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J Thorac Cardiovasc Surg 1995;110:1732-1744
© 1995 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

FRESH VENOUS ALLOGRAFTS IN PERIPHERAL ARTERIAL RECONSTRUCTION IN DOGSEffects of histocompatibility and of short-term immunosuppression with cyclosporine A and mycophenolate mofetil

Quebec, Quebec, Canada

Received for publication Nov. 30, 1994. Accepted for publication Feb. 16, 1995. Address for reprints: Raynald Roy, PhD, Rheumatology and Immunology Research Center, Laval University Medical Center, 2705 Laurier Blvd., Room 9800, Ste-Foy, Quebec, Canada G1V 4G2.

Abstract

To date, no arterial substitute has been shown to be as effective as the autologous saphenous vein in peripheral revascularization procedures. In the present study, the venous allograft was evaluated as a vascular substitute in terms of patency and induction of host immune reactivity, whether used in major histocompatibility complex–incompatible, major histocompatibility complex–compatible, or immunosuppressed major histocompatibility complex–incompatible dogs. The immunosuppressive drug therapies were given for a period of 31 days, beginning 1 day before transplantation, and consisted of the use of cyclosporine A, mycophenolate mofetil, or a combination of both. All histoincompatible allografts were thrombosed at 4 or 8 weeks after transplantation with antibody development and cell-mediated cytotoxicity in the graft, whereas histocompatible allografts showed late stenosis without immunologic reactions directed toward donor cells. Given alone, neither cyclosporine A nor mycophenolate mofetil improved the overall patency of venous allografts; thrombosis occurred shortly after cessation of immunosuppression. Still, the cyclosporine A–mycophenolate mofetil combination therapy led to a 100% patency rate at 20 weeks after implantation and immune reactions were markedly reduced. This study shows that the fresh vein allograft is still an attractive and functional alternative to the autologous saphenous vein if the host immunologic reactions are controlled by cyclosporine A–mycophenolate mofetil immunosuppression. (J THORAC CARDIOVASC SURG 1995;110:1732-42)

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