Fibrosis, Myofibroblasts, and Atrial Fibrillation

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Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia in the clinical setting, and traditional pharmacological approaches have proved to have important weaknesses. Structural remodeling has been observed in both clinical and experimental AF paradigms, and is an important feature of the AF substrate, producing fibrosis that alters atrial tissue composition and function. The precise mechanisms u...

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Atrial fibrosis progression in patients with Atrial Fibrillation

Methods Eighty-eight patients (58% male, mean age 60.4+/-14.7) with AF who underwent late gadolinium enhancement MRI (LGE-MRI) to assess the degree of atrial tissue fibrotic changes were included in this study. All patients underwent at least 2 or more LGE-MRI separated by more than 3 months of follow up. Progression of fibrosis was defined as an increase in fibrosis area by more than 5% (Figur...

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Atrial Fibrillation and Fibrosis: Beyond the Cardiomyocyte Centric View

Atrial fibrillation (AF) associated with fibrosis is characterized by the appearance of interstitial myofibroblasts. These cells are responsible for the uncontrolled deposition of the extracellular matrix, which pathologically separate cardiomyocyte bundles. The enhanced fibrosis is thought to contribute to arrhythmias "indirectly" because a collagenous septum is a passive substrate for propaga...

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Fibrosis in Atrial Fibrillation – Role of Reactive Species and MPO

Atrial fibrosis with enhanced turnover and deposition of matrix proteins leads to inhomogeneous atrial electrical conduction and gives rise to electrical reentry circuits resulting in atrial fibrillation. The multifactorial pathogenesis of atrial fibrosis involves resident cardiac cells as well as infiltrating leukocytes, both generating and sequestering matrix metalloproteinases (MMPs), a key ...

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ژورنال

عنوان ژورنال: Circulation: Arrhythmia and Electrophysiology

سال: 2015

ISSN: 1941-3149,1941-3084

DOI: 10.1161/circep.115.002881