title: Inflammatory markers in stable heart failure and their relationship with functional class.
abstract: OBJECTIVE
  While it appears to be clear that an inflammatory process occurs in heart failure (HF), it is still to be defined whether inflammation depends to a greater extent on HF etiology, functional class (FC), or the extent of depression of ejection fraction (EF). Our objectives were to analyze differences in inflammatory marker levels as compared to a healthy population, to assess differences depending on HF etiology, and to relate values with FC and EF.
  
  
  METHODS
  Fifty-nine consecutive outpatients with stable HF (57 + or - 9 years, 89% males) and 59 controls (55 + or - 8 years, 85% males) were enrolled into the study. Causes of HF included ischemic heart disease (n=24), idiopathic dilated cardiomyopathy (n=24), and miscellaneous conditions (n=11). Patients with decompensation in the past 6 months were excluded from the study. Protein fibrinogen, sialic acid, C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were measured. Echocardiography was performed in all study patients. FC was assessed using the NYHA classification.
  
  
  RESULTS
  A comparison of inflammatory marker levels between the HF and control groups showed significant differences in all markers, except for TNF-alpha. Protein fibrinogen in controls: 253 + or - 54 mg/dl, protein fibrinogen in HF: 294 + or - 67 mg/dl; p<0.05. Sialic acid in controls: 53 + or - 1 mg/dl, sialic acid in HF: 61 + or - 12 mg/dl; p<0.05. CRP in controls: 1.3 + or - 0.7 mg/dl, CRP in HF: 7.8 + or - 1.2 mg/dl; p<0.05. TNF-alpha in controls: 183 + or - 51 ng/ml, TNF-alpha in HF: 203 + or - 13 ng/ml; p=0.2. No differences were found between the different etiologies of HF. A positive association was seen between FC and protein fibrinogen and TNF-alpha (p<0.05), but not with EF.
  
  
  CONCLUSIONS
  Increased inflammatory marker levels related to FC of the patient, but not to EF, are found in chronic HF.
authors.affiliation: Avda. Ausias March 2, esc 2 pta 15. 46111, Rocafort, Valencia, Spain. igsanla@comv.es
authors.forename: Ignacio J
authors.initials: IJ
authors.lastname: Sánchez-Lázaro
authors.forename: Luis
authors.initials: L
authors.lastname: Almenar
authors.forename: Edelmiro
authors.initials: E
authors.lastname: Reganon
authors.forename: Virtudes
authors.initials: V
authors.lastname: Vila
authors.forename: Luis
authors.initials: L
authors.lastname: Martínez-Dolz
authors.forename: Vicenta
authors.initials: V
authors.lastname: Martínez-Sales
authors.forename: José
authors.initials: J
authors.lastname: Moro
authors.forename: Jaime
authors.initials: J
authors.lastname: Agüero
authors.forename: Víctor
authors.initials: V
authors.lastname: Ortiz-Martínez
authors.forename: Antonio
authors.initials: A
authors.lastname: Salvador
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000000981:diagnostic imaging* / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000097:blood / Q000145:classification* / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011859:Radiography
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators