par Milman, Anat;Behr, Elijah Raphael;Gray, Belinda;Johnson, David C;Andorin, Antoine;Hochstadt, Aviram;Gourraud, Jean-Baptiste;Maeda, Shingo;Takahashi, Yoshihide;Jm Juang, Jimmy;Kim, SungHwan;Kamakura, Tsukasa;Aiba, Takeshi;Postema, Pieter G;Mizusawa, Yuka;Denjoy, Isabelle;Giustetto, Carla;Conte, Giulio;Huang, Zhengrong;Sarquella-Brugada, Georgia;Mazzanti, Andrea;Jespersen, Camilla CH;Arbelo, Elena;Brugada, Ramon;Calo, Leonardo;Corrado, Domenico;Casado Arroyo, Ruben ;Allocca, Giuseppe;Takagi, Masahiko;Delise, Pietro;Brugada, Josep;Tfelt-Hansen, Jacob;Priori, Silvia G;Veltmann, Christian;Yan, Gan-Xin;Brugada, Pedro;Gaita, Fiorenzo;Leenhardt, Antoine;Wilde, Arthur A M;Kusano, Kengo F;Nam, Gi-Byoung;Hirao, Kenzo;Probst, Vincent;Belhassen, Bernard
Référence Circulation. Genomic and precision medicine, 14, 5, page (e003222)
Publication Publié, 2021-10-01
Référence Circulation. Genomic and precision medicine, 14, 5, page (e003222)
Publication Publié, 2021-10-01
Article révisé par les pairs
Résumé : | Brugada syndrome (BrS) is associated with mutations in the cardiac sodium channel gene, SCN5A. However, genetic studies of patients with BrS with arrhythmic events have been limited. We sought to compare various clinical, ECG, and electrophysiological parameters according to SCN5A genotype in a large cohort of BrS probands with first arrhythmic event. |