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J Thorac Cardiovasc Surg 1999;117:794-802
© 1999 Mosby, Inc.


CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

HEPARIN-COATED CARDIOPULMONARY BYPASS EQUIPMENT. I. BIOCOMPATIBILITY MARKERS AND DEVELOPMENT OF COMPLICATIONS IN A HIGH-RISK POPULATION

Vibeke Videm, MD, PhD, Tom Eirik Mollnes, MD, PhD, Erik Fosse, MD, PhD, Brit Mohr, MD, Kåre Bergh, MD, PhD, Tor-Arne Hagve, MD, PhD, Ansgar O. Aasen, MD, PhD, Jan L. Svennevig, MD, PhD

From the Department of Surgery A, Institute of Surgical Research, Department of Anaesthesiology, and Department of Clinical Chemistry, The National Hospital, Oslo University, Oslo; Department of Immunology and Blood Bank and Department of Microbiology, The Regional Hospital, Norwegian University of Science and Technology, Trondheim; and Department of Immunology and Transfusion Medicine, Nordland Central Hospital, Bodø, University of Tromsø, Tromsø, Norway.

The study was supported by The Norwegian Research Council, Medical Innovation at The National Hospital, and the Norwegian Council on Cardiovascular Research.

Received for publication March 10, 1998. Revisions requested July 9, 1998. Revisions received Oct 26, 1998. Accepted for publication Nov 6, 1998. Address for reprints: Vibeke Videm, MD, PhD, Department of Immunology and Blood Bank, The Regional Hospital, N-7006 Trondheim, Norway.

Objectives: 1. To study possible clinical benefits of heparin-coated cardiopulmonary bypass in patients with a broad range of preoperative risk factors. 2. To evaluate the correlation between the terminal complement complex and clinical outcome. 3. To identify clinical predictors of complement activation and correlates of granulocyte activation during cardiac surgery.
Methods: Blood samples from adults undergoing elective cardiac surgery with Duraflo II heparin-coated (n = 81) or uncoated (n = 75) cardiopulmonary bypass sets (Duraflo coating surface; Baxter International, Inc, Deerfield, Ill) were analyzed for activation of complement (C3 activation products, terminal complement complex), granulocytes (myeloperoxidase, lactoferrin), and platelets (ß-thromboglobulin) by enzyme immunoassays. Preoperative risk was assessed by means of the "Higgins' score." Complications (cardiac, renal, pulmonary, gastrointestinal, and central nervous system dysfunction, infections, death) were registered prospectively. Data were analyzed by analysis of variance, logistic regression, and linear regression.
Results and conclusions: Sixty-seven percent of the patients had predefined risk factors. Complications developed in 53 patients (34%), equivalently with and without heparin-coated bypass sets (P = .44-.82), despite a significant reduction in complement and granulocyte activation by heparin coating. No clear-cut relationship between the terminal complement complex and outcome was found, even if it was significant in the models for renal and central nervous system dysfunction and infections (P = .006). The Higgins' score was significantly related to complement activation (P < .05). Approximately 50% of the variation in granulocyte activation was explained by complement (P <= .01) and platelet activation (P < .05), heparin/protamine dose ratio (P = .02), duration of cardiopulmonary bypass (P < .01), and gender (P < .05). Therefore measures reducing complement activation alone will not necessarily reduce granulocyte activation sufficiently for clinical significance.




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