The Immunological Pathological Mechanism Of Dilated Cardiomyopathy

Objective To investigate the correlation between immune disorder and pathogenesis in the dilated cardiomyopathy(DCM) patients .Methods The lymphocytes, total T lymphocytes, help T lymphocytes(Th cells) and suppressor T lymphocytes(Ts cells) were counted in 36 DCM patients, 23 non-DCM patients and 21 normal controls with flow cytometry, and the serum concentration of autoantibody were measured in the patients or controls with indirect immunofluorescence technique . Results The lympocyte, total T cells, Th cells, and Ts cells were not significantly difference in tree groups (P> 0. 05). Th/Ts in DCM group was significantly higher than those in non-DCM group(P< 0.05) and normal control group (P < 0.05), and there was not significantly difference between non-DCM group(P> 0.05) and normal control group (P > 0.05). The geometric mean of the autoantibody is 1:62 in DCM group, 1:4 in non-DCM group, and 1:4 in normal control group. The geometric mean of the autoantibody in DCM group was significantly higher than those in non-DCM group(P< 0.05) or in normal control group (P< 0. 05), and there was not significantly difference between non-DCM group (P > 0.05) andnormal control group(P>0. 05) ;Th/Ts was positive correlation to the concentration of the serum concentration of autoantibody (rs' =0. 68, P<0. 01). Conclusion 1.The patients with DCM have immune disorder, expressed in their Th/Ts significantly higher, denoting the imbalance about the help and suppressor in the T lymphocyte. 2. All sorts of autoantibodies are in the serum of patients with DCM and the geometric mean of the autoantibody are significantly higher than those in non-DCM group or normal control group. 3. The geometric mean of the autoantibody in the serum of the patients with DCM is correlation to the imbalance in the cellular immunity.All sorts of autoantibodies result from the enhanced of help T cell and depressed of suppressor T cell. The Immunological disorders as was stated above may be involved in the immunopathogenesis of DCM.