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Immunoadsorption therapy reduces oxidative stress in patients with dilated cardiomyopathy

Authors :
Jun Koyama
Hiroki Kasai
Yusuke Miyashita
Uichi Ikeda
Taku Yoshio
Yuichiro Kashima
Atsushi Izawa
Takeshi Tomita
Yoshikazu Yazaki
Masafumi Takahashi
Makoto Higuchi
Source :
World Journal of Cardiovascular Diseases. :305-312
Publication Year :
2012
Publisher :
Scientific Research Publishing, Inc., 2012.

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.

Details

ISSN :
21645337 and 21645329
Database :
OpenAIRE
Journal :
World Journal of Cardiovascular Diseases
Accession number :
edsair.doi...........c5af6df6b71c9da1d931563ba3720661