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Structural changes of atrial myocardium during chronic atrial fibrillation
V L Thijssen1, J Ausma, G S Liu
1Department of Molecular Cell Biology & Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
Insights
Atrial fibrillation (AF) is a common arrhythmia linked to higher mortality. This review details structural changes in the atria during chronic AF, emphasizing the need for better animal models to understand these changes.
Area of Science:
- Cardiology
- Pathology
- Biomedical Engineering
Background:
- Atrial fibrillation (AF) is the most prevalent clinical arrhythmia, associated with increased mortality.
- While risk factors and mechanisms are known, the link between atrial structural remodeling and AF chronicity remains unclear.
- Structural changes in AF include adaptive dedifferentiation and maladaptive fibrosis of cardiomyocytes.
Purpose of the Study:
- To review structural changes in human and animal models of chronic atrial fibrillation.
- To discuss the time course and potential mechanisms of atrial structural remodeling in AF.
- To present methods for investigating the molecular mechanisms underlying AF-related structural changes.
Main Methods:
- Review of existing literature on structural remodeling in human patients with atrial fibrillation.
- Analysis of data from animal models mimicking chronic atrial fibrillation.
- Discussion of proposed mechanisms and methods for molecular investigation.
Main Results:
- Structural remodeling in the atria is a key feature of chronic atrial fibrillation.
- Both adaptive and maladaptive cellular changes occur, including cardiomyocyte dedifferentiation and fibrosis.
- Understanding the time course and mechanisms of remodeling is crucial for developing effective therapies.
Conclusions:
- Chronic atrial fibrillation induces significant structural changes in the atria.
- Accurate animal models are essential for studying the progression and mechanisms of AF-related remodeling.
- Further research into molecular pathways is needed to elucidate and potentially reverse these structural alterations.
Abstract:
Of all known arrhythmia's, atrial fibrillation (AF) is the most often met in the clinical setting and it is associated with an increase in mortality risk. Several risk factors for AF have been described and several mechanisms of induction and maintenance have been proposed. Studies in patients with AF have shown that structural changes occur in the atria, but the relationship between the structural remodelling and the chronicity of the arrhythmia are not well understood. The changes mainly concern adaptive (dedifferentiation of cardiomyocytes) and maladaptive (degeneration of cells with replacement fibrosis) features. In order to characterise the time course of the structural remodelling the need for animal models which adequately mimic chronic atrial fibrillation in humans is felt essential. In this review, the structural changes that are observed during prolonged sustained AF in patients and animal models, are described. Furthermore, the time course and potential mechanisms of structural remodelling are discussed and methods for elucidation of the underlying molecular mechanisms are presented.