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.

Mid-Term Results of Totally Thoracoscopic Ablation in Patients with Recurrent Atrial Fibrillation after Catheter Ablation

“…However, the sources of recurrent AF, especially permanent AF, are often difficult to identify. In patients with refractory AF, re-entrant activities induced by atrial remodeling are another possible causative factor [12]. In a previously published study, AF recurrence after PVI was predicted on the basis of the extent of fibrosis, and atrial fibrosis was present in all the cases [13].…”

Label-free proteomic analysis of serum exosomes from paroxysmal atrial fibrillation patients

“…The mechanisms underlying AF are classically described as mechanisms responsible for its initiation and mechanisms responsible for its perpetuation [ 23 ]. In this study, a multi-stage discovery-verification proteomic strategy was used to develop potential AF-related biomarkers from patients’ blood samples.…”

The impact of left atrial inferior wall isolation, in addition to pulmonary veins and left posterior wall, on long-standing persistent atrial fibrillation

“…AF is not a simple arrhythmia, and CA for AF becomes much more complicated for persistent and long-standing AF, which is related not only to focal triggers but also to atrial substrate and modulators. 8 Therefore, the ablation strategy for these patients is not fully constructed, being dependent on patient characteristics and a surgeon’s experience. Isolation of the LA posterior wall provides an additional treatment option to PV isolation, considering the large potential for AF triggers and substrates located in this area.…”