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Cardiovascular Research 2002 54(3):492-494; doi:10.1016/S0008-6363(02)00396-6
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Do we have a new early marker of chronic transplant dysfunction now?

Wilfried Briest*

Carl-Ludwig-Institute of Physiology, University of Leipzig, Liebigstrasse 27, D-04103 Leipzig, Germany

* Tel.: +49-341-971-5500; fax: +49-341-971-5509 briestw@medizin.uni-leipzig.de

Received 18 March 2002; accepted 19 March 2002

The first 10% of the full text of this article appears below.

See article by Subramanian et al. [9] (pages 539–548) in this issue.

The development of chronic transplant dysfunction (CTD) has become a limiting factor for long-term graft survival, and it is today's most important problem in clinical organ transplantation after the first perioperative year. To date, CTD cannot be prevented by current immunosuppressive protocols [1,2]. Depending on the type of organ transplanted (liver, kidney, heart, lung), the incidence of CTD 3 years after engraftment varies from 4 to >50% [3–5]. Irrespective of the organ grafted, graft vessels eventually develop so-called transplant vascular sclerosis (TVS), which is, however, . . . [Full Text of this Article]


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