Induced Brugada syndrome: Possible sources of arrhythmogenesis.

نویسندگان

  • Gonçalo Tomé
  • João Freitas
چکیده

Brugada syndrome is an inherited cardiac condition with the potential for development of life-threatening arrhythmias in relatively young individuals without significant structural cardiac abnormalities. The condition is characterized by a distinct coved-type ST segment elevation in the right precordial leads (V1-V3). This hallmark pattern (type 1) is often dynamic and sometimes concealed, and may be unmasked in certain conditions or under the effect of certain agents, which include variation of sympathovagal balance, hormones, metabolic factors and drugs. These factors may not only modulate electrocardiographic morphology and induce the characteristic type 1 pattern, but also predispose to ventricular arrhythmias. The risk of malignant arrhythmias in acute events with induced type 1 pattern may be imminent, particularly if the patient in fact has Brugada syndrome. The physician should be aware of the modulating factors that may underlie a Brugada pattern, and be able to recognize, identify and promptly correct them. The mechanisms responsible for the type 1 pattern and possible associated ventricular arrhythmias induced by these modulating factors have attracted growing attention and interest. Furthermore, not all induced Brugada ECG patterns are observed in patients with Brugada syndrome, existing the possibility for acquired Brugada patterns/syndrome and Brugada phenocopies. This paper reviews the modulating factors associated with induced type 1 pattern as possible causes of arrhythmogenesis, particularly in Brugada syndrome patients, describes some of the probable underlying mechanisms, and discusses the concepts of acquired Brugada syndrome and Brugada phenocopies.

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عنوان ژورنال:
  • Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology

دوره 36 12  شماره 

صفحات  -

تاریخ انتشار 2017