Cytokines and acute heart failure Review uri icon

Overview

MeSH Major

  • Heart Failure
  • Inflammation Mediators
  • Interleukin-6
  • Tumor Necrosis Factor-alpha

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-alpha 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.

publication date

  • January 2008

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1097/01.CCM.0000297160.48694.90

PubMed ID

  • 18158483

Additional Document Info

start page

  • S9

end page

  • 16

volume

  • 36

number

  • 1 SUPPL.