Related Experiment Video
Updated: Nov 14, 2025
Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Atrial fibrosis and substrate based characterization in atrial fibrillation: Time to move forwards
Jing X Quah1,2, Dhani Dharmaprani1,3, Kathryn Tiver2
1College of Medicine and Public Health, Flinders University of South Australia, Adelaide, Australia.
Insights
Atrial fibrosis (AF) significantly contributes to cardiac arrhythmia. Targeting fibrosis offers a promising therapeutic strategy for improving atrial fibrillation treatment outcomes.
Area of Science:
- Cardiology
- Electrophysiology
- Pathophysiology
Background:
- Atrial fibrillation (AF) is a common cardiac arrhythmia with limited therapeutic efficacy due to incomplete understanding of its mechanisms.
- Atrial fibrosis is increasingly recognized as a key factor in the maintenance and perpetuation of AF.
- Fibrosis leads to electrophysiological changes and is linked to adverse clinical outcomes, including thromboembolism and ablation recurrence.
Purpose of the Study:
- To review the pathophysiology of atrial fibrosis in AF progression.
- To explore the role of fibrosis in arrhythmogenesis.
- To discuss current and future therapeutic strategies targeting atrial fibrosis.
Main Methods:
- Review of existing literature on atrial fibrosis pathophysiology and its role in AF.
- Analysis of surrogate markers for fibrosis detection (cardiac MRI, echocardiography, electroanatomic mapping) and their limitations.
- Evaluation of current therapeutic interventions, including pharmacologic and ablation-based approaches.
Main Results:
- Atrial fibrosis alters conduction velocity, refractoriness, and promotes reentrant circuits, sustaining AF.
- Cardiac MRI, echocardiography, and electroanatomic mapping serve as surrogate markers for fibrosis detection.
- Current therapies targeting fibrosis include drugs and substrate-based catheter ablation, with potential for electrophenotyping.
Conclusions:
- Atrial fibrosis is a critical determinant of AF maintenance and progression.
- Accurate detection and targeted therapies for atrial fibrosis are essential for improving AF management.
- Future research should focus on advanced characterization techniques like electrophenotyping to refine treatment strategies.
Abstract:
Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia in clinical practice. However, current therapeutic interventions for atrial fibrillation have limited clinical efficacy as a consequence of major knowledge gaps in the mechanisms sustaining atrial fibrillation. From a mechanistic perspective, there is increasing evidence that atrial fibrosis plays a central role in the maintenance and perpetuation of atrial fibrillation. Electrophysiologically, atrial fibrosis results in alterations in conduction velocity, cellular refractoriness, and produces conduction block promoting meandering, unstable wavelets and micro-reentrant circuits. Clinically, atrial fibrosis has also linked to poor clinical outcomes including AF-related thromboembolic complications and arrhythmia recurrences post catheter ablation. In this article, we review the pathophysiology behind the formation of fibrosis as AF progresses, the role of fibrosis in arrhythmogenesis, surrogate markers for detection of fibrosis using cardiac magnetic resonance imaging, echocardiography and electroanatomic mapping, along with their respective limitations. We then proceed to review the current evidence behind therapeutic interventions targeting atrial fibrosis, including drugs and substrate-based catheter ablation therapies followed by the potential future use of electro phenotyping for AF characterization to overcome the limitations of contemporary substrate-based methodologies.
