It is now generally accepted that chronically extensive stimulation of the cytokine system-and of TNFalpha in particular-is detrimental to the heart and to peripheral tissue and that such stimulation may contribute to the pathogenesis of congestive heart failure of various causes. During the past decade, basic and clinical research has provided growing evidence for the role of systemic and local inflammatory responses that, however, have so far failed to translate into new treatments for patients. The present paper represents an attempt to critically review the general concepts that lie behind the dichotomy existing between an impressive bulk of biologic research showing the role of TNFalpha as a pathogen in congestive heart failure and the difficulties in translating this evidence into patients' treatment.
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