PMID- 14559127 OWN - NLM STAT- MEDLINE DCOM- 20040427 LR - 20190816 IS - 0167-5273 (Print) IS - 0167-5273 (Linking) VI - 91 IP - 2-3 DP - 2003 Oct TI - Treatment of acute inflammatory cardiomyopathy with intravenous immunoglobulin ameliorates left ventricular function associated with suppression of inflammatory cytokines and decreased oxidative stress. PG - 173-8 AB - Although an autoimmune mechanism has been postulated for myocarditis and dilated cardiomyopathy, immunosuppressive agents had not been shown to be effective. Potential benefits of intravenous immunoglobulin (IVIg) in the therapy of patients with myocarditis and recent onset of dilated cardiomyopathy were reported. Also, experimental studies showed that IVIg is an effective therapy for viral myocarditis by antiviral and anti-inflammatory effects. Accordingly, in the current study, the effects of IVIg in the patients were investigated with the analyses of inflammatory cytokines and oxidative stress. Nine patients (six in myocarditis, three in acute dilated cardiomyopathy) were treated with high-dose intravenous IVIg (1-2 g/kg, over 2 days). All were hospitalized with New York Heart Association (NYHA) class III to IV heart failure, left ventricular ejection fraction (LVEF) <40%, and symptoms for <6 months at the time of presentation. Five patients were diagnosed using endomyocardial biopsy. LVEF determined by echocardiography improved from 19.0+/-7.5% (mean+/-S.D.) at baseline to 35.4+/-9.1% at follow up (12.2+/-5.8 days after the treatment) (P<0.01). C-reactive protein and plasma inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) were decreased by this treatment. In addition, plasma level of thioredoxin, which regulates the cellular state of oxidative stress, was decreased by the treatment. All nine patients improved functionally to NYHA class I to II, and were discharged without side-effects. There have been no subsequent hospitalizations for heart failure during the course of follow-up (3 months-4.5 years). LVEF improved 16% of EF in the patients with myocarditis and acute dilated cardiomyopathy with the reduction of cytokines associated with improvement of oxidative stress state by high-dose of IVIg. Thus, IVIg seems to be a promising agent in the therapy of acute inflammatory cardiomyopathy in view of not only suppression of inflammatory cytokines but a reduction of oxidative stress. FAU - Kishimoto, Chiharu AU - Kishimoto C AD - Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, 54 Kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan. kkishi@kuhp.kyoto-u.ac.jp FAU - Shioji, Keisuke AU - Shioji K FAU - Kinoshita, Makoto AU - Kinoshita M FAU - Iwase, Tomoyuki AU - Iwase T FAU - Tamaki, Shunichi AU - Tamaki S FAU - Fujii, Manyo AU - Fujii M FAU - Murashige, Akihiro AU - Murashige A FAU - Maruhashi, Hiroyuki AU - Maruhashi H FAU - Takeda, Satoshi AU - Takeda S FAU - Nonogi, Hiroshi AU - Nonogi H FAU - Hashimoto, Tetsuo AU - Hashimoto T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - Int J Cardiol JT - International journal of cardiology JID - 8200291 RN - 0 (Biomarkers) RN - 0 (Cardiotonic Agents) RN - 0 (Cytokines) RN - 0 (Immunoglobulins, Intravenous) RN - 52500-60-4 (Thioredoxins) RN - 9007-41-4 (C-Reactive Protein) SB - IM MH - Acute Disease MH - Adult MH - Aged MH - Biomarkers/blood MH - C-Reactive Protein/drug effects/metabolism MH - Cardiomyopathy, Dilated/metabolism/physiopathology/*therapy MH - Cardiotonic Agents/therapeutic use MH - Cytokines/*biosynthesis/*drug effects MH - Female MH - Follow-Up Studies MH - Hospitalization MH - Humans MH - Immunoglobulins, Intravenous/*therapeutic use MH - Intra-Aortic Balloon Pumping MH - Male MH - Middle Aged MH - Myocarditis/metabolism/physiopathology/*therapy MH - Oxidative Stress/*drug effects MH - Pulmonary Wedge Pressure/drug effects/physiology MH - Statistics as Topic MH - Stroke Volume/drug effects/physiology MH - Thioredoxins/biosynthesis/blood/drug effects MH - Treatment Outcome MH - Ventricular Function, Left/*drug effects/*physiology EDAT- 2003/10/16 05:00 MHDA- 2004/04/28 05:00 CRDT- 2003/10/16 05:00 PHST- 2003/10/16 05:00 [pubmed] PHST- 2004/04/28 05:00 [medline] PHST- 2003/10/16 05:00 [entrez] AID - S0167527303000020 [pii] AID - 10.1016/s0167-5273(03)00002-0 [doi] PST - ppublish SO - Int J Cardiol. 2003 Oct;91(2-3):173-8. doi: 10.1016/s0167-5273(03)00002-0.