Circulating levels of cytokines and their site of production in patients with mild to severe chronic heart failure

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• 作者：Mario Petretta ; Gian L. Condorelli ; Letizia Spinelli ; Francesco Scopacasa ; Maurizio de Caterina ; Dario Leosco ; Maria L. E. Vicario ; Domenico Bonaduce
• 刊名：American Heart Journal
• 出版年：2000
• 出版时间：December 2000
• 年：2000
• 卷：140
• 期：6
• 页码：E28
• 全文大小：147 K

文摘

Background Patients with chronic heart failure have elevated levels of proinflammatory cytokines; however, the mechanism for their increased expression and the site of their production are unknown. Methods Twenty-two patients with heart failure, New York Heart Association functional class II to IV, underwent hemodynamic evaluation and echocardiographic study. Blood samples for cytokine evaluation were performed in the ascending aorta, coronary sinus, inferior vena cava, and hepatic vein. Levels of tumor necrosis factor-α (TNF-α), its soluble receptors sTNF-RI and sTNF-RII, interleukin-6 (IL-6), IL-6 soluble receptor, soluble gp130, interleukin-2 soluble receptor, and soluble Fas were measured with enzyme-linked immunosorbent assay kits. Results IL-6 concentrations were higher in class IV patients than in class III patients, which in turn were higher than those in class II. TNF-α, sTNF-RI, and sTNF-RII were higher in class IV patients than in class III and II patients. Significant correlations were found between IL-6 concentrations and left ventricular end-systolic volume (r = 0.64; P < .001), pulmonary wedge pressure (r = 0.56; P < .01), and left ventricular ejection fraction (r = –0.56; P < .01). No correlation was found between TNF-α and its soluble receptors and left ventricular volumes or hemodynamic measures. Finally, no difference in cytokine concentrations was found among the different sample sites. Conclusions Among inflammatory cytokines, IL-6 concentrations better reflect the hemodynamic derangement in patients with heart failure. No cardiac or gut production of cytokines occurs in patients with mild to severe heart failure. (Am Heart J 2000;140:e28.)