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J Thorac Cardiovasc Surg 2001;121:0331-0335
© 2001 The American Association for Thoracic Surgery


Cardiopulmonary Support and Physiology

Heparin antibodies and thromboembolism in heparin-coated and noncoated ventricular assist devices

Andreas Koster, MDa, Matthias Loebe, MD, PhDb, Ralf Sodian, MDb, Evgenij V. Potapov, MDb, Roland Hansen, MDc, Johannes Müller, MDb, Fritz Mertzlufft, MD, PhDd, George J. Crystal, PhDe, Herrmann Kuppe, MD, PhDa, Roland Hetzer, MD, PhDb

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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