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(Circulation. 1997;96:1386-1389.)
© 1997 American Heart Association, Inc.

Articles

Amiodarone Inhibits Production of Tumor Necrosis Factor- by Human Mononuclear Cells

A Possible Mechanism for its Effect in Heart Failure

Akira Matsumori, MD, PhD; Koh Ono, MD; Ryosuke Nishio, MD; Yoshisuke Nose, PhD; ; Shigetake Sasayama, MD, PhD

From the Department of Cardiovascular Medicine, Kyoto University, Japan.

Correspondence to Akira Matsumori, MD, PhD, Department of Cardiovascular Medicine, Kyoto University, 54 Kawaracho Shogoin, Sakyo-ku, Kyoto 606, Japan. E-mail amat{at}kuhp.kyoto-u.ac.jp

Background Recent studies suggest that cytokines such as tumor necrosis factor (TNF)- and interleukins (ILs) are capable of modulating cardiovascular function and that drugs used in the treatment of heart failure have various modulatory effects on the production of cytokines. This study was performed to examine the effects of amiodarone (a drug shown to be beneficial in some patients suffering from heart failure) versus other antiarrhythmic agents on the production of cytokines in vitro.

Methods and Results Human peripheral blood mononuclear cells (PBMC) were obtained from healthy volunteers. PBMC were cultured with 0.1, 1, and 10 µmol/L of amiodarone, quinidine, disopyramide, and lidocaine in the presence of lipopolysaccharide. After 24 hours' incubation, TNF-, IL-1ß, and IL-6 were measured in the culture supernatants by an enzyme-linked immunosorbent assay. TNF- production was inhibited by amiodarone but stimulated by quinidine in a concentration-dependent manner. Disopyramide and lidocaine tended to increase TNF- production. IL-6 production was decreased by amiodarone in all concentrations but was increased significantly by disopyramide. Modulation of IL-1ß production by amiodarone was biphasic and significantly increased at a concentration of 10 µmol/L.

Conclusions These previously unrecognized immunomodulatory effects of amiodarone may contribute to its beneficial effects in heart failure patients.

Key Words: amiodarone • heart failure • immune system • interleukins