Predictors of the voltage derived left atrial fibrosis in patients with long-standing persistent atrial fibrillation

Abstract

Background Left atrial (LA) arrhythmogenic substrate beyond the pulmonary veins (PV) seems to play a crucial role in the maintenance of atrial fibrillation (AF). The aim of this study was to evaluate the association of selected parameters with the presence and extent of voltage-defined LA fibrosis in patients with long-standing persistent AF (LSPAF) undergoing catheter ablation. Methods One hundred and sixteen consecutive patients underwent high density-high resolution voltage mapping of the LA with a multielectrode catheter following PV isolation and restoration of sinus rhythm with cardioversion. A non-invasive dataset, such as clinical variables, two- and three-dimensional echocardiography determined LA size and function and fibrillatory-wave amplitude on a standard surface electrocardiogram were obtained during AF before ablation. Results Low-voltage areas (LVA; 15 cm 2 [IQR 8–31]) were detected in 56% of patients. Twenty nine percent of them presented mild, 43% moderate and 28% severe global LVA burden. In univariate analysis, age ≥ 57 years old, female sex, body surface area ≤ 1.76 m 2 , valvular heart disease, moderate mitral regurgitation, chronic coronary syndrome, hypothyroidism, CHA 2 DS 2 -VASc score ≥ 3 and ≥ 4 predicted the presence of LVA. In multivariate analysis only female sex, valvular heart disease and CHA 2 DS 2 -VASc ≥ 4 remained statistically significant. AF duration, LA size and function and fibrillatory-waves amplitude were neither associated with the prediction of the LVA, nor severe LVA burden. Conclusions A LSPAF diagnosis does not indicate the presence of voltage defined fibrosis in many cases. Simple non-invasive screening of the LSPAF population could predict LVA prevalence.

Left and right atrial appendage functional features as predictors for voltage-defined left atrial remodelling in patients with long-standing persistent atrial fibrillation

“…Therefore, parameters predicting LVA burden still remain unclear. It was observed that left atrial appendage (LAA) remains intact despite the development of voltage-defined fibrosis in the body of LA [3,4], recently confirmed in LSPAF patients [2]. Hence, we hypothesised that the presence of LVA may influence the mechanical and electrical function of the left and right (RAA) atrial appendage.…”

“…Only patients who were able to maintain sinus rhythm following pulmonary vein isolation (PVI) and cardioversion (n = 140) underwent high-density high-resolution LA bipolar voltage mapping [2963(2213-3145) points per map] using the CARTO®3 system. The mapping protocol is described in detail elsewhere [2]. Briefly, this was performed during coronary sinus (CS) pacing with a Pentaray catheter, acquired with a CONFIDENSE™ module (BW).…”

“…The appendage was defined as an anatomical structure around the LAA orifice, determined internally from within the LA in the reconstructed shell. The extent of global LVA burden > 20% of the TSA was arbitrarily considered as severe on the basis of our observation that all detected LVA can be easily ablated if it occupies less than 20% of the TSA [2]. The body of LA was segmented into 5 areas: septum, anterior, posterior, inferior and lateral wall (Fig.…”

“…Left atrial (LA) fibrosis, that can be identified by the presence of low-voltage areas (LVA), is thought to play an important role in the development and maintenance of atrial fibrillation (AF) [1]. Some studies have shown evidence of LVA with several markers, however, with conflicting results, especially among the long-standing persistent AF (LSPAF) population [2]. Therefore, parameters predicting LVA burden still remain unclear.…”

New hope for patients and challenges for the multidisciplinary arrhythmia team: a hybrid convergent approach for atrial fibrillation treatment

“…Long-lasting episodes of AF (i.e., persistent forms) lead to pathophysiological changes within the atrial musculature, as a result of intensifying fibrosis, structural and electrical remodeling, especially within the posterior wall of the left atrium (LA) [2][3][4][5][6][7][8][9][10]. These changes have an adverse effect on the prognosis of the termination of arrhythmias and the maintenance of sinus rhythm, hence their inhibition may have a decisive impact on the further clinical course [11,12].…”