Relationship between triiodothyronine and proinflammatory cytokines in chronic heart failure

Cytokines and thyroid hormones are involved in the biochemical changes associated to heart failure (HF). Aim. - 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-TNF alpha 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 INF alpha and CRP. IL-6 and INF alpha 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 13 syndrome, IL-6 and TNF alpha 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 13 syndrome (p < 0.01). The inflammatory markers were all inversely correlated with FF3 levels. Conclusion. - 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. (C) 2009 Elsevier Masson SAS. All rights reserved.