• J. Cardiothorac. Vasc. Anesth. · Aug 1999

    Randomized Controlled Trial Clinical Trial

    Platelet function during cardiac surgery and cardiopulmonary bypass with low-dose aprotinin.

    • M Basora, C Gomar, G Escolar, M Pacheco, G Fita, E Rodriguez, and A Ordinas.
    • Department of Anesthesiology, Hospital Clínic, University of Barcelona, Spain.
    • J. Cardiothorac. Vasc. Anesth. 1999 Aug 1;13(4):382-7.

    ObjectiveTo determine whether two low-dose regimens of aprotinin influence platelet function.DesignProspective, randomized, single-blinded trial.SettingUniversity teaching hospital performing 600 cardiac operations per year.ParticipantsFifty-nine patients scheduled for cardiac surgery undergoing cardiopulmonary bypass (CPB) of expected duration of 60 minutes or more.InterventionsPatients were randomized into three groups. Group C (control) included 21 patients who did not receive aprotinin. In group A2, 17 patients received 14,286 kallikrein inhibitor units (KIU)/kg (2 mg/kg) of aprotinin before surgery, followed by a continuous infusion of 7,143 KIU/kg/h (1 mg/kg/h) until the end of surgery. In group A4, 19 patients received 28,572 KIU/kg (4 mg/kg) of aprotinin before surgery, followed by the same infusion.Measurements And Main ResultsPostoperative bleeding and transfusion requirements were significantly less in group A4. Changes in platelet number and function were similar in the three groups. Platelet aggregation was assessed in four periods: before CPB (T1), post-CPB (T2), and 2 hours (T3) and 4 hours (T4) after CPB. Platelet aggregation induced by adenosine diphosphate, 1 and 2 micromol/L; ristocetin, 1 mg/mL; and arachadonic acid (AA), 1.4 mmol/L, decreased at T2 (p < 0.001) in all groups, and for the ristocetin and AA groups, remained at less than baseline values at T3 and T4. In five patients from each group, platelet receptors for glycoprotein IIb-IIIa (GPIIb-IIIa) and expression of platelet activation markers, guanosine monophosphate 140 (GMP-140) and lysosomal protein, were measured by flow cytometry before and after CPB. Modifications in the expression of GPIIb-IIIa were always modest and without statistical significance. Platelet activation markers, GMP-140 or lysosomal protein, nearly doubled from baseline to post-CPB only in the A4 group, whereas they remained stable in both other groups (statistically not significant).ConclusionThe two regimens of aprotinin, both considered low dosage, did not exert a protective effect on platelet function. Neither dose produced changes in platelet GPIIb-IIIa or platelet activation markers. However, bleeding and transfusion needs were decreased.

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