Editorial
Copyright ©2014 Baishideng Publishing Group Co.
World J Cardiol. Mar 26, 2014; 6(3): 81-86
Published online Mar 26, 2014. doi: 10.4330/wjc.v6.i3.81
Table 1 Brugada phenocopy etiological categories
Etiological category
Metabolic conditions
Mechanical compression
Ischemia and pulmonary embolism
Myocardial and pericardial disease
ECG modulation
Miscellaneous
Table 2 Criteria to differentiate the Brugada electrocardiogram pattern, Brugada phenocopy and true congenital Brugada syndrome
Brugada ECG pattern
The ECG pattern has a type 1 or type 2 Brugada morphology as currently defined by Bayés de Luna et al[1]
Diagnostic criteria for BrP
The ECG pattern has a type 1 or type 2 Brugada morphology
The patient has an underlying condition that is identifiable
The ECG pattern resolves after resolution of the underlying condition
There is a low clinical pretest probability of true BrS determined by lack of symptoms, medical history and family history
Negative provocative testing with sodium channel blockers such as ajmaline, flecainide or procainamide
Provocative testing not mandatory if surgical RVOT manipulation has occurred within the last 96 h
The results of genetic testing are negative (desirable but not mandatory because the SCN5A mutation is identified in only 20% to 30% of probands affected by true BrS)
Features that suggest true congenital BrS
The ECG pattern has a type 1 or type 2 Brugada morphology
There is a high clinical pretest probability of true congenital BrS determined by presence of symptoms, medical history and family history
Positive provocative testing with sodium channel blockers such as ajmaline, flecainide or procainamide. This indicates sodium channel dysfunction consistent with true BrS
Genetic testing is positive in about 20% to 30% of probands