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Transplant Associated Coronary Artery Disease

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The Role of Immune Mechanisms in Cardiovascular Disease

Abstract

Heart transplantation is the clinically acceptable treatment for end-stage heart failure. Since the development of better immunosuppressive regimes and particularly the introduction of Cyclosporin A in 1983, which combats cellular rejection, short-term survival for heart transplant recipients has increased steadily with survival at 1 year being in the order of 85% (Kriett and Kaye 1990). The major medium to long-term complication is development of a proliferative occlusive disease of the vasculature of the allograft. This disease, variously described as transplant associated coronary artery disease (TxCAD; Rose and Dunn 1993), cardiac allograft vasculopathy (CAV; Hosenpud et al. 1992), accelerated coronary artery sclerosis (ACS; Yacoub and Rose, 1994) and graft coronary artery sclerosis (GCA; Schoen and Libby 1991), is a rapidly progressing disease which causes blockage of the coronary arteries. The incidence of TxCAD varies between heart transplant centres. Harefield Hospital, U.K. has an incidence of 6% at 1 year increasing to 17% at 3 years (see Dunn and Rose, 1993), however, other centres have reported incidences as high as 10%–20% at 1 year, 25%–40% at 3 years and at least 40%–50% at 5 years (Gao et al. 1989; Uretsky et al. 1987).

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© 1997 Springer-Verlag Berlin Heidelberg

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Wheeler, C.H., Collins, A.D., Dunn, M.J., Crisp, S.J., Yacoub, M.H., Rose, M.L. (1997). Transplant Associated Coronary Artery Disease. In: Schultheiss, HP., Schwimmbeck, P. (eds) The Role of Immune Mechanisms in Cardiovascular Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60463-8_14

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  • DOI: https://doi.org/10.1007/978-3-642-60463-8_14

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