Palmer D C, Tsai C C, Roodman S T, Codd J E, Miller L W, Sarafian J E, Williams G A
Transplantation. 1985 Apr;39(4):385-8.
Heart graft arteriosclerosis remains a severe and irreversible complication of allogeneic heart transplantation despite prophylactic therapy. Immunologically mediated endothelial damage has been proposed as a stimulus for the development of graft arteriosclerosis. The vascular lesions may accumulate large amounts of lipid resembling atheromas, or may be purely proliferative, as illustrated in the case of a 42-year-old heart transplant patient who developed slowly progressive graft dysfunction at eight months posttransplantation. Endomyocardial biopsy ten months posttransplantation revealed proliferative arteriolar occlusion, while changes on the coronary angiogram were minimal. Repeat biopsy at eleven months showed ischemic myocardial necrosis. The patient expired shortly thereafter. On postmortem examination, proliferative graft arteriosclerosis affecting both intramural and epicardial vessels was present, along with massive biventricular infarction. Tissue immunofluorescence studies demonstrated extensive vascular deposition of immunoglobulin and complement. We propose that (1) the presence of proliferative arteriolar occlusion on endomyocardial biopsy is predictive of poor heart graft survival; (2) proliferative graft arteriosclerosis may appear as advanced small vessel disease before extensive large vessel involvement is detected by coronary angiogram; and (3) immunofluorescence results support an immune-mediated mechanism of vascular injury in proliferative heart graft arteriosclerosis.
