Antiaggreganting Agents Do Not Influence the Sonoclot Profile

Abstract number: P1563

Paniccia R, Tellini I, Costanzo M, Ferrini S, Bolli P, Valente S, Giglioli C, Lombardi A, Gensini GF, Prisco D, Abbate R

Two new ‘point-of-care’ devices, which identify platelet function (PF) have recently become available. The PFA-100 system (DADE, USA) records the closure time (CT) taken by platelets to occlude a membrane coated with collagen and either epinephrine (CT/EPI) or ADP (CT/ADP). The Sonoclot analyzer (SIENCO Inc, USA) records changes in blood viscoelastic properties in the form of a graph. Sonoclot ‘signatures’ show a lag period (SonACT), corresponding to ACT, and a primary wave whose slope reflects the rate of fibrin formation (Clot rate – CR). Then, an inflection is produced as platelets are incorporated into the fibrin mesh and a secondary upslope leads to peak, which occurs at completion of fibrin formation. Subsequent downslope is produced as platelets induce further clot retraction The time to peak (minutes) (TP) reflects clot retraction, and is considered an indicator of PF. The purpose of this study was to investigate the changes of Sonoclot analysis and PFA 100 CT in 42 patients suffering from idiopathic sudden sensoneurinal hearing loss (ISSHL), treated with ASA (100 mg/die) for at least 1 month and in 54 patients undergoing PCI treated with ASA (325 mg/die) and clopidogrel (bolus: 300 mg followed by 75 mg/die) for a period of 2–5 days. A control group of 67 subjects, who had not taken any antiaggregating agent for 15 days before blood sampling, was also studied. In both patient groups the CT/EPI was prolonged compared to control group, so indicating ASA response. CT/ADP was prolonged in 22/42 ISSHL patients (52%) and in 18/56 PCI patients (33%). Instead, Sonoclot signature did not show any effect of ASA administration. In ISSHL patients TPs was similar compared to control group (11 ± 3.6 vs 11 ± 2.7 min) and only 1 patient showed a Sonoclot signature without clot retraction curve. In PCI patients a slight non significant prolongation of TP was observed in comparison with control group (11 ± 5.8 vs 11 ± 2.7 min) and only 2 patients showed a Sonoclot signature without clot retraction curve. The SonACTs were significantly (P < 0.05) shortened in ISSHL patients, whereas SonACTs of PCI patients did not show differences versus control group. In both patient groups CRs were signicantly higher than in control group (at least P < 0.05). These preliminary results suggest that antiaggregating agents in ASA responder patients – as evaluated by PFA 100 analysis – do not affect the Sonoclot profiles.