(Circulation. 1999;100:458-460.)
© 1999 American Heart Association, Inc.
Editorial |
Allograft Vasculopathy
Diagnosing the Nemesis of Heart Transplantation
From the Kaufman Center for Heart Failure, Department of Cardiology, the Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to James B. Young, MD, Medical Director, Kaufman Center for Heart Failure, Head, Section of Heart Failure and Cardiac Transplant Medicine, The Cleveland Clinic Foundation, Department of Cardiology (Desk F-25), 9500 Euclid Ave, Cleveland, OH 44195. E-mail youngj@cesmtp.ccf.org
Key Words: Editorials • transplantation • vasculopathy
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Introduction |
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Remarkable progress has been made with respect to cardiac transplantation over the past 3 decades.1 Few dramas are as compelling as a successful heart transplant in a patient who otherwise would die of cardiogenic shock. Improved outcomes relate to our greater (but yet incomplete) insight into the pathophysiology of allograft rejection. Still, the transplanted heart is not normal, and it is subjected to chronic immunologic assault. The long-term function of cardiac allografts is related primarily to the integrity of the organ at the time of transplantation and to rejection. More general systemic pathological processes, such as hypertension, lipid perturbation, diabetes, and infection, are also likely to take their toll.2 Although with contemporary immunomodulating strategies, cardiac allografts may perform satisfactorily for
20 years, a more reasonable expectation of
the half-life of these organs is between 7 and 10 years. It is
disturbing to note that the long-term survival of cardiac allografts
has changed little over the past 2 decades. Obviously, there is a
complicated interplay between immunologic and nonimmunologic factors
that determine the long-term function of the transplanted heart, but
so-called chronic rejection dictates outcome in large part. This
process (at times rapid) is a diffuse, obliterative
atherosclerosis, also referred to as allograft
arteriopathy or vasculopathy (veins rarely can be involved as well).
The pathophysiology of chronic cardiac allograft rejection is probably
analogous to that of chronic nephrosclerosis of
transplanted kidneys, biliary atresia of liver allografts, and
bronchiolitis obliterans after lung transplantation. Interestingly, we
still rather crudely separate rejection episodes into This article has been cited by other articles:
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