Key result
Cardiac autonomic dysfunction and complex nerve interactions play a key role in AF pathogenesis.
This review highlights the role of autonomic nervous system dysfunction in the pathophysiology of atrial fibrillation, suggesting potential new therapeutic targets beyond pure myocardial ablation.
Autonomic targets may merit exploration in AF; leaves open prospective trials to validate modulation beyond ablation.
There have been dramatic expansions of research in the field of atrial fibrillation (AF), both clinically and in basic science, which is propelled by advent of catheter ablation as the treatment option for patients with AF. Currently, the primary end point of the ablation procedure targets the isolation myocardial sleeves in the pulmonary vein (PV), i.e., PV isolation. However, the clinical outcome of the “purely” myocardial approach remains suboptimal despite of significant technological improvement in ablation procedures with better mapping and energy delivery systems. There has been increasing evidence that dysfunction of the autonomic nervous system that encompasses the sympathetic, parasympathetic and intrinsic neural network is involved in the pathogenesis of AF. Studies are under the way to evaluate the effects of targeting these neural components on improving the outcome of therapy for AF. We aimed to review the evidence in the literature on the role of autonomic dysfunction in the pathophysiology of AF.
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Xi et al. (2015) conducted a review in Atrial fibrillation. Autonomic dysfunction and complex interactions among different components of cardiac autonomic innervations play an important role in the pathogenesis of atrial fibrillation.
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