Abstract

Initial graft failure, especially in hearts from “marinal” or “expanded” donors, and cardiac allograft asculopathy (CAV), which develops in more than half f transplant recipients who survive beyond 3 to 5 ears, represent the major limitations for the recipients’ hortand long-term survival. The causes for both of hese pathophysiologic processes are largely undefined nd most likely multifactorial; however, activation of he allograft endothelium and the ensuing inflammatory eaction represent early events, serving as potential herapeutic targets (Figure 1). This article initially discusses the pathophysiology of ndothelial activation in cardiac allografts and then ocuses on possible therapeutic strategies to minimize he activation of the endothelium, thereby reducing the ncidence of early and late organ failure.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.