1. The Brugada syndrome: clinical, genetic, cellular, and molecular abnormalities 
Gerald V Naccarelli, MD, Charles Antzelevitch, PhD 
The American Journal of Medicine 
Volume 110, Issue 7, Pages (May 2001)
DOI: /S (01)

2. Figure 1
Twelve-lead electrocardiogram demonstrating right bundle branch block and ST segment elevation in the right precordial leads in a patient with Brugada syndrome. Reprinted with permission from Circulation(41).
The American Journal of Medicine  , DOI: ( /S (01) )

3. Figure 2
Mutations in the cardiac sodium gene SCN5A from different arrhythmic syndromes. In the Brugada syndrome, a splicing error at the donor site of intron 7 affects the first transmembrane segment of domain I (6). In Lenegre’s disease, a splicing error at exon 22 is associated with the disease (17). In long QT3, there is a delta KPQ deletion at position 1505–1507 in the intercellular linker between domains III and IV (27). Reprinted with permission from J Cardiovasc Electrophysiol(66).
The American Journal of Medicine  , DOI: ( /S (01) )

4. Figure 3
Schematic showing right ventricular epicardial action potential changes thought to underlie the electrocardiographic manifestation of the Brugada syndrome. Modified from Eur Heart J(67), with permission.
The American Journal of Medicine  , DOI: ( /S (01) )

5. Figure 4
Cellular mechanisms proposed to underlie arrhythmogenesis in the Brugada syndrome.
The American Journal of Medicine  , DOI: ( /S (01) )

6. Figure 5
Antiarrhythmic provocation of right bundle branch block and ST segment elevation in the right precordial leads by intravenous ajmaline in a patient with Brugada syndrome whose baseline electrocardiogram (left panel) demonstrated no electrocardiographic abnormalities. Panels 2 through 8 are changes noted over 5 minutes after intravenous ajmaline. The last panel on the right shows resolution of changes 10 minutes after administration of the drug. Modified from Am J Cardiol(64), with permission.
The American Journal of Medicine  , DOI: ( /S (01) )