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Pathophysiological changes after cardiac transplantation: the role of chronic inflammation and rejection
  1. Barry A Boilson1,
  2. Christopher G A McGregor2,
  3. Sudhir S Kushwaha1
  1. 1William J Von Liebig Transplant Center, Mayo Clinic, Rochester, Minnesota, USA
  2. 2Division of Surgery and Interventional Science, University College London, London, UK
  1. Correspondence to Dr Barry A Boilson, William J Von Liebig Transplant Center, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; boilson.barry{at}mayo.edu

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In their paper published in Heart, Goland et al provide novel insights into changes in function of the transplanted heart within the first year (in press).1 This paper, together with a recent article also published in this journal,2 contribute greatly in illuminating a field in which physiological investigation has been largely uncharted.

After the first heart transplant was performed by Christiaan Barnard in 1967, success was variable until immunosuppressive regimens were perfected.3 With these measures, and improved understanding of the immunology of rejection, the incidence of hyperacute allograft failure, largely due to hyperacute rejection, has become rare.4 However, acute rejection is still a concern, although its incidence decreases with time after transplantation5 most probably owing to the development of immune tolerance. Chronic rejection is a more difficult problem as it follows an insidious course. The histological hallmarks of chronic rejection in the transplanted heart are fibrosis and allograft vasculopathy.6 There is a clear association between donor-specific anti-HLA antibodies and the development of chronic rejection.6 7 However, exact criteria for the diagnosis of antibody-mediated rejection continue to be debated.8

The paper by Goland et al is unique in tracking endomyocardial biopsy findings, together with an assessment of structure and function of the transplanted heart before and …

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