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.

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AimsLocal activation time (LAT) mapping forms the cornerstone of atrial tachycardia diagnosis. Although anatomic and positional accuracy of electroanatomic mapping (EAM) systems have been validated, the effect of electrode sampling density on LAT map reconstruction is not known. Here, we study the effect of chamber geometry and activation complexity on optimal LAT sampling density using a combined in silico and in vivo approach.Methods and results In vivo 21 atrial tachycardia maps were studied in three groups: (1) focal activation, (2) macro-re-entry, and (3) localized re-entry. In silico activation was simulated on a 4×4cm atrial monolayer, sampled randomly at 0.25–10 points/cm2 and used to re-interpolate LAT maps. Activation patterns were studied in the geometrically simple porcine right atrium (RA) and complex human left atrium (LA). Activation complexity was introduced into the porcine RA by incomplete inter-caval linear ablation. In all cases, optimal sampling density was defined as the highest density resulting in minimal further error reduction in the re-interpolated maps. Optimal sampling densities for LA tachycardias were 0.67 ± 0.17 points/cm2 (focal activation), 1.05 ± 0.32 points/cm2 (macro-re-entry) and 1.23 ± 0.26 points/cm2 (localized re-entry), P = 0.0031. Increasing activation complexity was associated with increased optimal sampling density both in silico (focal activation 1.09 ± 0.14 points/cm2; re-entry 1.44 ± 0.49 points/cm2; spiral-wave 1.50 ± 0.34 points/cm2, P < 0.0001) and in vivo (porcine RA pre-ablation 0.45 ± 0.13 vs. post-ablation 0.78 ± 0.17 points/cm2, P = 0.0008). Increasing chamber geometry was also associated with increased optimal sampling density (0.61 ± 0.22 points/cm2 vs. 1.0 ± 0.34 points/cm2, P = 0.0015).ConclusionOptimal sampling densities can be identified to maximize diagnostic yield of LAT maps. Greater sampling density is required to correctly reveal complex activation and represent activation across complex geometries. Overall, the optimal sampling density for LAT map interpolation defined in this study was ∼1.0–1.5 points/cm2.

It was hypothesised that left atrial (LA) fibrosis identified by the presence of low-voltage areas (LVA) may influence the mechanical and electrical function of the left (LAA) and right (RAA) atrial appendage among the long-standing persistent atrial fibrillation (LSPAF) population. 140 consecutive patients underwent voltage mapping of LA with a multielectrode catheter following pulmonary vein isolation and restoration of sinus rhythm with cardioversion. Echocardiography determined LAA peak outflow and inflow velocities and intracardiac catheter-based mean LAA and RAA AF cycle length (AFCL) were obtained during AF before ablation. The impact of flow velocities and AFCL on the prevalence and location of LVA was further evaluated. LVA were detected in 54% of the patients. 14% of the patients presented severe global LVA burden > 20% of the total LA surface area. 29% of the patients presented a disseminated pattern of remodelling as 3 out of 5 LA segments were affected. LAA AFCL, RAA AFCL, LAA flow velocities did not predict the absolute presence of LVA. However LAA AFCL > 155 ms predicted disseminated LVA pattern and LAA AFCL > 165 ms severe LVA incidence. LAA AFCL > 155 ms was predictive for existence of LVA within antero-septal LA segments whilst LAA emptying velocity ≤ 0.2 m/s within lateral wall. Moreover RAA AFCL > 165 ms was strongly related to the presence of LAA AFCL > 15 ms and > 165 ms. LAA and RAA functional assessment was predictive of the presence of advanced stages of voltage-defined LA fibrosis and its regional distribution among LSPAF population