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Ann Thorac Surg 2004;78:1522
© 2004 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, University Hospital of Groningen, Groningen, the Netherlands
b Department of Biomedical Engineering, Groningen University Medical Center, Groningen, the Netherlands
* Address reprint requests to Dr Boonstra, Department of Cardiothoracic Surgery, Groningen University Medical Center, Hanzeplein 1, 9713 EZ Groningen, the Netherlands (E-mail: p.w.boonstra{at}thorax.azg.nl).
Clopidogrel,also known as Plavix, is an inhibitor of adenosine diphosphate–induced platelet aggregation (thienopyridine derivate). In combination with aspirin, which blocks the thromboxane-mediated pathway, it is recommended as the standard therapy for prevention of coronary artery stent thrombosis [1]. These two drugs ensure that platelet function will be inhibited and that stent thrombosis will be prevented. As a consequence of the widespread use of these drugs in treating acute coronary syndromes and using percutaneous coronary interventions, patients will have an increased risk of major bleeding [2]. In this issue of The Annals, Chu and associates prospectively assessed hemostasis after operations performed in 80 patients having used clopidogrel and aspirin until the day of their operation [3]. Results were compared with those from 232 patients who did not have these drugs on board, or in a very low dose. This excellent paper confirms the widespread belief among cardiac surgeons that exposure of patients to clopidogrel in combination with aspirin before surgery increases blood loss and blood transfusion significantly. The conclusive advice of Chu and colleaagues is "waiting when possible." However, sometimes there is no time to wait. See page 1536
Clopidrogel and aspirin inhibit only two of seven important platelet activation pathways [4]. However, platelet function and the rest of the clotting system will be inhibited further when an on-pump operation will be performed in the patients having used clopidogrel and aspirin until the day of their operation.Several mechanisms are responsible for this. The first mechanism is caused by the damaging effects of shear stresses that are induced in the extracorporeal circuit, by cardiotomy suction, by heparin and protamine, and by thrombin and plasmin generation [5]. The second mechanism is caused by the dilution of clotting factors during cardiopulmonary bypass (CPB). The third mechanism is the one that is due to the direct use of clopidogrel and aspirin. These mechanisms together exceed the capacity of platelets to respond adequately on the activation of the clotting system. Chu and colleagues [3] found that hemostasis was normalized after 4 days of discontinuation of clopidrogel and aspirin, or when about 50% of the platelet pool was renewed. Their advice "waiting when possible" is based on this finding. To overcome such an increased risk of bleeding when there is no time to wait, aprotinin can be administered. Furthermore, platelets from healthy donors can be infused immediately after discontinuation of CPB.
When the pump is not used during coronary artery bypass graft surgery in patients having used clopidogrel and aspirin,the additional negative effect of CPB on platelet function will be absent. But it must be realized that, in particular with these off-pump procedures, patients have an increased procoagulant activity postoperatively: in other words, these off-pump patients are prone to graft closure [6]. As a consequence, hemostasis should not be improved in these patients, for example, by giving them aprotinin. Unfortunately, the Chu study contained too few patients who underwent off-pump coronary artery bypass graft surgery to perform a realistic statistical analysis that could support this suggestion. Further studies will be needed to help cardiac surgeons and interventional cardiologists to further reduce the morbidity and probably mortality rates of such patients.
References
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