[Tumor necrosis factor-alpha in heart failure: more questions than answers].

24 Heart failure (HF) as a clinical syndrome is posing an increasing social and economic burden, particularly in developed countries with their ageing populations.1 No single pathophysiological mechanism can explain the clinical manifestations of HF, which presents as the unfavourable endpoint of a many cardiac diseases; most commonly ischaemic heart disease, hypertension, idiopathic dilated cardiomyopathy (IDC), and advanced valvular disease. Our emerging understanding of the pathophysiologic mechanisms that underpin HF implicates inflammatory processes and the vascular endothelium in the progression of this disease. Heart failure is characterised by immune activation. Specific and non-specific inflammatory markers are elevated in patients with HF regardless of aetiology, and have been associated with the severity and progression of disease.2,3 Indeed, tumor necrosis factor alpha (TNF-α) levels, in particular, appear to provide incremental prognostic information in heart failure patients (reviewed by Baumgarten et al).4 Levine et al in 1990 were the first to demonstrate that TNF-α levels were significantly increased in patients with HF compared to controls and that increased TNF-α levels were associated with increased severity of disease.5 Other studies have consistently confirmed elevated levels of this cytokine in HF patients,4 indeed, pathophysiologically relevant concentrations seem to mimic aspects of the syndrome.4 Thus, in experimental stuED I TO R I A L S