The Brugada Syndrome-An Update-

Brugada Syndrome

“…These drugs create additional conduction delay between the other part of the ventricles and the right ventricular outflow tract (RVOT) (the depolarization theory) or induce the transmural gradient of AP by shortening AP more in the RVOT epicardium than endocardium (the repolarization theory), which, theoretically, both lead to the manifestation of coved-type ECG. 95 Procainamide or flecainide may lead to false-negative results, as procainamide creates less conduction delay because it blocks less I Na compared to other sodium channel blockers 96 and flecainide induces less ST-segment elevation presumably because of its stronger I to blocking effect (less shortening of AP in the RVOT epicardium) (see the Mechanism of Ventricular Arrhythmia section of this article). 97 Close monitoring with continuous ECG recording and full equipment for resuscitation is necessary in every test.…”

“…Some of the follow-up periods are of the whole study population (including symptomatic cases). Event rates of the studies by Brugada et al (1998), 90 Brugada et al (2003), 96 and Delise et al (2011) 94 include all asymptomatic patients (both spontaneous and drug-induced type 1 ECG) because the data were not available separately.…”

Sensitivity and specificity of sodium channel blocking test in the diagnosis of Brugada syndrome

“…Greater inhibition of I to current by flecainide may render it less effective [7]. Psilicanaide, a pure class 1C agent, is considered more effective than flecanaide [8]. On the contrary, procainamide exhibits a less use-dependent block of the fast I Na channel, and therefore is less effective compared to all other agents [8].…”

Genetic aspects and investigation of sudden death in young people

“…12 It is defined by coved ST segment elevation in leads V1-V3 with a partial RBBB pattern. Inheritance is autosomal dominant, arising in 20-30% of cases from mutations in the sodium channel gene (SCN5A).…”