Abstract
Atrial fibrosis plays a key role in atrial myopathy, resulting in the genesis of atrial fibrillation (AF). The abnormal distribution of fibrotic tissue, electrical coupling, paracrine interactions, and biomechanical–electrical interactions have all been suggested as causes of fibrosis-related arrhythmogenesis. Moreover, the regional difference in fibrogenesis, specifically the left atrium (LA) exhibiting a higher arrhythmogenesis and level of fibrosis than the right atrium (RA) in AF, is a key contributor to atrial arrhythmogenesis. LA fibroblasts have greater profibrotic cellular activities than RA fibroblasts, but knowledge about the regional diversity of atrial regional fibrogenesis remains limited. This article provides a comprehensive review of research findings on the association between fibrogenesis and arrhythmogenesis from laboratory to clinical evidence and updates the current understanding of the potential mechanism underlying the difference in fibrogenesis between the LA and RA.
Highlights
Atrial fibrosis is a distinctive pathological finding of atrial myopathy and contributes to the genesis of various cardiovascular diseases
atrial fibrillation (AF) increases the area of fibrosis in patients with heart failure (HF) [5], and the crosstalk between fibrogenesis and arrhythmogenesis plays a pivotal role in AF
This review provides an update on the existing body of laboratory and clinical evidence, for fibrosis-related electrophysiological diversity between the left atrium (LA) and right atrium (RA)
Summary
Atrial fibrosis is a distinctive pathological finding of atrial myopathy and contributes to the genesis of various cardiovascular diseases. Abnormal Distribution of Fibrotic Tissue in Atrial Electrical Coupling and Arrhythmogenesis. Propagation waves perpendicular to the collagen fiber exhibit slower conduction velocity [23]; the organization of fibrotic tissue may be highly correlated with reentry stability. Atrial myofibroblasts isolated from the surgical specimens of the patients with AF exhibit high Cx43 expression [27]. This finding indicates that fibrogenesis may induce the remolding of the gap junction and activate arrhythmogenesis. Myocytes, when coupled with an increased number of myofibroblasts, exhibit greater depolarized resting membrane potential, thereby inactivating sodium channels, decreasing conduction velocity, and increasing the complexity of wave propagation [28]. The distribution and density of atrial myofibroblasts–cardiomyocytes heterocellular coupling may be a key element of atrial arrhythmogenesis
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