Regional Diversities in Fibrogenesis Weighed as a Key Determinant for Atrial Arrhythmogenesis

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.

Correlation between Electrocardiogram Changes and Right Ventricular Systolic Function in Patients with Chronic Atrial Fibrillation

“…The pathophysiology of AF consists in the activation of profibrotic signals and abnormal calcium handling at the atrial level [15]. The abnormal distribution of fibrotic tissue, electrical coupling, paracrine interactions, and biomechanical-electrical interactions are considered to be the causes of fibrosis-related arrhythmogenesis [16]. The pressure on the right side of the heart is significantly reduced because of thinness and poor elasticity in the right ventricular myocardium and low resistance in pulmonary arteries with high expansion [17].…”