Atrial fibrillation (AF) is a complex disease with many possible mechanisms. Studies indicate that the arrhythmogenic foci within the thoracic veins are AF initiators. Once initiated, AF alters atrial electrical and structural properties in a way that promotes its own maintenance and recurrences and may alter the response to antiarrhythmic drugs. The exact mechanisms by which the initiators trigger AF remain elusive, however. Evidence to date suggests that autonomic modulation does have an adjunctive role to play in catheter AF ablation, especially when applied selectively. Further mechanistic and clinical studies are warranted before a wider application can be recommended.
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