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Autoantibodies produced against sarcolemmal Na-K-ATPase: possible upstream targets of arrhythmias and sudden death in patients with dilated cardiomyopathy

Akiyasu Baba, MD, PhD^*,*, Tsutomu Yoshikawa, MD and Satoshi Ogawa, MD

^* Department of Medicine, Kitasato Institute Hospital, Tokyo, Japan
Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.

View larger version (19K): [in a new window]   Figure 1 Enzyme-linked immunosorbent assay of autoantibodies produced against Na-K-ATPase in patients with dilated cardiomyopathy (DCM). O.D. = optical density.

View larger version (21K): [in a new window]   Figure 2 Na-K-ATPase enzyme activity incubated with purified IgG of patients with dilated cardiomyopathy (DCM) and of CTL. *p < 0.01.

View larger version (69K): [in a new window]   Figure 3 Western blots of autoantibodies produced against alpha subunit of Na-K-ATPase. (a) Immunopurified IgG of patients without autoantibodies; (b) with autoantibodies; (c) preincubation of Na-K-ATPase with (b), and (d) anti–Na-K-ATPase (alpha subunit) polyclonal antibodies.

View larger version (19K): [in a new window]   Figure 4 Total number of PVCs and the prevalence of nonsustained ventricular tachycardia (NSVT) in patients with or without Na-K-ATPase autoantibodies. *p < 0.001.

View larger version (13K): [in a new window]   Figure 5 Kaplan-Meier survival curves for cardiac sudden death according to the presence or absence of autoantibodies.