IL-33/ST2 pathway and classical cytokines in end-stage heart failure patients submitted to left ventricular assist device support: a paradoxic role for inflammatory mediators?

Mediators Inflamm. 2013:2013:498703. doi: 10.1155/2013/498703. Epub 2013 Dec 10.

Abstract

Background: Inflammation is a critical process contributing to heart failure (HF). We hypothesized that IL-33/ST2 pathway, a new mechanism regulated during cardiac stress, may be involved in the functional worsening of end-stage HF patients, candidates for left ventricular assist device (LVAD) implantation, and potentially responsible for their outcome.

Methods: IL-33, ST2, and conventional cytokines (IL-6, IL-8, and TNF-α) were determined in cardiac biopsies and plasma of 22 patients submitted to LVAD implantation (pre-LVAD) and compared with (1) control stable chronic HF patients on medical therapy at the moment of heart transplantation without prior circulatory support (HT); (2) patients supported by LVAD at the moment of LVAD weaning (post-LVAD).

Results: Cardiac expression of ST2/IL-33 and cytokines was lower in the pre-LVAD than in the HT group. LVAD determined an increase of inflammatory mediators comparable to levels of the HT group. Only ST2 correlated with outcome indices after LVAD implantation.

Conclusions: IL-33/ST2 and traditional cytokines were involved in decline of cardiac function of ESHF patients as well as in hemodynamic recovery induced by LVAD. IL-33/ST2 pathway was also associated to severity of clinical course. Thus, a better understanding of inflammation is the key to achieving more favorable outcome by new specific therapies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytokines / physiology*
  • Female
  • Heart Failure / etiology*
  • Heart Failure / immunology
  • Heart Failure / therapy
  • Heart Transplantation
  • Heart-Assist Devices*
  • Humans
  • Inflammation Mediators / physiology*
  • Interleukin-1 Receptor-Like 1 Protein
  • Interleukin-33
  • Interleukins / physiology*
  • Male
  • Middle Aged
  • Receptors, Cell Surface / physiology*
  • Signal Transduction

Substances

  • Cytokines
  • IL1RL1 protein, human
  • IL33 protein, human
  • Inflammation Mediators
  • Interleukin-1 Receptor-Like 1 Protein
  • Interleukin-33
  • Interleukins
  • Receptors, Cell Surface