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Ablation of electrical drivers during atrial fibrillation (AF) has been proved as an effective therapy to prevent recurrence of fibrillatory episodes. This study presents a new methodology based on causality analysis that is able to identify the hierarchical dominance of atrial areas driving AF. Realistic mathematical models of the atrial electrical activity during AF were used to assess the validity of our method. Identification of the dominant atrial propagation patterns was achieved by computing causal relations between multiple electrogram signals. The causal relationships between atrial areas during the fibrillatory processes were summarized into a recurrence map, highlighting the hierarchy and dominant areas. Recurrence maps computed from causality analysis allowed the identification of sites responsible for maintenance of the arrhythmia. These maps were able to locate the position of the atrial driver in fibrillatory processes with a single rotor, with 2 rotors or with several drivers. Additionally, the correspondence between the nodal values of the recurrence map and the distance to the rotor core has been established. Causal analysis consistently estimated propagation patterns and location of atrial drivers during AF. This methodology could guide ablation procedures in AF patients.

Current techniques for atrial flutter (AFL) treatment involve radiofrequency ablation. This is a relatively simple and short procedure for typical AFL, whereas becomes more complex and unpredictable in the case of atypical AFL. Therefore, non-invasive characterization of AFL would be helpful for the management of ablation procedures. In this study the behavior of typical and atypical AFL groups is characterized from the vectorcardiographic AFL loops. The initial hypothesis is that typical AFL loops resemble each other, whereas atypical AFL loops differ from typical AFL ones. All patient loops were compared to a reference, by analyzing the global trajectory, pathway complexity and distance to the reference loop. The distance was the most significative parameter, being 0.445 ± 0.135 and 0.799 ± 0.144 for typical and atypical AFL (p = 8.00 e-5). In addition, an intrapatient analysis revealed a higher stability of typical AFL loops than in the case of atypical AFL.

Brugada syndrome (BrS) causes sudden death in patients with structurally normal hearts. Manifestation of BrS in the ECG is dynamic and most patients do not show unequivocal signs of the syndrome during ECG screening. Electrograms (EGMs) of BrS patients show conduction delay and fractionation at the right ventricular outflow tract area (RVOT) and thus could be used for diagnosis, but their recording requires an invasive procedure. We have obtained 67-lead body surface potential mapping recordings (BSPM) of 6 BrS patients and 6 controls and computed their EGMs by solving the inverse problem of electrocardiography by using Tikhonov's regularization method. Inverse-computed EGMs presented similar activation times and durations in controls and BrS patients for apex and septum. However, RVOT EGMs showed a later activation in BrS patients than in controls (58 ± 7 vs. 39 ± 5 ms, p<0.01) and EGMs were longer (122 ± 22 vs. 85 ± 8 ms, p<0.01). Inverse-computed EGMs of BrS patients showed abnormalities consistent with those observed in electrophysiological studies and could be used for a non-invasive diagnosis and characterization of Brugada syndrome.

Role of dual AV nodal pathway physiology in the atrioventricular nodal (AVN) conduction during atrial arrhythmias remains unclear. By using His electrogram alternans (HEA), we have developed a functional model of the atrioventricular conduction that incorporates the dual AV nodal pathway physiology. Experiments performed on 5 rabbit atrial-AVN preparations were used to develop and test the presented AV nodal functional model. HEAs from the inferior margin of the His bundle were used to identify fast and slow wavefront propagations (FP and SP). Conduction curves were calculated by using the model and compared with the real experiments, the root mean square error of the FP and SP were 7 ± 4ms and 3 ± 3 ms respectively. In addition, the model has been used for illustrating the effects of the atrioventricular node modification, which has emerged as one of the alternatives for ventricular rate control during atrial fibrillation. The presented model can help in understanding some of the unclear AV node conduction mechanisms and should be considered as a step forward in understanding the AV node and specifically its dual pathway physiology.

Brugada syndrome (BrS) causes sudden death in patients with structurally normal hearts. Manifestation of BrS in the ECG is dynamical and most patients do not show unequivocal signs of the syndrome during ECG screening. We have obtained 67-lead body surface potential mapping recordings of 25 patients with BrS and analyzed their spatial distribution of surface potentials during ventricular activation. Six patients presented spontaneous type I ECGs during the recording. These patients showed non-dipolarities in isopotential maps at the right ventricular outflow tract (RVOT) region during the development of terminal R waves in right precordial leads. Same finding was observed in 95% of BrS patients not presenting a type I ECG. Conduction delay in the RVOT may be a consistent finding in BrS patients that can be identified by Body Surface Potential Mapping.