title: Tumor necrosis factor-alpha serum activity during treatment of acute decompensation of cachectic and non-cachectic patients with advanced congestive heart failure.
abstract: Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that produces left ventricular dysfunction and a negative inotropic effect in cardiac tissue when overexpressed in human subjects. Previous studies have shown that levels of circulating TNF-alpha are elevated in patients with advanced congestive heart failure (CHF) and especially in those with cardiac cachexia. To clarify the potential role of TNF-alpha in the unstable state of decompensated advanced CHF, we investigated the TNF-alpha serum activity in 25 cachectic and 22 non-cachectic CHF patients (New York Heart Association, NYHA functional classes III or IV), who were treated with intravenous diuretics and positive inotropic agents for acute decompensation of the disease, during a 5-day hospitalization period, as well as in 15 age-matched healthy control subjects. Cachectic CHF patients needed higher dosages of inotropic agents than non-cachectic patients and the determination of TNF-alpha serum concentrations in this patient group showed high levels of TNF-alpha at hospital admission (18.3 +/- 3.2 pg/ml) and a transient increase in circulating TNF-alpha during the treatment period with the highest levels on the 2nd day of hospitalization (32.5 +/- 7.1 pg/ml). The TNF-alpha serum levels were low in non-cachectic CHF patients and healthy controls on the 1st day (4.0 +/- 0.9 and 3.7 +/- 0.6 pg/ml, respectively) and did not change substantially during the course of the study. The present results show that TNF-alpha serum activity is transiently increased during the treatment of decompensated cachectic CHF patients only and may be related to the clinical instability and the consequent therapeutic interventions in this category of CHF patients.
authors.affiliation: 1st Department of Cardiology, Amalia Fleming Hospital, Athens, Greece.
authors.forename: J T
authors.initials: JT
authors.lastname: Parissis
authors.forename: K F
authors.initials: KF
authors.lastname: Venetsanou
authors.forename: D G
authors.initials: DG
authors.lastname: Mentzikof
authors.forename: N G
authors.initials: NG
authors.lastname: Ziras
authors.forename: C G
authors.initials: CG
authors.lastname: Kefalas
authors.forename: S M
authors.initials: SM
authors.lastname: Karas
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002100:Cachexia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004077:Digoxin / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D004280:Dobutamine / Q000008:administration & dosage / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005665:Furosemide / Q000008:administration & dosage / Q000627:therapeutic use; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D011379:Prognosis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D004232:Diuretics; D014409:Tumor Necrosis Factor-alpha; D004280:Dobutamine; D004077:Digoxin; D005665:Furosemide