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J Thorac Cardiovasc Surg 2001;121:0331-0335
© 2001 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
From the Departments of Anesthesiologya and Cardiothoracic and Vascular Surgery,b Deutsches Herzzentrum Berlin; Institute of Laboratory Medicine and Pathobiochemistry,c Campus Virchow Klinikum, Charité, Berlin; Department of Anesthesiology and Intensive Care Medicine,d University of Homburg, Saar, Germany; Department of Anesthesiology,e Illinois Masonic Medical Center; and the Departments of Anesthesiology and Physiology and Biophysics, University of Illinois College of Medicine, Chicago, Ill.
Received for publication Feb 1, 2000. Revisions requested April 11, 2000; revisions received May 8, 2000. Accepted for publication Sept 5, 2000. Address for reprints: Andreas Koster, MD, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany (E-mail: koster{at}dhzb.de).
Objective: Coating of ventricular assist devices (VADs) with heparin improves the biocompatibility and may reduce the need for systemic anticoagulation. However, heparins are associated with the risk of formation of heparin/platelet factor 4 antibodies (HPF4/A) and the development of heparin-associated thromboemboli. We analyzed the occurrence of HPF4/A and thromboembolism in patients with heparin-coated and noncoated VADs.
Methods: One hundred patients were enrolled in the investigation. Fifty-seven received a heparin-coated (group 1) and 43 a noncoated (group 2) VAD. HPF4/A testing was performed before and 2 and 12 weeks after implantation by the heparin platelet factor 4 enzyme-linked immunosorbent assay.
Results: There was no significant difference in the occurrence of HPF4/A in the 2 groups (P = .102). Before the operation, 21 of the patients in group 1 had positive test responses and 25 in group 2. No patient had HPF4/A after termination of systemic heparinization. In group 1 there was no significant difference in the incidence of recurrent pump thromboses in patients who had positive test responses for HPF4/A (n = 11) when compared with those who had negative test responses (n = 9, P = .89). Twenty-one patients had HPF/A but no thromboembolism. However, all 22 patients who had thromboembolism had HPF4/A.
Conclusions: Heparin coating of the VAD surface does not enhance the occurrence of HPF4/A-associated immunologic or thrombogenic reactions. However, the presence of these antibodies is strongly associated with an increased risk of thromboembolism in patients with a VAD.
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