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.