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J Thorac Cardiovasc Surg 1997;113:802-804
© 1997 Mosby, Inc.
BRIEF COMMUNICATIONS |
Yamanashi, Japan
Received for publication Oct. 8, 1996 accepted for publication Oct. 22, 1996. Address for reprints: Junya Katoh, MD, Second Department of Surgery, Yamanashi Medical University, 1110 Shimokato, Tamaho-cho, Nakakoma-gun, Yamanashi, 409-38 Japan.
Excessive bleeding after cardiac operations involving cardiopulmonary bypass (CPB), mostly a result of activated fibrinolysis and platelet dysfunction, remains a problem. Intraoperative administration of aprotinin significantly decreases postbypass blood loss; however, its use is limited because of complications such as inadequate heparinization during CPB and high cost.
1 Alternatively, Karski and associates
2 revealed that high-dose administration of tranexamic acid (TA) before CPB prevents excessive postoperative blood loss and reduces the need for blood transfusions. TA inhibits fibrinolysis by binding to the lysine binding site on plasminogen and plasmin, which is the binding site for fibrin.
It was reported that to counteract post-CPB fibrinolytic status and achieve hemostasis, high-dose TA administration was needed.
3 The elimination half-life of TA is about 80 minutes. To maintain concentrations of TA in the blood during hemostasis after CPB, we gave an additional half of the pre-CPB dose of TA during the post-CPB period. The objective of this study was to investigate whether an additional postbypass dose of TA affects post-CPB blood loss after cardiac operations.
Methods.
Ninety-three patients undergoing either coronary artery bypass grafting or heart valve operation were studied with their informed consent. Approval for the study was received from our hospital's ethics review board. Only one cardiac surgeon (K. T.) was involved in the study. In this prospective, randomized trial, the patients were divided into three groups of equal size. Patient characteristics are summarized in
Table I.
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Data are presented as means plus or minus the standard error of the mean. Comparisons of the mean values in the three groups were computed by one- and two-way analyses of variance.
Results.
Patient characteristics were similar among groups, as shown in
Table I.
Table II summarizes the volume of post-CPB mediastinal blood loss, blood product requirements, and postoperative hemoglobin levels. Blood loss during the operation, but after CPB, in the TA-2 group was significantly lower than that in the TA-1 group (reduced 40%, p = 0.0238) and that in the control group (reduced 242%, p = 0.0047). Blood loss during the first 6 hours after operation was also significantly reduced compared with that in the TA-1 (reduced 42%, p = 0.0050) and the control group (reduced 134%, p = 0.0003). Blood loss from 6 to 24 hours in the TA-2 group was significantly lower than that in the control group (reduced 49%, p = 0.0298); however, there was no significance compared with the TA-1 group (p = 0.1197).
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Comment.
TA may improve hemostasis after operation by two mechanisms. First, TA inhibits post-CPB plasmin-induced fibrinolysis by binding to the lysine binding site on plasmin and plasminogen. Second, TA inhibits plasmin-induced platelet activation, consequently preserving platelet function.
4 Concentrations of the TA administered before the CPB period may fall to less than half of the original level after CPB, because the elimination half-life of TA is about 80 minutes. To counteract a post-CPB fibrinolytic status, maintenance of the concentration of TA may be important. Therefore we hypothesized that an additional bolus dose of TA given soon after CPB might prevent reactivation of fibrinolysis and reinforce hemostasis.
The results proved our hypothesis was right. Blood loss in the TA-2 group was significantly reduced during each of the tested periods except from 6 to 24 hours after the operation. Furthermore, our study failed to show any increased incidence of perioperative thrombotic complications. We conclude that with additional administration of TA after CPB, blood loss after cardiac operations involving CPB will be safely reduced.
References
-aminocaproic acid. J Cardiothorac Vasc Anesth 1993;7:431-5.[Medline]This article has been cited by other articles:
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D. Zabeeda, B. Medalion, M. Sverdlov, S. Ezra, A. Schachner, T. Ezri, and A. J. Cohen Tranexamic acid reduces bleeding and the need for blood transfusion in primary myocardial revascularization Ann. Thorac. Surg., September 1, 2002; 74(3): 733 - 738. [Abstract] [Full Text] [PDF] |
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