Related Experiment Video

Updated: Nov 19, 2025

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
08:10

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation

Published on: July 20, 2022

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Implications of Inflammation and Fibrosis in Atrial Fibrillation Pathophysiology

Masahide Harada1, Stanley Nattel2

  • 1Department of Cardiology, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukakecho, Toyoake 4701192, Japan.

Cardiac Electrophysiology Clinics
|January 31, 2021
PubMed

Insights

Inflammation and fibrosis drive atrial fibrillation by promoting cardiac remodeling and conduction issues. Targeting these processes may offer new therapeutic strategies for atrial fibrillation.

Area of Science:

  • Cardiology
  • Pathophysiology
  • Fibrosis Research

Background:

  • Atrial fibrillation (AF) pathophysiology involves inflammation and fibrosis.
  • Atrial fibrosis disrupts normal heart rhythm by causing conduction disturbances.
  • Systemic inflammation activates cardiac fibroblasts, leading to fibrosis.

Purpose of the Study:

  • To review current knowledge on inflammation and fibrosis in atrial fibrillation.
  • To highlight the interplay between inflammation and fibrosis in AF progression.
  • To discuss the potential of targeting inflammation and fibrosis as therapeutic strategies for AF.

Main Methods:

  • Literature review of existing research on atrial fibrillation, inflammation, and fibrosis.
  • Analysis of the mechanisms linking inflammatory mediators to cardiac fibroblast activation.
  • Synthesis of data on the role of fibrosis in atrial remodeling and AF maintenance.

Main Results:

  • Inflammation and fibrosis are key components in the pathophysiology of atrial fibrillation.
  • A complex interplay exists between inflammation and fibrosis, creating a cycle of atrial remodeling.
  • This cycle contributes to the maintenance of atrial fibrillation and increases thrombogenicity.

Conclusions:

  • Inflammation and fibrosis are critical targets for managing atrial fibrillation.
  • Understanding the interplay between these factors is crucial for developing effective therapies.
  • Targeting inflammation and fibrosis holds promise for treating atrial fibrillation and reducing associated risks.

Keywords:
Atrial fibrillationAtrial remodelingFibrosisInflammasomeInflammation

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