Abstract
Until some decades ago chronic heart failure (CHF) has been considered a haemodynamic disorder with neurohormonal activation. Thus, the therapeutic strategies were oriented to correct cardiovascular disarrangement and counteract neurohormones. Although these therapeutic interventions improved CHF prognosis, mortality and morbidity CHF related remained high. In the recent years experimental and clinical researches increased our knowledge on CHF pathophysiology. Specifically, the involvement of inflammatory cytokines in the progression of CHF become more and more evident. Therefore, correction of cytokine network may represent a new therapeutic strategy approach in the management of CHF. However, results obtained from the first clinical trials with engineered anti-cytokine molecules, such as Infliximab and Etanercept, are discouraging. More knowledge on the complex interplay among inflammatory molecules in heart failure will allow its transfer to the design of more effective therapeutic candidates. The present review addresses current information on this controversial issue.
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