Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

• Published in: The American journal of cardiology Vol. 83; no. 3; pp. 376 - 382
• Main Authors: Aukrust, Pål, Ueland, Thor, Lien, Egil, Bendtzen, Klaus, Müller, Fredrik, Andreassen, Arne K, Nordøy, Ingvild, Aass, Halfdan, Espevik, Terje, Simonsen, Svein, Frøland, Stig S, Gullestad, Lars
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.02.1999; Elsevier; Elsevier Limited
• Subjects: Adult; Aged; Biological and medical sciences; Biomarkers - blood; Cardiology; Cardiology. Vascular system; Cardiomyopathy, Dilated - blood; Cardiomyopathy, Dilated - complications; Cardiomyopathy, Dilated - physiopathology; Cardiovascular disease; Cytokines - blood; Female; Heart; Heart failure; Heart Failure - blood; Heart Failure - etiology; Heart Failure - physiopathology; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Immunoenzyme Techniques; Interleukin-1 - blood; Interleukin-10 - blood; Interleukin-6 - blood; Male; Medical sciences; Middle Aged; Monocytes - metabolism; Myocardial Ischemia - blood; Myocardial Ischemia - complications; Myocardial Ischemia - physiopathology; Receptors, Cytokine - blood; Receptors, Interleukin-6 - blood; Receptors, Tumor Necrosis Factor - blood; Stroke Volume; Transforming Growth Factor beta - blood; Tumor Necrosis Factor-alpha - metabolism; Human; Heart failure; Congestive hypertrophic cardiomyopathy; Pathogenesis; Heart disease; Cytokine; Cardiovascular disease; Myocardial disease; Blood plasma
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/S0002-9149(98)00872-8

Inflammatory cytokines may play a pathogenic role in the development of congestive heart failure (CHF). Elevated circulating levels of inflammatory cytokines have been reported in CHF, but most studies have focused on only a few cytokine parameters. However, the activity of these cytokines are modulated by soluble cytokine receptors and cytokines with anti-inflammatory activities, and in the present study several of these interacting factors were examined simultaneously in 38 CHF patients with various degrees of heart failure and in 21 healthy controls. Patients with CHF had increased plasma concentrations of tumor necrosis factor (TNF)α, interleukin-6, soluble TNF receptors and the soluble interleukin-6 receptor, glycoprotein (gp)130. They also had elevated ratios of TNFα/soluble TNF receptors and interleukin-6/soluble gp130 as well as enhanced interleukin-6 bioactivity in serum, suggesting inflammatory net effects. In addition to raised circulating levels of inflammatory cytokines, CHF patients with severe heart failure also had abnormalities in the levels of anti-inflammatory cytokines, with decreased levels of transforming growth factor β1 and inadequately raised interleukin-10 in relation to the elevated TNFα concentrations. This dysbalance between inflammatory and anti-inflammatory cytokines was also found in monocyte supernatants from CHF patients. The abnormalities in the cytokine network were most pronounced in patients with the most severe heart failure, and several of the immunologic parameters, in particular soluble gp130, were correlated with variables reflecting deranged hemodynamic status. The present study analyzing the complexity of the cytokine network in CHF, demonstrates profound disturbances in the levels of both inflammatory and anti-inflammatory mediators with a marked dysbalance favoring inflammatory effects.