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.