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Cardiac adipose tissue and atrial fibrillation: the perils of adiposity
Stéphane N Hatem1, Alban Redheuil2, Estelle Gandjbakhch3
1Sorbonne University, Faculté de médicine, Assistance Publique-Hôpitaux de Paris, GH Pitié-Salpêtrière Hospital, INSERM UMR_S1166, Cardiology Department, Institute of Cardiometabolism and Nutrition-ICAN, 91, boulevard de l'hôpital, 75013 Paris, France stephane.hatem@upmc.fr.
Insights
Adipose tissue around the atria contributes to atrial fibrillation (AF) risk and severity through inflammatory crosstalk with the heart. Managing risk factors like obesity may improve AF treatment by addressing these structural changes.
Area of Science:
- Cardiology
- Biomedical Science
- Pathophysiology
Background:
- Accumulation of adipose tissue around the atria is linked to atrial fibrillation (AF) risk, persistence, and severity.
- This association is driven by complex interactions between atrial adipose tissue and the myocardium, not merely a coincidental finding.
Purpose of the Study:
- To explore the intricate relationship between epicardial adipose tissue and atrial myocardium in the context of atrial fibrillation.
- To highlight the role of inflammatory mediators and oxidative stress from adipose tissue in cardiac remodeling.
- To underscore the potential of risk factor management, particularly obesity, in treating AF.
Main Methods:
- Review of clinical and experimental evidence linking epicardial adipose tissue to atrial remodeling.
- Analysis of the mechanisms by which adipokines, inflammatory cytokines, and reactive oxidative species affect atrial myocardium.
- Consideration of fibro-fatty infiltrations and their impact on atrial function.
Main Results:
- Epicardial adipose tissue releases inflammatory mediators and oxidative species, promoting fibrotic remodeling of the atrial myocardium.
- Fibro-fatty infiltration in the subepicardium contributes to functional disorganization of the atrial myocardium.
- Obesity is associated with specific structural and functional atrial remodeling, offering therapeutic targets for AF.
Conclusions:
- The interplay between adipose tissue and atrial myocardium is a key factor in atrial fibrillation pathogenesis.
- Aggressive risk factor management, especially addressing obesity, presents a promising strategy for managing AF.
- Advancements in cardiac imaging are crucial for visualizing myocardial fat and localizing AF substrates.
Abstract:
The amount of adipose tissue that accumulates around the atria is associated with the risk, persistence, and severity of atrial fibrillation (AF). A strong body of clinical and experimental evidence indicates that this relationship is not an epiphenomenon but is the result of complex crosstalk between the adipose tissue and the neighbouring atrial myocardium. For instance, epicardial adipose tissue is a major source of adipokines, inflammatory cytokines, or reactive oxidative species, which can contribute to the fibrotic remodelling of the atrial myocardium. Fibro-fatty infiltrations of the subepicardium could also contribute to the functional disorganization of the atrial myocardium. The observation that obesity is associated with distinct structural and functional remodelling of the atria has opened new perspectives of treating AF substrate with aggressive risk factor management. Advances in cardiac imaging should lead to an improved ability to visualize myocardial fat depositions and to localize AF substrates.
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