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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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Atrial fibrosis and the mechanisms of atrial fibrillation

Thomas H Everett1, Jeffrey E Olgin

  • 1Division of Cardiology and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, California 94143-1354, USA.

Heart Rhythm
|March 6, 2007
PubMed

Insights

Congestive heart failure (CHF) promotes atrial fibrosis, increasing atrial fibrillation (AF) vulnerability. Targeting angiotensin and transforming growth factor-beta (TGF-beta) may prevent AF development in heart failure patients.

Area of Science:

  • Cardiology
  • Pathophysiology
  • Biomedical Research

Background:

  • Atrial fibrillation (AF) frequently coexists with congestive heart failure (CHF).
  • CHF is linked to atrial structural remodeling, specifically interstitial fibrosis, which impairs conduction and increases AF susceptibility.
  • The exact mechanisms driving AF in CHF remain under investigation, with both focal and reentrant drivers observed.

Purpose of the Study:

  • To elucidate the signaling pathways involved in atrial fibrosis development in the context of heart failure.
  • To investigate the role of angiotensin and transforming growth factor-beta (TGF-beta) in mediating atrial fibrosis and AF.
  • To understand how atrial fibrosis contributes to AF vulnerability in CHF.

Main Methods:

  • Review of existing literature on AF, CHF, atrial fibrosis, and related molecular signaling pathways.
  • Analysis of findings from animal models of pacing-induced heart failure and genetic overexpression of TGF-beta1.
  • Examination of studies involving angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and TGF-beta inhibition.

Main Results:

  • Atrial interstitial fibrosis is a hallmark of CHF, contributing to conduction abnormalities and increased AF risk.
  • Angiotensin signaling, modulated by ACE inhibitors or ARBs, appears to play a role in blunting atrial fibrosis and reducing AF incidence in heart failure.
  • Transforming growth factor-beta (TGF-beta) signaling is critical, as evidenced by profound atrial fibrosis and AF in TGF-beta1 overexpressing mice and prevention of fibrosis with TGF-beta inhibition in canine models.

Conclusions:

  • Atrial fibrosis is a key substrate for AF development, particularly in the setting of CHF.
  • Inhibition of angiotensin and TGF-beta signaling pathways shows promise in preventing atrial fibrosis and mitigating AF risk associated with heart failure.
  • Further research into these signaling mechanisms could lead to novel therapeutic strategies for managing AF in CHF patients.

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