Articles
| Open Access |
https://doi.org/10.55640/
METABOLIC DYSFUNCTION AND ATRIAL REMODELING: THE LINK BETWEEN ETIOLOGY AND PATHOGENESIS IN ATRIAL FIBRILLATION
Panjiyev Jonibek Abdumajidovich , Department of Preclinical Sciences of the Asian International University, Bukhara, UzbekistanAbstract
Atrial fibrillation (AF) increasingly emerges as a metabolic disease rather than an isolated electrophysiological disorder. Metabolic dysfunction—including obesity, insulin resistance, dyslipidemia, mitochondrial injury, chronic inflammation, and epicardial adipose tissue (EAT) expansion—creates a structural and electrophysiological atrial substrate that predisposes to AF. Etiologic metabolic stressors induce oxidative injury, abnormal intracellular calcium cycling, ion-channel remodeling, gap junction disruption, mitochondrial dysfunction, fibroblast activation, and autonomic imbalance. Together, these mechanisms generate conduction heterogeneity, ectopic firing, rotor stabilization, and progressive atrial cardiomyopathy. This review integrates metabolic etiologies with mechanistic pathways of AF pathogenesis, providing a comprehensive conceptual model linking systemic metabolism to atrial arrhythmogenesis. Understanding AF as a metabolic-inflammatory-fibrotic disorder offers new opportunities for prevention and personalized therapy.
Keywords
Atrial fibrillation, Rate control, Rhythm control, Obesity, insulin resistance, reentry circuits
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