Introduction
Atrial fibrillation (AF) is the most common prevalent arrhythmia, estimated to affect approximately 33 million individuals worldwide (1). The cumulative incidence of progression from paroxysmal AF (PAF) to persistent AF (PersAF) and long-standing persistent AF (LSPAF) is estimated at 8.1 per 100 patient-years (2). AF is associated with an elevated risk of thromboembolism, stroke, impaired quality of life, and even mortality (3,4), and achieving rhythm control with catheter ablation (CA) has shown to improve outcomes in recent studies (5). Ectopic foci originating in the pulmonary veins (PVs) represent the main arrhythmia mechanism in PAF as established by Haissaguerre et al. in a landmark trial (6), and as such pulmonary vein isolation (PVI) is the mainstay treatment for PA. However, in patients with non-PAF, long-term conditions such as hypertension, heart failure, obesity, and sleep apnea lead to structural and cellular changes induced by chronic inflammation, myocyte death and lymphocyte and fatty infiltration, all leading to fibrosis (7). These structural changes within the atria serve as a conduit for fibrillatory waves as they facilitate re-entrant circuits through the fibrotic tissues (8), and the effectiveness of PVI alone for PersAF and LSPAF is far from acceptable (9).
Given these suboptimal results, different ablation strategies and lesion sets have been proposed to increase CA success in the treatment of non-PAF. We will review current evidence surrounding the different approaches for CA of non-PAF and provide evidence-based guidance on best clinical practice.