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Atrial fibrillation, the most common sustained cardiac arrhythmia, has a complex and multifaceted pathophysiology.1 The presence of a predisposing substrate, frequently encompassing atrial hypertrophy, fibrosis, and significant alterations of the extracellular matrix, is contributing to intra-atrial electric conduction delay as well as shortening and dispersion of atrial refractory periods. Triggers such as short-coupled supraventricular extrasystoles can initiate the arrhythmia acting on this pathological milieu with the potential contribution of modulating factors, such as the autonomic nervous system, ischemia, and hormones.See Article by Yang et al The initial clinical experiences of transcatheter ablation of atrial fibrillation (AF) were reported 20 years ago almost simultaneously by different groups.2,3 Mimicking atrial debulking and compartmentalization provided by surgical techniques such as the classical Maze procedure, these transcatheter approaches aimed at substantial atrial substrate modification. A few years later, the recognition by Haissaguerre et al4 that most of the ectopic foci initiating AF were located in the pulmonary veins, shifted the attention of the electrophysiological community from substrate to triggers of the arrhythmia. The observation that ablation with local radiofrequency energy of the ectopic foci achieved 62% freedom from AF, paved the way for circumferential pulmonary vein isolation widespread use, which soon became the cornerstone of paroxysmal AF interventional treatment showing higher efficacy when compared with antiarrhythmic drugs.5 However, in patients presenting with persistent AF, pulmonary vein isolation proved to be insufficient if used as stand-alone ablation strategy showing only modest long-term success rates.6,7 These findings suggested the existence of a more complex electrophysiological substrate in patients with persistent AF with structures and mechanisms involved in facilitation and maintenance of the arrhythmia residing outside the pulmonary veins.8 As a consequence, efforts were redirected toward AF substrate modification with several non–pulmonary veins targets used as …

Electrophysiologically Guided Substrate Modification During Sinus Rhythm