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J Thorac Cardiovasc Surg 1997;114:117-122
© 1997 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Received for publication July 19, 1996; revisions requested Sept. 12, 1996; revisions received Jan. 30, 1997. accepted for publication Jan. 31, 1997. Address for reprints: H. te Velthuis, PhD, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Department of Pathophysiology of Plasma Proteins, P.O. Box 9190, 1006 AD Amsterdam, The Netherlands.
Abstract
Objective: Heparin coating reduces complement activation on the surface of extracorporeal circuits. In this study we investigated its effect on activation of the contact system in 30 patients undergoing coronary artery bypass grafting with the use of a heparin-coated (Duraflo II, Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.; n = 15) or an uncoated extracorporeal circuit (n = 15). Methods: Plasma markers that reflect activation of contact (kallikrein-C1-inhibitor complexes), coagulation (prothrombin fragments F1+2), or fibrinolytic (plasmin-
2-antiplasmin complexes) systems were determined before and during the operation. The generation of kallikrein-C1-inhibitor complexes was reduced by 62% (p = 0.06) after the onset of cardiopulmonary bypass and by 43% (p = 0.026) after the cessation of bypass in the group in which a heparin-coated circuit was used compared with the group in which the circuit was uncoated. Generation was reduced by 58% (p = 0.06) when the ratio of kallikrein-C1-inhibitor to prekallikrein after onset of bypass was considered. We detected significant increases in F1+2 levels in both groups and increases in plasmin-2-antiplasmin complexes in the heparin-coated group at cessation of bypass, but no intergroup differences were observed. Thus use of heparin-coated extracorporeal circuits during cardiac operations reduces formation of kallikrein-C1-inhibitor complexes when compared with use of uncoated circuits. The heparin coating is not accompanied by similar reductions in coagulation or fibrinolysis, suggesting that thrombin and plasmin formation during cardiopulmonary bypass occurs mainly independently of the contact system activation
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