Evidence for increased peripheral production of tumor necrosis factor-α in advanced congestive heart failure

Although cytokines have been associated with the progression of congestive heart failure (CHF) by multiple mechanisms,(1) the origin of these inflammatory mediators remains controversial. Myocardial tissue has been postulated as a relevant source of proinflammatory mediators, because both tissue necrosis factor (TNF)-alpha and TNF-alpha messenger ribonucleic acid (mRNA) have been detected in human failing hearts.(2,3) In addition, it has been recently proposed that bacterial translocation caused by mesenteric congestion, leading to endotoxemia and increased TNF-alpha levels, could be a trigger for peripheral immunoinflammatory activation in CHF.(4) Comparison between cytokine levels from peripheral venous and coronary sinus blood could help to indicate whether their production is predominantly peripheral or cardiac. To date, however, only 2 studies attempted to compare cytokines levels from arterial, venous, and coronary sinus blood in patients with CHF, demonstrating no significant differences between withdrawal sites.(5,6) In the present study, we evaluated patients with advanced CHF and compared TNF-alpha and soluble receptors I TNF-alpha and II TNF-alpha circulating levels from venous blood drawn from a peripheral anterocubital vein and from the coronary sinus.