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Related Experiment Videos

Cytokines and heart failure.

W J Paulus1

  • 1Cardiovascular Center, OLV Ziekenhuis, Aalst, Belgium.

Heart Failure Monitor
|March 14, 2003
PubMed
Summary
This summary is machine-generated.

Pro-inflammatory cytokines like TNF-alpha contribute to heart failure by impairing cardiac function and causing muscle wasting. Therapies targeting these cytokines show promise in improving left ventricular (LV) performance.

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Area of Science:

  • Cardiology
  • Immunology
  • Molecular Biology

Background:

  • Pro-inflammatory cytokines, including interleukin-1, interleukin-6, and tumor necrosis factor-alpha (TNF-alpha), are rapidly expressed in the myocardium during left ventricular (LV) dysfunction.
  • This expression is triggered by factors like inflammation in myocarditis or elevated LV wall stress in conditions such as ischemic cardiomyopathy and chronic LV pressure/volume overload.

Purpose of the Study:

  • To investigate the role of myocardial cytokine expression in the pathogenesis of left ventricular dysfunction and heart failure.
  • To explore the mechanisms by which cytokines depress cardiac contractility and promote adverse LV remodeling.
  • To review therapeutic strategies targeting the cardioinflammatory response in heart failure.

Main Methods:

  • Analysis of myocardial and plasma cytokine concentrations in heart failure patients and experimental models.

Related Experiment Videos

  • Investigation of cytokine-mediated signaling pathways, including sphingosine production and calcium handling.
  • Review of pharmacological interventions affecting cytokine levels and activity.

    • Main Results:

    • Cytokine overexpression, particularly TNF-alpha, correlates with the progression of LV dilatation in transgenic mice.
    • Cytokines contribute to contractile dysfunction and adverse LV remodeling, potentially via sphingosine-induced interference with calcium handling.
    • Elevated cytokine levels in both myocardium and plasma contribute to systemic effects like muscle wasting and cachexia.

    Conclusions:

    • Cytokines play a significant role in the pathophysiology of heart failure, mediating both local myocardial effects and systemic consequences.
    • Potential sources of cytokine production include gut-derived endotoxins and peripheral tissue hypoperfusion.
    • Pharmacological agents and direct cytokine blockade (e.g., soluble TNF-alpha receptor fusion protein) demonstrate potential for improving cardiac function and exercise tolerance in heart failure.