Background: Dilated cardiomyopathy (DCM) is linked to inflammatory cardiomyopathy (InfCM). To gain a profound insight into the underlying mechanisms, we phenotypically characterized pan leukocytes (CD18), naive T-lymphocytes (CD3, CD2, CD4, CD8), activated lymphocytes (LFA-1, LFA-3, VLA-4, ICAM-1, CD69, CD45R0), macrophages (Mac-1, 27E10), B-lymphocytes (CD19) and NK-cells (CD57) in DCM and control hearts.
Material/Methods: Biopsies from DCM patients (n=164, LVEF<40%) and specimens from non-cardiac death causes (controls; n=17) were immunostained. Biopsies exceeding >2.0 CD3+ lymphocytes per high power field/hpf and/or >1.5 CD3+ lymphocytes/hpf with numerous foci and HLA class I/DR abundance were evaluated positive for InfCM.
Results: InfCM+ biopsies (n=102; 63%) demonstrated significantly increased infiltrates with respect to all studied phenotypes except for CD19 and CD57 when compared with both DCM biopsies negative for InfCM (n=62) and the controls, whereas the latter two groups did not differ (Tukey-Kramer analysis). Virtually all phenotypes correlated with one another in multivariate
analysis (except for B-lymphocytes and NK cells). Whereas HLA class I/DR abundance was present in 14% of the controls and 26% of the DCM biopsies not yielding InfCM, InfCM+ biopsies demonstrated significantly (<0.001) higher frequencies of HLA abundance (76%).
Conclusions: The inflammatory process in InfCM comprises T-lymphocytes and macrophages, whereas Blymphocytes and NK-cells are not significantly increased. InfCM is associated with HLA induction. CD69+, CD45R0+ and adhesion molecule bearing infiltrates indicate the activated state of lymphocytes, and 27E10 of macrophages in InfCM, respectively. Our data are in accordance with the hypothesis of a ‘chronic active inflammatory process’ involved in DCM.

Keywords: Macrophages, Lymphocytes, Diagnosis, dilated cardiomyopathy, dilated cardiomyopathy