Ongoing myocardial damage in chronic heart failure is related to activated tumor necrosis factor and Fas/Fas ligand

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Koichi Setsuta1, Yoshihiko Seino, Takeshi Ogawa

  • 1Division of Cardiology, Department of Medicine, Tokyo Metropolitan Komagome Hospital, Japan.

Circulation Journal : Official Journal of the Japanese Circulation Society
|July 28, 2004
PubMed

Insights

Elevated heart-type fatty acid-binding protein (H-FABP) indicates ongoing myocardial damage in chronic heart failure (CHF). This damage is linked to increased tumor necrosis factor (TNF) and Fas/Fas ligand (FasL) system activation.

Area of Science:

  • Cardiology
  • Biomarkers
  • Heart Failure Pathophysiology

Background:

  • Elevated cardiac troponin T and H-FABP identify chronic heart failure (CHF) patients with ongoing myocardial damage (OMD) at high risk.
  • Cardiomyocyte necrosis/apoptosis via TNF and Fas/FasL may contribute to OMD development.

Purpose of the Study:

  • To investigate the relationship between H-FABP, TNF, and Fas/FasL system activation in CHF patients.
  • To assess if these markers correlate with heart failure severity.

Main Methods:

  • Serum concentrations of H-FABP, soluble Fas (sFas), and TNF-alpha were measured in 38 CHF patients.
  • Patients were categorized by New York Heart Association (NYHA) functional class (II vs. III+IV).
  • Correlations between markers and renal function were analyzed.

Main Results:

  • H-FABP, TNF-alpha, and sFas levels were significantly higher in NYHA III+IV patients compared to NYHA II patients.
  • Increased H-FABP concentrations strongly correlated with elevated TNF-alpha (r=0.57, p=0.0001) and sFas (r=0.69, p<0.0001).
  • These correlations were independent of renal function.

Conclusions:

  • OMD, indicated by H-FABP, is associated with activated TNF and the Fas/FasL system in CHF.
  • This suggests a pathophysiological role for cardiomyocyte necrosis/apoptosis in worsening heart failure.
  • H-FABP serves as a marker for membrane damage related to these inflammatory pathways.
Abstract

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