Arrhythmia-Induced Cardiomyopathy in Atrial Fibrillation: Pathogenesis, Diagnosis, and Treatment

Arrhythmia-induced cardiomyopathy (AIC) represents a potentially reversible form of LV dysfunction in which sustained atrial fibrillation (AF) and irregular, often rapid, ventricular activation drive maladaptive electrical, structural, and metabolic remodeling. Beyond simple rate effects, AIC reflects perturbed calcium handling, oxidative stress, and fibro-inflammatory signaling that propagate atrial-ventricular crosstalk and energetic failure. Clinically, attribution remains challenging because AF may be the cause, consequence, or marker of underlying myocardial disease; however, substantial improvement in LVEF after durable rhythm control is strongly supportive of an AIC component. A disciplined diagnostic pathway-integrating rhythm burden quantification, echocardiographic deformation indices, cardiac magnetic resonance, and natriuretic peptide trajectories-can refine pre-test probability and guide treatment intensity. Early rhythm control has emerged as a disease-modifying strategy in AF with HF, with catheter ablation often central to burden reduction and reverse remodeling; in parallel, rapid initiation of guideline-directed HF therapy and targeted cardiometabolic interventions may favor substrate regression and facilitate durable sinus rhythm. Uncertainties persist regarding standardized AIC case definition, arrhythmia burden thresholds that secure sustained recovery, optimal sequencing of rhythm- and substrate-directed therapies, and criteria for de-escalation of HF treatment after recovery. This review synthesizes contemporary mechanistic, diagnostic, and therapeutic evidence on AIC in AF and delineates priorities for future trials.