Atrial Fibrosis as a Dominant Factor for the Development of Atrial Fibrillation: Facts and Gaps

Anastasia Xintarakou; Stylianos Tzeis; Stelios Psarras; Dimitrios Asvestas; Panos Vardas


Europace. 2020;22(3):342-351. 

In This Article

Abstract and Introduction


Atrial fibrillation (AF), the most commonly diagnosed arrhythmia, affects a notable percentage of the population and constitutes a major risk factor for thromboembolic events and other heart-related conditions. Fibrosis plays an important role in the onset and perpetuation of AF through structural and electrical remodelling processes. Multiple molecular pathways are involved in atrial substrate modification and the subsequent maintenance of AF. In this review, we aim to recapitulate underlying molecular pathways leading to atrial fibrosis and to indicate existing gaps in the complex interplay of atrial fibrosis and AF.


Atrial fibrillation (AF) is the most common cardiac arrhythmia with diverse pathophysiological background. Rarely, AF is not associated with any concomitant condition or underlying comorbidity, but in the vast majority of cases, an underlying pathology coexists.[1] Diverse pathological processes affecting the atria, including collagen fibre accumulation, fatty infiltration, and amyloid deposition, contribute to the genesis and perpetuation of AF. The term 'atrial cardiomyopathy' has been introduced to describe these histological/pathophysiological changes and a classification scheme has been proposed to outline the dominant underlying pathology. A key contributor in the development of atrial cardiomyopathy and subsequently AF is atrial fibrosis.[2,3]