical impact, and pharmacological modulation].

In the vasculature, platelets contribute to thrombotic and inflammatory responses, key processes in atherothrombosis. During percutaneous coronary interventions, several studies have emphasized the deleterious impact of enhanced platelet aggregation on early clinical outcome. However, despite the significant interest of determining platelet responsiveness appears worth, the clinically accurate and practical platelet function assay is still not widespread available. Furthermore, standardized definitions of platelet "low-responders" are still lacking. Up to now, light transmission platelet aggregometry remains the "gold-standard". Platelets "points of care" assays might overcome the limitations of conventional optical platelet aggregation but need further validation in clinical settings. The most recent ACC/AHA guideline endorses a strategy of platelet monitoring in the highest risk patients (IIb C). In "low-responders" patients, clopidogrel dose escalation was demonstrated to improve platelet responsiveness. Others potential pharmacological solutions could include the switch for another thienopyridine. Indeed, prasugrel a P2Y12 receptor inhibitor was demonstrated to provide higher levels of inhibition of ADP-induced platelet aggregation.