Several autoantibodies directed against cardiac cellular proteins including G-protein-linked receptors, contractile proteins and mitochondrial proteins, have been identified in patients with dilated cardiomyopathy (DCM). Among these autoantibodies, anti-β1-adrenoreceptor (AR) antibodies have long been discussed in terms of their pathogenetic role in DCM. Anti-β1-AR antibody-positive patients with DCM showed significant deterioration of NYHA functional class as well as reduced cardiac function compared to those in autoantibody-negative patients. Various studies with a limited number of patients indicate that the use of immunoadsorption to eliminate immunoglobulin G (IgG) significantly improves cardiac performance and clinical status in heart failure patients. Since removal of autoantibodies of the IgG3 subclass induces hemodynamic improvement and an increase in the left ventricular ejection fraction, antibodies belonging to IgG3 such as anti-β1-AR antibodies might play an important role in reducing cardiac function in patients with DCM. According to a recent report, however, the effect of hemodynamic improvement by immunoadsorption threapy was similar among patients who were positive and negative for anti-β1-AR antibodies, indicating that the beneficial effects of immunoadsorption might be not directly associated with the selective elimination of the β1-AR autoantibodies. Immunoadsorption therapy is a new therapeutic option for patients with DCM and heart failure, but further investigations are required to elucidate the specific antigens of cardiac autoantibodies responsible for the hemodynamic effects.
Keywords: Cardiomyopathy, adrenoreceptor, autoantibody, immunoadsorption, heart failure
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