High-density atrial mapping, P-wave analysis, and computational simulations in Brugada syndrome: Enhancing the understanding of atrial fibrillation

Background An increased risk of atrial fibrillation (AF) has been reported in patients with Brugada syndrome (BrS). The pathophysiology of AF susceptibility in BrS is largely unknown. Objective This study aimed to characterize the atrial electrical properties of patients with BrS with and without AF based on P-wave and high-density atrial mapping analysis with a focus on conduction velocity (CV) and provide mechanistic insights on AF susceptibility using computer modeling. Methods Electrocardiographic signals were processed, and P-wave parameters were analyzed in a consecutive series of patients with and without BrS. High-density atrial mapping was performed in patients with BrS undergoing an electrophysiological procedure. CV vectors were numerically approximated at each recording point using polynomial surface fitting. AF initiation susceptibility was simulated in a 3-dimensional atrial model and compared with control simulations. Results A total of 133 subjects (89 patients with BrS and 44 controls) were included. AF history was present in 11% of patients with BrS. Patients with BrS had longer mean P-wave duration than controls (135 ms vs 124 ms, P < .01), whereas no P-wave parameter was able to discriminate between patients with BrS with and without AF. CVs correlated with total atrial activation time (TAAT) (R2 = 0.706), and TAATs mildly correlated with P-wave duration (R2 = 0.12). A significantly higher conduction pattern complexity, quantified as the number of coexisting fibrillation waves, was observed in BrS than in control simulations. In all simulations, regardless of the degree of fibrosis, AF initiation rates were significantly higher in BrS than in control simulations. Conclusion Conventional P-wave parameters do not identify patients with BrS prone to AF. Increased TAAT is related to reduced local CVs, explaining the prolonged P-wave duration observed in patients with BrS. Simulation studies showed significantly higher AF susceptibility initiation in patients with BrS than in controls.