This editorial refers to ‘Atrial fibrillation following lung transplantation: double but not single lung transplant is associated with long-term freedom from paroxysmal atrial fibrillation’†, by G. Lee et al., on page 2774
Atrial fibrillation (AF) is a complex disease most probably due to multiple aetiopathogenic mechanisms. This arrhythmia usually requires a trigger for initiation and a vulnerable electrophysiological and/or anatomic substrate for maintenance. It is still unclear whether the trigger mechanisms for AF initiation include focal enhanced automaticity, triggered activity, or microre-entry from myocardial tissue inside the pulmonary vein (PV). In spite of an incomplete understanding of the anatomo-functional basis for the initiation and maintenance of AF, various catheter and surgical ablation techniques have been shown to modify the substrate of this arrhythmia, achieving a stable sinus rhythm, free from AF, in a high proportion of cases.
In the past 10 years, catheter ablation techniques in patients with AF have evolved from an initial approach focused on the PVs and their junctions with the left atrium (LA), to a more extensive intervention, mainly, but not exclusively, on the LA myocardium and its neuro-vegetative innervation (Figure 1). It is now recognized that the cornerstone of most catheter and surgical ablation approaches is to isolate the PVs electrically from the LA wall. Despite more or less substantial differences among the various catheter techniques that are currently utilized worldwide, results seem to be uniformly similar, with success rates in the range from 50% to 80% in patients with long-standing, persistent, or paroxysmal AF. Notably, a median of two AF ablation procedures are usually necessary for a successful outcome.1,2
Schematic of the anatomo-functional arrhythmic mechanism and common ablation strategies in paroxysmal and long-standing/persistent AF. (A) Active triggers arising from the atrial myocardium within the PVs and other thoracic veins (CS, vein/ligament …