Item Type: | Article |
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Title: | Hemodynamic improvement and removal of autoantibodies against beta-1-adrenergic receptor by immunoadsorption therapy in dilated cardiomyopathy |
Creators Name: | Mobini, R., Staudt, A., Felix, S.B., Baumann, G., Wallukat, G., Deinum, J., Svensson, H., Hjalmarson, A. and Fu, M. |
Abstract: | The removal of {beta}1-adrenergic receptor ({beta}1AR) autoantibodies by immunoadsorption (IA) has been proposed as a potential mechanism for the improvement of the left ventricular function in dilated cardiomyopathy (DCM). In the present study, the possible association between removal of the autoantibodies against the human {beta}1AR with the hemodynamic improvement induced by IA was investigated. IA was performed in 22 DCM patients (n=22; NYHA III-IV, EF<30%, stable medication). The {beta}1AR autoantibodies from column eluents (CE) were detected by enzyme-linked immunosorbent assay (ELISA) and BIAcore methods. CE of 32% (7/22) of the patients was found to be antibody-positive with ELISA or BIAcore. In addition, a bioassay system was also used for the detection of this autoantibody. Seventy-three percent (16/22) of the patients were found to be antibody-positive by this method. However, independent of the {beta}1AR antibody detection method, both antibody-positive and antibody-negative groups showed similar acute and prolonged hemodynamic improvements during IA therapy. Furthermore, antibody-positive and -negative groups received a comparable improvement of left ventricular ejection fraction. These results suggest that different mechanisms are involved in the hemodynamic improvement induced by IA. The beneficial hemodynamic effects induced by IA are not directly associated with the removal of {beta}1AR autoantibodies. |
Keywords: | {beta}1-Adrenergic Receptor, Autoantibodies, Immunoadsorption |
Source: | Journal of Autoimmunity |
ISSN: | 0896-8411 |
Publisher: | Academic Press |
Volume: | 20 |
Number: | 4 |
Page Range: | 345-350 |
Date: | June 2003 |
Official Publication: | https://doi.org/10.1016/S0896-8411(03)00042-8 |
PubMed: | View item in PubMed |
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