Haematologica 2004;89: supplement no. 8 - Supplements ...

XVIII Congress of the Italian Society for Hemostasis and Thrombosis Research, Rome, Sept. 30-Oct. 3, 200453be used for the rapid detection of adequate in vivoinhibition of platelet TxA2 by aspirin. Only prospectiverandomised trials correlating PFA100 resultswith long-term incidence of events, on one hand,and the evaluation of whether PFA100-based adjustmentof aspirin dosage affects the rate of success oftreatment, on the other, can validate the use ofPFA100 for the detection of aspirin resistance.CO-064COLLAGEN-INDUCED PLATELET THROMBOXANE A2PRODUCTION IN PATIENTS CHRONICALLY TREATED WITHASPIRINPulcinelli FM, Riondino S, Celestini A, Pignatelli P,Trifirò E, Di Renzo L, Violi FDipartimento di Medicina Sperimentale e Patologia,Università degli Studi di Roma "La Sapienza", ItalyA certain number of patients chronically treatedwith aspirin shows a reduced sensitivity to itsantiplatelet effect. Aim of the present study was toverify whether such a reduced sensitivity dependson a persistent thromboxane A2 (TxA2) formationand whether this production is caused by an incompleteinhibition of cyclooxygenase (COX)-1, or by thepresence of COX-2. We enrolled 196 patients takingaspirin (100-330 mg/day) in whom collagen-inducedplatelet aggregation and thromboxane A2 productionwere measured. In a subgroup of 96 patientsplatelet aggregation and TxA2 production were alsoinvestigated after in vitro treatment with a TxA2receptor antagonist (13-Azaprostanoic acid), aspirinor a COX-2 inhibitor (NS-398). Results: Patients weredivided into quartiles defined by the distribution ofthe TxA2 values. Platelet still produced TxA2 inresponse to collagen (128.7±21.6 pg/10 8 cells); TxA2production is significantly correlated with plateletaggregation (Spearman correlation coefficient=0.44; p