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Ann Thorac Surg 1997;64:1025
© 1997 The Society of Thoracic Surgeons
| The first 20% of the full text of this article appears below. |
See also page 1019.
DR JAMES K. KIRKLIN (Birmingham, AL):
Perhaps you could educate us for a moment about two points. I was intrigued with the rapidity of the development of this vasculitis lesion, which seems to be much more rapid than you would find in a human model of cardiac transplantation. First, do you believe that this is the same lesion, and, if so, how do you explain the very accelerated nature of it in these inbred swine? Second, I thought that perhaps an anti-CD4 antibody, which is necessary for induction of B cells might play some role in blocking this response, but instead it was an anti-CD8. Could you comment on what you believe the mechanism is?
DR ALLAN:
Doctor Kirklin's first question raises a commonly asked point concerning the validity of animal models in which cardiac allograft vasculopathy develops over several weeks to several months' time, whereas in patients we tend to think of this disease as a manifestation of chronic rejection, occurring several years after transplantation. First, I
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