ENDOMYOCARDIAL HLA EXPRESSION IS INCREASED TO THE SAME EXTENT IN IDIOPATHIC AND SECONDARY DILATED CARDIOMYOPATHY

In a total of 22 failing hearts from human transplant recipients, the expression of major histocompatibility complex (MHC) molecules, the CD phenotype of infiltrating mononuclear cells, and the number of fibrob lasts were analyzed by immunohistochemistry. Compared with 10 non-fail ing control hearts, significantly higher morphometric area fractions o f HLA-ABC and HLA-DR with a concomitant increase of CD3-, CD4- and CD8 -positive cells were found to be comparable in 12 patients with idiopa thic dilated cardiomyopathy and in 10 patients with secondary heart fa ilure. Furthermore, the similarity of T-cell activation in idiopathic and secondary variants of the disease were substantiated by the follow ing observations: (1) the site-specific distribution of MHC molecules and mononuclear cells in the myocardium was comparable in idiopathic a nd secondary dilated cardiomyopathy; (2) 6 individuals with lymphocyti c aggregates in their myocardium in association with the highest level s of HLA-ABC expression were equally distributed among idiopathic and secondary patient subsets; and (3) expression of HLA-ABC and HLA-DR co rrelated with that of an endothelial cell marker, von Willebrand facto r, in failing myocardia of both study groups. In conclusion, no differ ence was found in increased MHC molecule expression in failing myocard ium of idiopathic and secondary variants of dilated cardiomyopathy, an d these entities were not differentially associated with infiltration by increased numbers of T lymphocytes. Hence, we postulate that these immunopathological features are consequences rather than causative fac tors of myocardial degeneration and dilatation. This view contrasts wi th the current concept that specific abnormalities of T cell-mediated immunity would reflect postinfectious autoimmunity and that this type of immune reaction was restricted to the idiopathic form of dilated ca rdiomyopathy.