title: Relationship between triiodothyronine and proinflammatory cytokines in chronic heart failure.
abstract: Cytokines and thyroid hormones are involved in the biochemical changes associated to heart failure (HF).
  
  
  OBJECTIVE
  Aims of the study were to investigate: plasma circulating levels of the cytokines Interleukine-6 (IL-6) TNF alpha and C reactive protein (CRP) in patients with stable HF in relation to the severity of left ventricular dysfunction; the relationship between these inflammatory markers and thyroid hormones.
  
  
  METHODS
  One-hundred and sixty-six patients (121 males, age 64+/-12), with non-ischemic cardiomyopathy, were admitted to the Institute of Clinical Physiology for progressive deterioration of symptoms. Forty-eight healthy subjects (30 males, age range 26-75 years) were also enrolled as control group (Group N). High sensitivity (hs)-IL-6 and hs-TNFalpha were quantified using solid phase sandwich ELISA kits. Hs-CRP was measured by Immulite System.
  
  
  RESULTS
  In the whole population (HF and N), the association between inflammatory markers and age resulted statistically significant only for IL-6 serum concentration (p<0.001) but not for TNFalpha and CRP. IL-6 and TNFalpha were strongly higher in the HF in comparison with N (p<0.001) while CRP showed a less significant difference (p<0.05). Whole population showed a negative association between IL-6 and EF% and between CRP and EF% (respectively p<0.01, r=-0.23; p<0.05, r=0.19). Comparing normal subjects with two classes of patients, respectively with EF>35% and EF<35%, we clearly observed the progressive enhancement of the inflammatory markers. Considering normal subjects, patients without and with low T3 syndrome, IL-6 and TNFalpha increased progressively from normal to patients with fT3<2 pg/ml (p<0.01 and p<0.01) while CRP only respect to the group with low T3 syndrome (p<0.01). The inflammatory markers were all inversely correlated with FT3 levels.
  
  
  CONCLUSIONS
  Because low FT3 serum concentration represents a negative prognostic index, it is likely that impairment of T3 production and enhanced inflammation represent pathogenic mechanisms linked to HF progression.
authors.affiliation: G. Monasterio Foundation, Pisa, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Lubrano
authors.forename: A
authors.initials: A
authors.lastname: Pingitore
authors.forename: A
authors.initials: A
authors.lastname: Carpi
authors.forename: G
authors.initials: G
authors.lastname: Iervasi
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D018450:Disease Progression; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000150:complications; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000150:complications; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D013318:Stroke Volume; D014284:Triiodothyronine / Q000097:blood* / Q000172:deficiency; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*; D018487:Ventricular Dysfunction, Left / Q000097:blood
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D014284:Triiodothyronine; D002097:C-Reactive Protein