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J Thorac Cardiovasc Surg 1998;116:1083-1084
© 1998 Mosby, Inc.
LETTERS TO THE EDITOR |
To the Editor:
We read with interest the brief communication by Alvarez
1 regarding his experience with 3 patients undergoing emergency coronary artery bypass grafting after platelet glycoprotein (Gp) IIb-IIIa inhibition. We also have observed excessive mediastinal bleeding and increased transfusion requirements when operating on patients exposed to the GpIIb-IIIa inhibitor abciximab. 2 Although the use of these potent inhibitors of platelet aggregation is a major breakthrough in the treatment of acute coronary syndromes, it is becoming clear that operating on patients with active GpIIb-IIIa inhibition represents a major challenge for the surgeon and a significant risk for the patient.
In our small, retrospective series, we noted that the interval from cessation of abciximab administration to operation was critical in determining the degree of coagulopathy after the operation. Patients who underwent an emergency operation within 12 hours of administration had significantly greater transfusion requirements and bleeding than did patients for whom the operation could be delayed longer than 12 hours. This clinical observation correlates with pharmacodynamic studies of abciximab, which demonstrate a half-life of approximately 12 hours. Platelet aggregation is severely dysfunctional in patients operated on within this period.
Optimal management of patients undergoing emergency cardiac operations after GpIIb-IIIa inhibition is evolving. We believe that there are 3 critical components for the surgical management of these patients: (1) transfusion therapy, (2) reduced heparinization, and (3) delay of surgical intervention when possible until after clearance of the inhibitor.
Transfusion therapy with pooled platelets is essential to increase the number of functional platelets. Abciximab is a chimeric human-murine monoclonal antibody fragment that tightly binds the GpIIb-IIIa receptor, so the pool of circulating, unbound drug is negligible. Transfused platelets therefore remain functional. The timing of platelet administration is as yet unclear; we transfuse after weaning from cardiopulmonary bypass. Additionally, because abciximab increases the activated clotting time in patients receiving heparin, we recommend a reduced heparin dosage for patients undergoing cardiopulmonary bypass, with the caveat that optimal heparin dosage in the presence of GpIIb-IIIa inhibitors is as yet undefined. We currently use a 150-µg/kg heparin dose and target an activated clotting time of 500 seconds. It is also critical that surgeons recognize the importance of delay between administration of the particular GpIIb-IIIa inhibitor and the operation; if possible, waiting for a period equivalent to the effective circulating half-life of the drug should be considered. This factor takes on additional relevance as newer, shorter-acting GpIIb-IIIa reach the market (tirofiban and eptifibitide have recently been approved by the Food and Drug Administration). The use of various "off-pump" techniques to avoid cardiopulmonary bypass and full heparinization should be considered when anatomically feasible and appropriate. Finally, delay of the operation until after clearance of the GpIIb-IIIa inhibitor is a reasonable strategy.
Alvarez 1 recommends the use of aprotinin as an adjunct to hemostasis in patients requiring an emergency operation in the face of GpIIb-IIIa inhibition. Aprotinin reduces mediastinal bleeding in patients at high risk; however, its salutory effect on platelet function is mediated through the GpIb receptor, affecting platelet adhesion rather than aggregation. Although it is tempting to try anything when faced with this difficult clinical problem, further information regarding the interaction between aprotinin and GpIIb-IIIa inhibitors is certainly needed.
The importance of the platelet thrombus in acute coronary ischemic syndromes and the ability to affect this process has been called a "new frontier in myocardial reperfusion therapy."3 For the significant numbers of patients who face cardiac surgery after profound platelet inhibition, however, these inhibitors of platelet aggregation are a 2-edged sword. In light of the number of percutaneous interventions performed annually in the United States and the number of various GpIIb-IIIa inhibitors (oral and intravenous) coming to market, the magnitude of this problem is certain to rise. To treat patients in these difficult cases, cardiac surgeons will need an effective management strategy that is based on an understanding of the pharmacodynamics of the different platelet inhibitors and the pathophysiology of platelet adhesion and aggregation.
Cornelius Dyke, MD
Carolinas Heart Institute
Carolinas Medical Center
Charlotte, NC 28232
James S. Gammie, MD
University of Pittsburgh Medical Center
Pittsburgh, PA 15213
12/8/92806
References
This article has been cited by other articles:
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  A. M. Lincoff, L. A. LeNarz, G. J. Despotis, P. K. Smith, J. E. Booth, R. E. Raymond, S. K. Sapp, C. F. Cabot, J. E. Tcheng, R. M. Califf, et al. Abciximab and bleeding during coronary surgery: results from the EPILOG and EPISTENT trials Ann. Thorac. Surg., August 1, 2000; 70(2): 516 - 526. [Abstract] [Full Text] [PDF]
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