Cytokines and acute heart failure

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

86 Scopus citations

Abstract

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)
Pages (from-to)S9-S16
JournalCritical care medicine
Volume36
Issue number1 SUPPL.
DOIs
StatePublished - Jan 2008

Keywords

  • Chronic heart failure
  • Myocardial injury
  • Proinflammatory cytokines

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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