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Activated nuclear transcription factor kappaB in patients with myocarditis and dilated cardiomyopathy--relation to

Peter Alter1, Heinz Rupp, Bernhard Maisch

  • 1Philipps University of Marburg, Department of Internal Medicine-Cardiology, Germany. palter@med.uni-marburg.de

Biochemical and Biophysical Research Communications
|November 22, 2005
PubMed

Insights

Nuclear factor-kappaB (NFkappaB) activation is elevated in myocarditis, correlating with preserved left ventricular function. This suggests NFkappaB plays a role in early inflammatory stages and may protect against cardiac dilation.

Area of Science:

  • Cardiology
  • Immunology
  • Molecular Biology

Background:

  • Myocarditis, an inflammation of the heart muscle, can be triggered by infections or autoimmune conditions.
  • The role of persistent viral genomes and ongoing adverse processes in myocarditis pathogenesis remains unclear.
  • Nuclear factor-kappaB (NFkappaB) is a key transcription factor implicated in inflammatory and remodeling processes.

Purpose of the Study:

  • To investigate the activation status of NFkappaB in patients with myocarditis and its association with cardiac function and viral persistence.
  • To determine if NFkappaB activation is linked to adverse cardiac remodeling in myocarditis.

Main Methods:

  • Echocardiography and cardiac catheterization were used to assess hemodynamics in 93 patients with suspected myocarditis/cardiomyopathy.
  • Endomyocardial biopsies were analyzed using immunohistochemistry and PCR for viral genomes and activated NFkappaB.
  • Statistical analyses correlated NFkappaB levels with clinical parameters and viral presence.

Main Results:

  • NFkappaB activation was significantly higher in myocarditis patients compared to controls, but not in dilated cardiomyopathy.
  • Increased NFkappaB correlated with preserved left ventricular function and inversely with left ventricular end-diastolic volume.
  • Adenovirus persistence was associated with increased NFkappaB activation, while cytomegalovirus and parvovirus B19 showed no significant association.

Conclusions:

  • Elevated NFkappaB activation is linked to inflammatory processes in myocarditis.
  • NFkappaB activation may occur in early inflammatory stages and potentially protect cardiomyocytes from apoptosis and cardiac dilation.
  • The prognostic and therapeutic relevance of NFkappaB in myocarditis warrants further investigation.
Abstract

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