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Factor VIII/von Willebrand factor concentrate therapy for ventricular assist device–associated acquired von Willebrand disease

Authors

  • Melissa Cushing,

    Corresponding author
    1. From the Department of Pathology and Laboratory Medicine and the Department of Internal Medicine, Weill Cornell Medical Center, New York, New York; and the BloodCenter of Wisconsin, Milwaukee, Wisconsin.
      Melissa M. Cushing, MD, Department of Pathology and Laboratory Medicine, Weill Cornell Medical Center, 525 E. 68th Street, Box 251, New York, NY 10065; e-mail: mec2013@med.cornell.edu.
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  • Kathy Kawaguchi,

    1. From the Department of Pathology and Laboratory Medicine and the Department of Internal Medicine, Weill Cornell Medical Center, New York, New York; and the BloodCenter of Wisconsin, Milwaukee, Wisconsin.
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  • Kenneth D. Friedman,

    1. From the Department of Pathology and Laboratory Medicine and the Department of Internal Medicine, Weill Cornell Medical Center, New York, New York; and the BloodCenter of Wisconsin, Milwaukee, Wisconsin.
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  • Tomer Mark

    1. From the Department of Pathology and Laboratory Medicine and the Department of Internal Medicine, Weill Cornell Medical Center, New York, New York; and the BloodCenter of Wisconsin, Milwaukee, Wisconsin.
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Melissa M. Cushing, MD, Department of Pathology and Laboratory Medicine, Weill Cornell Medical Center, 525 E. 68th Street, Box 251, New York, NY 10065; e-mail: mec2013@med.cornell.edu.

Abstract

BACKGROUND: Acquired von Willebrand disease (aVWD) can lead to a propensity to bleed, and many different modalities have been used to treat this condition. The efficacy of these agents in patients with aVWD secondary to cardiac assist devices is not fully understood.

STUDY DESIGN AND METHODS: A case is reported of a patient with two risk factors for aVWD, multiple myeloma and ventricular assist device (VAD), who was successfully treated with von Willebrand factor (VWF)/Factor VIII concentrate (Humate-P, CSL Behring) during the bridge to VAD replacement.

RESULTS: Although continued absence of high-molecular-weight VWF persisted after VWF replacement with Humate-P, the patient's VWF antigen and activity increased and clinical hemostasis was achieved. The VAD clotted on a few occasions, despite a continuous heparin infusion; however, these events were resolved with temporarily holding the Humate-P. A VAD exchange was performed and the patient was successfully bridged to heart transplant.

CONCLUSION: The treatment of VAD-associated aVWD may be augmented with Humate-P, and successful treatment can allow a bridge to heart transplantation. However, careful monitoring for thrombosis in the VAD circuit must be undertaken.

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