Brugada syndrome is a heterogeneous genetic channelopathy that predisposes to ventricular arrhythmias and sudden cardiac death (SCD). The electrocardiogram (ECG) findings only suggest a diagnosis of Brugada syndrome but are not confirmatory. The ECG pattern is known to vary with time in some patients and many have a normal baseline ECG [1,2]. There are two distinctly described ECG patterns, type I Brugada is characterized by ST elevation (≥2mm) with a “coved” pattern or a T-wave which is inverted with an upward convexity, in other cases the elevated ST segment descends and rises again forming a “saddleback” type pattern, this is called the type II Brugada. The electrophysiological and clinical manifestations of this syndrome have been found to be secondary to various factors [3-10]. Of these, mutations in cardiac sodium channel SCN genes (SCN5A and SCN10A) are the most well-known [11]. Since all affected families do not have these mutations, it is believed that other mutations in sodium channel genes or mutations in non-sodium channel genes may also cause Brugada syndrome [12-15].
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Published on: Jul 3, 2017 Pages: 24-25
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DOI: 10.17352/ac.000008
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