Cardiac Transplantation in Man

Abstract

To date, 12 of 18 patients receiving cardiac allografts at the Stanford Medical Center have died. Five of these died with some degree of graft failure resulting from rejection injury. The remaining seven demonstrated some morphologic evidence of rejection, but death was due to other causes including pulmonary hypertension in two, hemorrhage and sepsis in one, infection in two, cerebral embolism in one, and hepatic failure in one. Acute rejection injury was defined in 10 allografts, accelerated acute rejection in one, and chronic rejection in nine. The clinical signs of allograft rejection and their morphologic correlates were essentially as predicted from the study of orthotopic canine cardiac allografts. The clinical features and most of the anatomic lesions of acute rejection were usually reversible by current methods of immunosuppressive therapy. Chronic rejection, manifested primarily by obliterative intimal proliferation in coronary arteries, was present in most allografts obtained from patients surviving at least 1 month. Its severity was apparently not related to the quality of the host-donor leukocyte antigen match, and it was not routinely detectable clinically. This intimal thickening may limit long survival of patients undergoing cardiac transplantation.