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J Thorac Cardiovasc Surg 1996;111:1-12
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

SURFACE-BOUND HEPARIN FAILS TO REDUCE THROMBIN FORMATION DURING CLINICAL CARDIOPULMONARY BYPASS

Robert C. Gorman, MDa(by invitation), Nicholas P. Ziats, PhDc (by invitation), A. Koneti Rao, MDb (by invitation), Nicolas Gikakis, BSa (by invitation), Ling Sun, MDb (by invitation), Mohammed M. H. Khan, MDb (by invitation), Nina Stenach, CCPa (by invitation), Suneeti Sapatnekar, MDc (by invitation), Vibhuti Chouhan, PhDb (by invitation), Joseph H. Gorman, III, MD (by invitation), Stefan Niewiarowski, MD, PhDb (by invitation), Robert W. Colman, MDb (by invitation), James M. Anderson, MD, PhDc (by invitation), L. Henry Edmunds, Jr., MDa


Philadelphia, Pa., and Cleveland, Ohio

Supported by grants HL47186, HL33849, and HL48771 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

Address for reprints: L. Henry Edmunds, Jr., MD, Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA 19104.

Abstract

The hypothesis that heparin-coated perfusion circuits reduce thrombin formation and activity; fibrinolysis; and platelet, complement, and neutrophil activation was tested in 20 consecutive, randomized adults who had cardiopulmonary bypass. Twenty identical perfusion systems were used; in 10, all blood-contacting surfaces were coated with partially degraded heparin (Carmeda process; Medtronic Cardiopulmonary, Anaheim, Calif.). All patients received a 300 U/kg dose of heparin. Activated clotting times were maintained longer than 400 seconds. Cardiopulmonary bypass lasted 36 to 244 minutes. Blood samples for platelet count, platelet response to adenosine diphosphate, plasmaß-thromboglobulin, inactivated complement 3b, neutrophil elastase, fibrinopeptide A, prothrombin fragment F1.2, thrombin-antithrombin complex, tissue plasminogen activator, plasminogen activator inhibitor-1, plasmin{alpha}2-antiplasmin complex, and D-dimer were obtained at these times: after heparin was given, 5 and 30 minutes after cardiopulmonary bypass was started, within 5 minutes after bypass was stopped, and 15 minutes after protamine was given. After cardiopulmonary bypass, tubing segments were analyzed for surface-adsorbed antithrombin, fibrinogen, factor XII, and von Willebrand factor by radioimmunoassay. Heparin-coated circuits significantly (p < 0.001) reduced platelet adhesion and maintained platelet sensitivity to adenosine diphosphate (p = 0.015), but did not reduce release ofß-thromboglobulin. There were no significant differences between groups at any time for fibrinopeptide A, prothrombin fragment F1.2, or thrombin-antithrombin complex or in the markers for fibrinolysis: D-dimer, tissue plasminogen activator, plasminogen activator inhibitor-1, and{alpha}2-antiplasmin complex. In both groups, concentrations of prothrombin fragment F1.2 and thrombin-antithrombin complex increased progressively and significantly during cardiopulmonary bypass and after protamine was given. Concentrations of D-dimer,{alpha}2-antiplasmin complex, and plasminogen activator inhibitor-1 also increased significantly during bypass in both groups. Fibrinopeptide A levels did not increase during bypass but in both groups increased significantly after protamine was given. No significant differences were observed between groups for levels of inactivated complement 3b or neutrophil elastase. Radioimmunoassay showed a significant increase in surface-adsorbed antithrombin on coated circuits but no significant differences between groups for other proteins. We conclude that heparin-coated circuits used with standard doses of systemic heparin reduce platelet adhesion and improve platelet function but do not produce a meaningful anticoagulant effect during clinical cardiopulmonary bypass. The data do not support the practice of reducing systemic heparin doses during cardiac operations with heparin-coated extracorporeal perfusion circuitry. (J THORACCARDIOVASCSURG1996;111:1-12)




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