Prevalence of Brugada sign in a Greek tertiary hospital population

Abstract

The Brugada-type ECG pattern is infrequently seen in a Greek hospital-based population. All subjects with Brugada sign and structurally normal hearts displayed a benign clinical course without arrhythmic events during a relatively long follow-up period.

Brugada Syndrome

“…Type 1 ECG appears more frequently in Asia (0%-0.36%) [55][56][57][58][59][60][61][62][63][64][65][66] and Europe (0%-0.25%) [67][68][69][70][71][72][73][74] than in the United States (0.03%). [75][76][77][78][79] Type 2 and type 3 ECG is more prevalent in Asia (0.12%-2.23%) [56][57][58][59][60][61][62][63][64][65][66] than in Europe (0.0%-0.6%) [67][68][69][70][71][72][73][74] or the United States (0.02%). [76][77][78][79] The low prevalence of Brugada-type ECG in the United States may be explained by different ethnic backgrounds among the studies.…”

Cardiac amyloidosis and Brugada-like ECG pattern

“…The Brugada syndrome (BS) is an inherited channelopathy associated with a high propensity of polymorphic ventricular tachycardia, ventricular fibrillation and sudden cardiac death in individuals with structurally normal hearts [6]. The characteristic (ECG) pattern referred as Brugada sign consists of complete or incomplete right bundle branch block (RBBB) and ST-segment elevation in leads V 1 through V 3 [5,6].…”

“…The characteristic (ECG) pattern referred as Brugada sign consists of complete or incomplete right bundle branch block (RBBB) and ST-segment elevation in leads V 1 through V 3 [5,6]. The ECG features of BS could be intermittent, requiring a pharmacological challenge with a class I antiarrhythmic agent to unmask the characteristic ST-segment elevation in right precordial leads [5,12].…”

Genetics of Sudden Cardiac Death

“…Patients are at high risk for SCD with cardiac event rate per year of 0.5 % in asymptomatic patients, 1.9 % in patients with syncope, and 7.7 % in patients with aborted SCD [22]. The syndrome is estimated to be responsible for up to 12 % of all sudden deaths and 20 % of SCD among patients with structurally normal hearts [22][23][24][25]. The syndrome has a genetic basis, and several mutations have been identified in genes encoding subunits of cardiac sodium, potassium, and calcium channels, as well as in genes involved in the trafficking or regulation of these channels.…”

“…The syndrome has a genetic basis, and several mutations have been identified in genes encoding subunits of cardiac sodium, potassium, and calcium channels, as well as in genes involved in the trafficking or regulation of these channels. Hundreds of variants in more than 25 genes have been associated with BrS [22,[24][25][26][27][28].…”