Cytokines and acute heart failure

David Chen, Christian Assad-Kottner, Carlos Orrego, Guillermo Torre

Research output: Contribution to journalArticlepeer-review

91 Scopus citations


In patients with chronic heart failure, ongoing myocardial injury partially results from activation of the inflammatory system, with production and release of proinflammatory cytokines, activation of the complement system, production of autoantibodies, overexpression of major histocompatibility complex molecules, and expression of adhesion molecules that may perpetuate the inflammatory state. Acute decompensated heart failure modifies the course of chronic heart failure and worsens outcomes via a combination of potential mechanisms, including neurohormonal activation, apoptosis, and the inflammatory cascade. Proinflammatory cytokines, including tumor necrosis factor-α and interleukin-6, play a pathogenetic role in chronic heart failure, and anti-inflammatory immune therapy is currently under investigation. In acute decompensation of chronic heart failure, the change in the inflammatory cytokine activation cascade is less clear. Larger investigational studies are needed to assess the exact roles of circulating and intracardiac cytokines in this particular patient population.

Original languageEnglish (US)
JournalCritical Care Medicine
Issue number1 SUPPL.
StatePublished - Jan 1 2008


  • Chronic heart failure
  • Myocardial injury
  • Proinflammatory cytokines

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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