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

Citation
M. Basora et al., Platelet function during cardiac surgery and cardiopulmonary bypass with low-dose aprotinin, J CARDIOTHO, 13(4), 1999, pp. 382-387
Citations number
43
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA
ISSN journal
10530770 → ACNP
Volume
13
Issue
4
Year of publication
1999
Pages
382 - 387
Database
ISI
SICI code
1053-0770(199908)13:4<382:PFDCSA>2.0.ZU;2-E
Abstract
Objective: To determine whether two low-dose regimens of aprotinin influenc e platelet function. Design: Prospective, randomized, single-blinded trial. Setting: University teaching hospital performing 600 cardiac operations per year. Participants:Fifty-nine patients scheduled for cardiac surgery undergoing c ardiopulmonary bypass (CPB) of expected duration of 60 minutes or more. Interventions: Patients were randomized into three groups. Group C (control ) included 21 patients who did not receive aprotinin. In group A(2), 17 pat ients received 14,286 kallikrein inhibitor units (KIU)/kg (2 mg/kg) of apro tinin before surgery, followed by a continuous infusion of 7,143 KIU/kg/h ( 1 mg/kg/h) until the end of surgery. In group A(4), 19 patients received 28 ,572 KIU/kg (4 mg/kg) of aprotinin before surgery, followed by the same inf usion. Measurements and Main Results: Postoperative bleeding and transfusion requi rements were significantly less in group A(4) Changes in platelet number an d function were similar in the three groups. Platelet aggregation was asses sed in four periods: before CPB (T-1), post-CPB (T-2), and 2 hours (T-3) an d 4 hours (T-4) after CPB. Platelet aggregation induced by adenosine diphos phate, 1 and 2 mu mol/L; ristocetin, 1 mg/mL; and arachadonic acid (AA), 1. 4 mmol/L, decreased at T-2 (p < 0.001) in all groups, and for the ristoceti n and AA groups, remained at less than baseline values at T-3 and T-4 In fi ve patients from each group, platelet receptors for glycoprotein IIb-IIIa ( GPIIb-IIIa) and expression of platelet activation markers, guanosine monoph osphate 140 (GMP-140) and lysosomal protein, were measured by flow cytometr y before and after CPB. Modifications in the expression of GPIIb-IIIa were always modest and without statistical significance. Platelet activation mar kers, GMP-140 or lysosomal protein, nearly doubled from baseline to post-CP B only in the A(4) group, whereas they remained stable in both other groups (statistically not significant). Conclusion: The two regimens of aprotinin, both considered low dosage, did not exert a protective effect on platelet function. Neither dose produced c hanges in platelet GPIIb-IIIa or platelet activation markers. However, blee ding and transfusion needs were decreased. Copyright (C) 1999 by W.B. Saund ers Company.