PMID- 10072229 OWN - NLM STAT- MEDLINE DCOM- 19990325 LR - 20190622 IS - 0002-9149 (Print) IS - 0002-9149 (Linking) VI - 83 IP - 3 DP - 1999 Feb 1 TI - Effects of amiodarone on tumor necrosis factor-alpha levels in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. PG - 388-91 AB - Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of congestive heart failure and may be associated with an increase in mortality. A recent in vitro study showed that amiodarone decreases TNF-alpha production by human blood mononuclear cells in response to lipopolysaccharide. However, no previous clinical studies have determined the effect of chronic amiodarone therapy on TNF-alpha levels. Thus, the purpose of this study was to determine whether amiodarone affects TNF-alpha levels in patients with ischemic and nonischemic cardiomyopathy. TNF-alpha levels were analyzed by an enzyme-linked immunoassay using plasma samples at baseline, 1, and 2 years of follow-up in New York Heart Association class III patients (n = 40 in each of the placebo and amiodarone groups, mean ejection fraction 0.25+/-0.09) who were randomized in the Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy, a multicenter, double-blind, placebo-controlled study in which the effect of amiodarone on survival was investigated. TNF-alpha levels were elevated in both groups of patients at baseline, 6.6+/-3.1 and 7.7+/-5.3 pg/ml in the amiodarone and placebo groups, respectively (p = 0.3). There were no significant differences in demographic or clinical variables between the 2 groups. Amiodarone treatment was associated with a significant increase in TNF-alpha levels in patients with ischemic cardiomyopathy, 12.7+/-12.5 and 6.8+/-3.7 pg/ml in the amiodarone and placebo groups, respectively (p = 0.03) at 1 year. No change in TNF-alpha levels was observed in patients with nonischemic cardiomyopathy. In contrast to the in vitro data, amiodarone treatment is associated with an increase in TNF-alpha levels in patients with ischemic cardiomyopathy. This increase is not associated with an adverse effect on survival. FAU - Oral, H AU - Oral H AD - Division of Cardiology, University of Michigan, Ann Arbor, USA. FAU - Fisher, S G AU - Fisher SG FAU - Fay, W P AU - Fay WP FAU - Singh, S N AU - Singh SN FAU - Fletcher, R D AU - Fletcher RD FAU - Morady, F AU - Morady F LA - eng PT - Clinical Trial PT - Comparative Study PT - Journal Article PT - Multicenter Study PT - Randomized Controlled Trial PL - United States TA - Am J Cardiol JT - The American journal of cardiology JID - 0207277 RN - 0 (Anti-Arrhythmia Agents) RN - 0 (Biomarkers) RN - 0 (Tumor Necrosis Factor-alpha) RN - N3RQ532IUT (Amiodarone) SB - IM MH - Aged MH - Amiodarone/*therapeutic use MH - Anti-Arrhythmia Agents/*therapeutic use MH - Biomarkers/blood MH - Cardiomyopathy, Dilated/blood/*complications/drug therapy MH - Double-Blind Method MH - Electrocardiography MH - Enzyme-Linked Immunosorbent Assay MH - Follow-Up Studies MH - Heart Failure/*blood/*drug therapy/etiology MH - Hemodynamics/drug effects MH - Humans MH - Myocardial Ischemia/blood/*complications/drug therapy MH - Prognosis MH - Prospective Studies MH - Survival Rate MH - Tumor Necrosis Factor-alpha/*metabolism EDAT- 1999/03/11 00:00 MHDA- 1999/03/11 00:01 CRDT- 1999/03/11 00:00 PHST- 1999/03/11 00:00 [pubmed] PHST- 1999/03/11 00:01 [medline] PHST- 1999/03/11 00:00 [entrez] AID - S0002-9149(98)00874-1 [pii] AID - 10.1016/s0002-9149(98)00874-1 [doi] PST - ppublish SO - Am J Cardiol. 1999 Feb 1;83(3):388-91. doi: 10.1016/s0002-9149(98)00874-1.