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Heart Program

Investigators: Drs. Phil Halloran, Daniel Kim, , Ian Paterson,  Konrad Famulski, Jeff Reeve.

From our recent work on human heart allograft biopsies, we have obtained new evidence that there is a correlation between invasive Quilty lesions (Quilty B) and a pathological molecular phenotype in human endomyocardial allograft biopsies. The ‘Quilty’ lesion is a type of inflammation in heart transplants.  Two histological variants of Quilty lesions were described: one where the dense lymphocytic infiltrates are confined to the endocardium (Quilty A), and another where the infiltrates extend (“spill-over”) invasively into the adjacent underlying myocardium and shows extensive proliferation of small capillaries (Quilty B).

Since its first description, several hypotheses have been proposed to explain the pathogenesis of these sub-endomyocardial infiltrates. Some of these include the use of cyclosporine-based immunosuppression, variants of post-transplant lymphoproliferative disorders, viral infections, and chronic rejection. In this regard, Quilty B lesions are known to be frequently misdiagnosed as acute rejection episodes. However, none of these hypotheses have been proven conclusively. Clear and consistent associations of Quilty lesions with cellular or antibody mediated rejection, viral infection, subsequent development of transplant vasculopathy, or allograft survival have not been established. Nevertheless, it is striking to observe that Quilty lesions are not found in the hearts of patients who receive immunosuppression for organ transplants other than the heart. Thus the Quilty lesion seems to be a phenomenon that occurs only in the transplanted heart, and we propose to elucidate its pathogenesis, immuno-pathological role and clinical relevance.