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Aprotinin reduces the antiplatelet effect of clopidogrel

^a From the Karolinska Institute, Department of Cardiothoracic Surgery and Anesthesiology, Karolinska University Hospital, SE-17176 Stockholm, Sweden
^b From the Karolinska Institute, Department of Cardiology, Länssjukhuset i Sundsvall/Härnösand, Sundsvall, Sweden

*Corresponding author. Tel.: +46-8-51770830; fax: +46-8-331931.

E-mail address: gabriella.lindvall{at}karolinska.se (G. Lindvall).

Aprotinin reduces bleeding and transfusion rates in patients undergoing coronary surgery while on clopidogrel. However, safety studies have indicated that aprotinin may have a possible adverse effect related to an increased incidence of thromboembolic events. We therefore studied the adenosinediphosphate (ADP) mediated platelet aggregation before and after administration of aprotinin in patients on clopidogrel. Fifteen clopidogrel-treated patients with acute coronary syndrome undergoing coronary surgery were studied. ADP-mediated platelet aggregation and platelet count ratio (%) were measured before and after a bolus dose [2x10⁶ kallikrein inhibiting units (KIU)] of aprotinin. Aprotinin induced an increased aggregation in 11 of 15 patients (73%), and a decrease was registered in two patients (13%). The median (25th/75th percentile) ADP-mediated platelet aggregation before and after aprotinin was 84% (76/91) and 94% (86/97, P<0.01). Clopidogrel non-responders with >90% aggregation (n=4) had a median aggregation of 94.5% (91.5/97.5) vs. 82% (73/87, P<0.01) in the responders (n=11). The median increase in platelet aggregation after aprotinin was 8% (5/20) in the responders vs. 0% (–5.25/3, P<0.01) in the non-responders. Aprotinin increased ADP induced platelet aggregation from 84 to 94% in patients on clopidogrel, which corresponds to a median decrease in relative platelet inhibition of >50%.

Key Words: Coronary artery bypass surgery; Pathology/pharmacology/physiology; Blood; Coagulation; Platelets