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Review
. 2021 Mar;25(6):2764-2775.
doi: 10.1111/jcmm.16350. Epub 2021 Feb 11.

Left atrial fibrosis in atrial fibrillation: Mechanisms, clinical evaluation and management

Affiliations
Review

Left atrial fibrosis in atrial fibrillation: Mechanisms, clinical evaluation and management

Jin Ma et al. J Cell Mol Med. 2021 Mar.

Abstract

Atrial fibrillation (AF), the commonest arrhythmia, shows associations with various disease conditions. Mounting evidence indicates that atrial fibrosis is an important part of the arrhythmogenic substrate, with an essential function in the generation of conduction abnormalities that underlie the transition from paroxysmal to persistent AF, which in turn contributes to AF perpetuation. Left atrial (LA) fibrosis is considered a possible major factor and predictor in AF treatment. The present review provides insights into LA fibrosis' association with AF. The information is focused on clinical aspects and mechanisms, clinical evaluating methods that evaluate fibrosis changes and examining possible options for the prevention of atrial fibrosis.

Keywords: arrhythmia; atrium; cardiovascular imaging; electrophysiology; fibrosis.

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Conflict of interest statement

None declared.

Figures

FIGURE 1
FIGURE 1
The malignant cycle of atrial fibrosis and AF. The development and maintenance of AF require both a trigger and a susceptible substrate. Triggers are mainly represented by ectopic discharges originating in the PV ostia, due to changes in calcium homeostasis or autonomic activation which can trigger activity involving early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs). These ectopic discharges can initiate AF by premature atrial electrical activation. In addition to this process, an AF substrate is essential to maintain the arrhythmia. Structural remodelling, particularly atrial interstitial fibrosis, is the main arrhythmogenic substrate and leads to local conduction disturbances and block, which increases the risk of re‐entry circuits. AF itself can further perpetuate the progression of atrial fibrosis. ECG, electrocardiogram; ESO, oesophageal electrocardiogram
FIGURE 2
FIGURE 2
Activated fibroblasts are the main effector cells in heart fibrosis. Under pathological conditions, different stresses stimulate Ca2+ entry in fibroblasts via TRP channels (TRPC) that promote a Ca2+ concentration increase. Subsequently, the expression levels of specific markers were assessed, such as collagen, α‐SMA, profibrotic cytokine (TGF‐β1) and different isoforms of TRPC, which activate cardiac fibroblasts leading to their migration, proliferation, cytokine secretion and exacerbated extracellular matrix synthesis

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