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Abstract
Several literatures have reported that the elimination of autoantibodies by immunoadsorption (IA) therapy induced short- and long-term improvements in cardiac function of patients with dilated cardiomyopathy (DCM). We assessed whether reduction in oxidative stress was related to the mechanism underlying left ventricular functional benefit from IA. We studied 7 patients with DCM (New York Heart Association (NYHA) functional class III/IV). Autoantibodies were removed with IA by passing patients’ plasma over tryptophan columns. The level of anti-β1-adrenoreceptor (AR) autoantibodies was measured by enzyme- linked immunosorbent assay. The level of diacron- reactive oxygen metabolite (d-ROM) was determined as a marker of oxidative stress. During IA, the anti- β1-AR autoantibodies titers of all the patients decreased significantly from 27.8 ± 5.0 to 18.7 ± 5.5 U/ml (p < 0.01). IA induced the following hemodynamic improvements: cardiac index increased from 1.71 ± 0.40 to 1.97 ± 0.41 l/min/m2 and left ventricular ejection fraction (LVEF) increased from 22.8 ± 6.1 to 29.1±9.1% (p < 0.05). d-ROM level decreased significantly from 392.7 ±17.0 to 314.1 ± 22.0 Carratelli units (p < 0.05), and was negatively correlated with LVEF before and after IA therapy (r = －0.601, p < 0.05). The anti-β1-AR autoantibodies, LVEF and d- ROM returned to the baseline levels at 12 months after IA. In conclusion, oxidative stress reduction may be responsible for the beneficial effect of IA therapy in patients with DCM.
Highlights
Dilated cardiomyopathy (DCM) is a chronic myocardial disease characterized by progressive ventricular enlargement and myocardial contractile malfunction [1]
Several literatures have reported that the elimination of autoantibodies by immunoadsorption (IA) therapy induced short- and long-term improvements in cardiac function of patients with dilated cardiomyopathy (DCM)
Several literatures reported that the elimination of anti-β1-AR autoantibodies with immunoadsorption (IA) therapy induced short- and long-term improvements in the left ventricular ejection fraction (LVEF), cardiac output, and New York Heart Association (NYHA) functional class in patients with DCM, who were refractory to conventional medical therapy
Summary
Dilated cardiomyopathy (DCM) is a chronic myocardial disease characterized by progressive ventricular enlargement and myocardial contractile malfunction [1]. The fundamental mechanisms responsible for the development and progression of left ventricular failure have not yet been completely elucidated, a variety of experimental studies suggest that alterations in the immune system might be involved in the pathogenesis of DCM [3]. Several autoantibodies directed against cardiac cellular proteins, including G-protein-linked receptors, contractile proteins, and mitochondrial proteins, have been identified in patients with DCM. Several literatures reported that the elimination of anti-β1-AR autoantibodies with immunoadsorption (IA) therapy induced short- and long-term improvements in the left ventricular ejection fraction (LVEF), cardiac output, and New York Heart Association (NYHA) functional class in patients with DCM, who were refractory to conventional medical therapy
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