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Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal

Dirk Westermann1, Diana Lindner, Mario Kasner

  • 1Department of Cardiology and Pneumology, Charité, Universititäts-Medizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, Germany. dirk.westermann@web.de

Circulation. Heart Failure
|November 16, 2010
PubMed

Insights

Cardiac inflammation drives extracellular matrix accumulation, worsening diastolic dysfunction in heart failure with normal ejection fraction (HFNEF). This fibrosis is linked to increased inflammatory cells and reduced collagen breakdown.

Area of Science:

  • Cardiology
  • Pathophysiology
  • Molecular Biology

Background:

  • The underlying mechanisms of heart failure with normal ejection fraction (HFNEF) remain incompletely understood.
  • Investigating the role of cardiac inflammation in extracellular matrix (ECM) remodeling is crucial for understanding HFNEF.

Purpose of the Study:

  • To determine the influence of cardiac inflammation on ECM remodeling in patients with HFNEF.
  • To explore the relationship between inflammation, fibrosis, and diastolic dysfunction in HFNEF.

Main Methods:

  • Utilized conductance catheter methods and echocardiography to assess left ventricular function in HFNEF patients and controls.
  • Analyzed endomyocardial biopsy samples for ECM proteins and inflammatory cells, and cultured cardiac fibroblasts to study gene expression.
  • Stimulated cardiac fibroblasts with transforming growth factor-beta (TGF-β) to investigate its effect on ECM production.

Main Results:

  • HFNEF patients exhibited diastolic dysfunction, increased cardiac collagen accumulation, and decreased matrix metalloproteinase-1 (MMP-1) levels compared to controls.
  • Inflammatory cells expressing the profibrotic factor TGF-β were identified in HFNEF patients.
  • In vitro, TGF-β stimulation induced fibroblast to myofibroblast transdifferentiation, increasing collagen and decreasing MMP-1 production.

Conclusions:

  • Cardiac inflammation contributes significantly to diastolic dysfunction in HFNEF.
  • Inflammation triggers ECM accumulation, specifically fibrosis, which directly impacts diastolic function in HFNEF.
Abstract

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