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J Thorac Cardiovasc Surg 1995;110:813-0818
© 1995 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Groningen, Leiden, and Amsterdam, The Netherlands
Financially supported by Bayer AG, Leverkusen, Germany.
Received for publication July 20, 1994. Accepted for publication Dec. 22, 1994. Address for reprints: C. R. H. Wildevuur, MD, Department of Cardiopulmonary Surgery, Research Division, University Hospital, Oostersingel 59, 9713 EZ Groningen, The Netherlands.
Abstract
The impaired hemostasis of aspirin-treated patients is an annoying problem during and after cardiopulmonary bypass. The hemostatic function of platelets comprises two mechanisms: the shear-induced and the cyclooxygenase pathways. Because the latter is inhibited in aspirin-treated patients, the hemostatic function depends mainly on the former pathway. To investigate the effect of cardiopulmonary bypass on the shear-induced pathway, a double-blind study of preoperative aspirin treatment (325 mg) and placebo was conducted in 40 patients undergoing coronary artery bypass grafting. Postoperative blood loss was higher in the aspirin-treated patients than in the placebo-treated patients (p < 0.05). The shear-induced hemostasis was monitored by the in vitro bleeding test (Thrombostat), which mimics bleeding through an injured arteriole. The shear-induced pathway of aspirin-treated platelets was not affected before cardiopulmonary bypass, but it was impaired more during the operation (p < 0.01) and remained worse afterward (p < 0.05), compared with that of placebo-treated platelets. The inhibitory effects of aspirin on thromboxane production and on collagen-induced platelet aggregation remained throughout the operation. In aspirin-treated platelets, the aggregation capacity induced by adenosine diphosphate was inhibited before the operation (p < 0.05) and showed substantial recovery during the operation (p < 0.05). These results suggest that the shear-induced pathway of aspirin-treated platelets is more vulnerable to cardiopulmonary bypass than the pathway in normal platelets and causes severe impairment of hemostasis afterward. (J THORACCARDIOVASCSURG1995;110: 813-8)
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