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J Thorac Cardiovasc Surg 2007;133:1147-1153
© 2007 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
a Department of Surgery, New York Presbyterian Hospital, College of Physicians & Surgeons, Columbia University, New York, NY
b Department of Medicine, New York Presbyterian Hospital, College of Physicians & Surgeons, Columbia University, New York, NY
c Department of Pathology, New York Presbyterian Hospital, College of Physicians & Surgeons, Columbia University, New York, NY.
Received for publication June 14, 2006; revisions received October 7, 2006; accepted for publication October 25, 2006. * Address for reprints: Mario C. Deng, MD, FACC, FESC, Director of Cardiac Transplantation Research, Department of Medicine, Columbia University College of Physicians & Surgeons, New York, NY 10032. (Email: md785{at}columbia.edu).
Objective: Infections are among the most common and serious complications of ventricular assist device implantation. These infections generally occur within the first 2 months after surgery. The basis for this high incidence of infection is not well established, so a murine intravascular infection model was developed with aortic implantation of the textured polyurethane patch material currently used in HeartMate ventricular assist devices (Thoratec Corporation Pleasanton, Calif).
Methods: Polyurethane patch material was placed in the wall of the mouse descending aorta. Mice were then infected with Staphylococcus aureus 1 or 14 days after implantation. In vitro adhesion studies were conducted with polyurethane membranes coated with endothelial cells and membranes coated with fibrinogen.
Results: Mice were susceptible to infection in both dose- and time-dependent fashions. The patch material was significantly more susceptible to infection at day 1 than day 14. Immunohistologic and morphologic studies demonstrated that the CD31+ cells deposited on the membrane surface phenotypically appeared to be endothelial cells. In vitro adhesion studies of polyurethane membranes coated with endothelial cells showed them to be less susceptible to S aureus binding than were membranes coated with fibrinogen.
Conclusion: Textured polyurethane membranes are less susceptible to infection as cellular deposition occurs. The time frame within which these membranes become populated with cellular material is consistent with the time-dependent clinical incidence of infection. Cellular coating of polyurethane may provide a strategy for reducing the risk of infection.
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