Epicardial origin of cardiac arrhythmias: clinical evidences and pathophysiology

Corentin Chaumont1,2, Nadine Suffee3, Estelle Gandjbakhch3

  • 1Cardiology Department, Rouen University Hospital, Rouen, France.

Insights

The epicardial region is crucial for both ventricular and atrial arrhythmias, driven by structural changes like fibro-fatty infiltration. Understanding epicardial reactivation offers new therapeutic targets for heart rhythm disorders.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Cardiac Pathophysiology

Background:

  • The epicardium plays a critical role in ventricular arrhythmias (e.g., Brugada syndrome, cardiomyopathies) and atrial fibrillation.
  • Shared substrates include altered repolarization gradients and subepicardial fibro-fatty infiltration.
  • Epicardial reactivation is increasingly recognized in arrhythmogenic substrate formation.

Purpose of the Study:

  • To review the pathophysiological mechanisms of epicardial-driven arrhythmias.
  • To highlight the role of epicardial progenitor cells and immune-inflammatory processes.
  • To explore potential novel biomarkers and therapeutic strategies.

Main Methods:

  • Review of recent literature on cardiac imaging, mapping, and ablation.
  • Analysis of pathophysiological data linking epicardial alterations to arrhythmias.
  • Synthesis of evidence on cellular and inflammatory contributions to arrhythmogenesis.

Main Results:

  • Epicardial alterations are common to various ventricular and atrial arrhythmias.
  • Epicardial progenitor cell recruitment and immune-inflammatory processes contribute to subepicardial fibrosis.
  • Epicardial reactivation is a key factor in developing arrhythmogenic substrates.

Conclusions:

  • The epicardium represents a critical 'electrical fragility' zone in the heart.
  • Further understanding of epicardial mechanisms can lead to new diagnostic and therapeutic approaches for arrhythmias.
  • Targeting epicardial pathways may offer novel treatment strategies for complex cardiac arrhythmias.

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