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Exploring mechanisms of Brugada syndrome using noninvasive electrocardiographic imaging

This paper is available in a repository.
This paper is available in a repository.

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Abstract

Noninvasive electrocardiographic imaging (ECGI) allows to reconstruct endocardial and epicardial local unipolar electrograms (EG) using body surface mapping based on CT or MRI data. The goal of this study was to investigate electrophysiological characteristics of Brugada syndrome (BrS) using ECGI. 10 patients with a BrS (BrS group, 8 male, 37,7±11,4 years) had a spontaneous or ajmaline­induced BrS coved type ECG. For comparison, 5 patients without ECG abnormalities (control group, 2 male, 45,8±14 years) were also studied. All BrS patients were genotyped (6 SCN5A mutation carriers). ECGI procedure was performed in all patients using Amycard 01C System (EP Solutions SA, Switzerland). All patients with BrS had a zone of abnormal EGs in right ventriclar outflow tract (RVOT). EG changes included: fractionation of QRS (N=9; 90%), ST­segment elevation > 2 mV (N=7; 70%) and activation­ recovery interval (ARI) prolongation due to the early repolarization (N=8; 80%). This changes significantly more expressed on the epicardium. Ajmaline challenge was strengthening existing and expanding the area of abnormal EGs (Fig.). The control patients had no abnormal EGs in RVOT. EG characteristics were not significantly different in patients with and without SCN5A mutations. In contrast, ST segment elevation, ARI prolongation and Epi­Endo voltage gradient were prevalent in symptomatic BrS patients (with spontaneous or induced VF; p≤0,05) (Tab.). Results of this study have demonstrated that myocardial depolarization and repolarization abnormalities in BrS patients are located in the RVOT and prevailed in the epicardium cluster.