Brugada syndrome unmasked by fever and paradoxical lower degree of dromotropic disturbance in the right ventricular outflow tract


  • Javier Garcia-Niebla a Profesor colaborador Escuela Universitaria de Enfermería. Hospital Universitario de La Candelaria en Universidad de La Laguna. Valle del Golfo Health Center, Servicio Canario de Salud, El Hierro, Spain
  • Andrés Ricardo Pérez-Riera b Laboratório de Delineamento de Estudos e Escrita Científica. Faculdade de Medicina do ABC, Santo André, São Paulo (SP) Brasil e Disciplina de Clínica Médica, Centro Universitário Uninove, Mauá, Brasil;
  • Rodrigo de Souza Abreu c Laboratório de Delineamento de Estudos e Escrita Científica. Universidade Federal do Espírito Santo. Vitória, Espírito Santo, Brasil
  • Raimundo Barbosa-Barros d Centro Coronário, Hospital Messejana Dr. Carlos Alberto Studart Gomes, Fortaleza, Ceará, Brasil
  • Díaz Muñoz d Servicios Sanitarios del Área de Salud de El Hierro, Valle del Golfo Health Center, Islas Canarias, Spain
  • Kjell Nikus f Heart Center, Tampere University Hospital and Faculty of Medicine and Life Sciences, University of Tampere, Finland



Brugada syndrome, fever, dromotropic disturbance, right ventricular outflow tract


Brugada syndrome (BrS) is an inherited clinical-electrocardiographic arrhythmic entity with an autosomal dominant genetic pattern of inheritance or de novo variant. The syndrome has low worldwide prevalence, but is endemic in Southeast Asian countries (Thailand, Philippines and Japan). The BrS is a subtle structural heart disease (SHD), and the diagnosis is only possible when the so-called type 1 Brugada ECG pattern is spontaneously present or induced for example with fever. Repolarization-depolarization disturbances in BrS patients can be caused by genetic mutations, abnormal neural crest cell migration, low expression of connexin-43 gap junction protein, or connexome disturbances. A recent autopsy study revealed increase in biventricular collagen with myocardial fibrosis when compared with control subjects although the main affected cardiac territory is the right ventricular outflow tract (RVOT). In this location, there is abnormally low expression of significant connexin-43 gap junction responsible for the electro-vectorcardiographic manifestations of terminal QRS conduction delay in the right standard precordial leads (V1-V2), high right precordial leads (V1H-V2H), as well as in the unipolar aVR lead (“the forgotten lead”). Based on their location, these leads reflect the electrical activity of the RVOT.


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