Atrial Fibrillation Mechanisms and Implications for Catheter Ablation

Abstract

AF is a heterogeneous rhythm disorder that is related to a wide spectrum of etiologies and has broad clinical presentations. Mechanisms underlying AF are complex and remain incompletely understood despite extensive research. They associate interactions between triggers, substrate and modulators including ionic and anatomic remodeling, genetic predisposition and neuro-humoral contributors. The pulmonary veins play a key role in the pathogenesis of AF and their isolation is associated to high rates of AF freedom in patients with paroxysmal AF. However, ablation of persistent AF remains less effective, mainly limited by the difficulty to identify the sources sustaining AF. Many theories were advanced to explain the perpetuation of this form of AF, ranging from a single localized focal and reentrant source to diffuse bi-atrial multiple wavelets. Translating these mechanisms to the clinical practice remains challenging and limited by the spatio-temporal resolution of the mapping techniques. AF is driven by focal or reentrant activities that are initially clustered in a relatively limited atrial surface then disseminate everywhere in both atria. Evidence for structural remodeling, mainly represented by atrial fibrosis suggests that reentrant activities using anatomical substrate are the key mechanism sustaining AF. These reentries can be endocardial, epicardial, and intramural which makes them less accessible for mapping and for ablation. Subsequently, early interventions before irreversible remodeling are of major importance. Circumferential pulmonary vein isolation remains the cornerstone of the treatment of AF, regardless of the AF form and of the AF duration. No ablation strategy consistently demonstrated superiority to pulmonary vein isolation in preventing long term recurrences of atrial arrhythmias. Further research that allows accurate identification of the mechanisms underlying AF and efficient ablation should improve the results of PsAF ablation.

Keywords: atrial fibrillation; catheter ablation; fibrosis; mapping; pulmonary vein ablation; reentrant drivers.

Figure 1

Coumel triangle summarizing the different contributors to AF.

Figure 2

Schematic representation of the mechanisms maintaining AF. (A) Single stable focal or reentrant source (star) with fibrillatory conduction. (B) Multiple wavelets: multiple waves propagate randomly and give birth to new daughter wavelets. (C) Multiple reentries (red arrows) around areas of scar and fibrosis. (D) Combination of the different mechanisms that sustain AF in humans. These mechanisms are typically meandering and last for few consecutive beats.

Figure 3

Different reentrant activities maintaining AF (adapted from reference Allessie et al., 1977).

Figure 4

Phase maps acquired during AF in patients with PAF (A), PsAF of 4 months (B) and long lasting PsAF >12 months (C). Red spots identify sites of phase singularity.

Figure 5

Unipolar signals recorded during a one second window of AF. Electrograms at the site of reentrant activities (red spots) show a complex and turbulent activity while the activity in the remaining atria is homogeneous. A reentry can be identified by analyzing the surrounding electrograms (white arrows) that show a sequential temporal activation. LA, left atrium; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RA, right atrium; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.