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J Thorac Cardiovasc Surg 2001;122:630-632
© 2001 The American Association for Thoracic Surgery
Brief Communications |
From the Departments of Heart Surgery,a Cardiology,b and Anaesthesiology,c Triemli City Hospital, Zurich, Switzerland.
Received for publication Jan 18, 2001. Accepted for publication March 9, 2001. Address for reprints: Dr med Michele Genoni, Leit. Arzt, Department of Heart Surgery, Triemli City Hospital, Birmensdorferstr 397, CH-8063 Zurich (E-mail: michele.genoni{at}triemli.stzh.ch).
Interest in the development of new strategies to prevent platelet aggregation in acute coronary syndrome has been stirred by a growing appreciation of the role of platelet aggregation in thrombosis and of the resistance of platelet-rich thrombi to conventional fibrinolytic therapy. A highly effective approach is inhibition of the final platelet aggregation pathway, by blocking the activated platelet receptor glycoprotein (GP) IIb/IIIa. Kong and associates
1 have surveyed 16 clinical trials using a variety of inhibitors of GP IIa/IIIa and reported an overall 35% reduction in risk of 30-day mortality and myocardial infarction. However, other authors have reported increased hemorrhage in patients receiving the synthetic inhibitors eptifibatide 2 and abciximab. 3
Tirofiban (Aggrestat; Merck & Co, Inc, Whitehouse Station, NJ) is a nonpeptide tyrosine derivative that acts as a reversible, selective antagonist of GP IIb/IIIa. It induces more than 90% inhibition of platelet aggregation after a 30-minute infusion, with platelet function returning to near-baseline levels by 4 to 8 hours after the end of infusion. The use of tirofiban together with heparin in the treatment of acute coronary syndrome has given particularly promising results. Thus, in the PRISM trial, 4 patients who received tirofiban plus heparin showed a 33% risk reduction in the composite end point and a 36% risk reduction in refractory ischemia at 48 hours. In the RESTORE study, 5 the tirofiban group showed a 38% risk reduction in composite end point and a 39% risk reduction in myocardial infarction alone at 48 hours. In both studies the incidence of major bleeding was higher among patients in the tirofiban group, but the difference was not statistically significant. Because of concern over the potential disruption of blood coagulation during surgery after the use of inhibitors of platelet aggregation, current recommendations require tirofiban treatment to be halted at least 8 hours before the start of a surgical intervention. Clearly, this may put at risk some patients who have received tirofiban and who urgently require surgical intervention.
We have retrospectively compared the risk of hemorrhage in patients whose tirofiban infusion was stopped at different times preceding the start of surgery. Between December 1998 and April 2000, 40 patients who were already being treated with tirofiban in the Triemli City Hospital, Zurich, also required either emergency surgical procedures or operations that had to be performed earlier than planned. Seventeen of these 40 patients (Early Stop) had their tirofiban infusion stopped more than 8 hours previously (mean = 40.5 ± 39.1 hours), whereas in the other 23 (Late Stop) the tirofiban infusion was stopped less than 8 hours (mean = 3.4 ± 1.8 hours) before surgery. The high incidence of the need for preoperative intravenous heparin (Early Stop, 36%, Late Stop, 100%, P = .01) and an intra-aortic balloon pump (Early Stop, 29%, Late Stop, 69%, P = .01) in these patients demonstrates their clinical instability and the corresponding risk involved in delaying surgical intervention. On assessment before surgery, the two groups were comparable for the measured coagulation parameters (Table 1).
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). The amount of blood drained in the first 24 postoperative hours and the transfusion volumes (of erythrocytes, thrombocyte concentrate, and fresh frozen plasma) required during postoperative hospitalization were also recorded (Table 2). The results showed no clinically or statistically significant intergroup differences in the postoperative coagulation parameters, nor was any relationship observed between the volume of blood lost in the first 24 hours and the interval between the end of tirofiban infusion and surgery. All patients were monitored for perioperative myocardial infarction, including analysis of the electrocardiogram, creatine kinase, troponin, and myoglobin. Only 1 patient had a postoperative myocardial infarction, and this patient was in the Late Stop group.
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References
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