1014-94 Activated Endothelial and Interstitial Cells in Chronic Myocarditis – Expression of Endothelial Adhesion Molecules

A chronic immunological process — based on an initial event of myocarditis, probably triggered by a viral infection — is considered as a possible pathogenetic mechanism for dilated cardiomyopathy (DCM). The cytokine-respondent induction of adhesion molecules on endothelial cells (EC) enables the adhesion of immunocompetent cells to activated EC and the consecutive transmigration. We studied the expression pattern of adhesion molecules (immunoglobulin-superfamily and β1-integrins) in biopsies from patients with clinically suspected DCM (n=134). Immunohistologically negative specimens (n=61: poor lymphocytic infiltration) presented a missing or weak immunoreactivity of adhesion molecules on EC. An enhanced intensity of expression was noticed in the percentage of positive biopsies (n=73: pathologically increased lymphocytic infiltration >2.0 CD 3-lymphocytes per high power field/HPF, x400-fold magnification) depicted at the following table:Negative (n=61)Positive (n=73)AntigenEndothelInterstitiumEndothelInterstitiumHLA class I15%13%63%68%HLA DR20%18%55%64%ICAM-l/CD 5425%11%84%77%VCAM-123%–88%–VLA-β/CD 2926%26%89%70%VLA-β/CDw49d15%13%66%37%LFA-3/CD 5818%16%66%36%ConclusionsPathologically increased lymphocytic infiltrates in chronic myocarditis are associated with an endothelial and interstitial inflammatory activation. This phenomenon is independent of focally concentrated infiltrates. Thus, the implication of adhesion molecules in the immunohistological diagnosis of myocarditis could provide further information apart from the sole criterion “lymphocytic infiltration” and minimize the “sampling-error-effect”