PICTURE 1 Typical electrocardiogram of Brugada syndrome. Note the pattern resembling a right bundle branch block, the P-R prolongation and the ST elevation in leads V1-V3.		PICTURE 2 Spontaneous polymorphic ventricular tachycardia recorded during monitoring in a patient with Brugada syndrome. The arrhythmias are fast and need DC shock to terminate.
PICTURE 3 The electrocardiograms of the two first patients ever seen. They were siblings of age 2 and 3 at the time of the recordings. Compare to picture 1.		PICTURE 4
PICTURE 5 Spontaneous changes on the electrocardiogram in a patient with Brugada syndrome. Note how the ST elevation changes. On February 1993 the electrocardiogram was completely normal (arrow).		PICTURE 6 Six precordial leads showing spontaneous changes of the electrocardiogram in five different days. Note that the panel in the right shows a less typical electrocardiogram. This pattern has been called saddle-back by the Japanese investigators.
PICTURE 7 12-lead ECG during administration of ajmaline (50 mg in 5 min). Note the progressive appearance of the ST elevation in V1-V3.		PICTURE 8 Leads V1 to V3 are shown from two patients with two different mutations in the sodium channel. It is possible that the electrocardiogram varies depending upon the type of mutation.
PICTURE 9 Modulation of the electrocardiogram by atrial pacing, isoproterenol and procainamide. Note the right bundle branch block in panel the third panel (ISOPRO) after the ST elevation has been normalized by isoproterenol.		PICTURE 10 In contrast to picture 9, this patient shows no right bundle branch block when the electrocardiogram normalizes during followup
PICTURE 11 Schematic drawing showing the mechanism of phase 2 re-entry in Brugada syndrome. A selective shortening of the duration of the action potential on the epicardium because of an increased activity of the Ito results in an electric gradient and re-entry.		PICTURE 12 Early repolarization. Compare with the electrocardiograms of patients with Brugada syndrome to note the important differences.
PICTURE 13 Electrophysiologic differences between early repolarization, long QT syndrome and Brugada syndrome. In early repolarization there exists a voltage gradient but no dispersion of duration of action potentials. That is why these patients show ST elevation but do not develop arrhythmias. In the long QT syndrome there exist a voltage gradient because of prolongation of the action potential in some areas because of early afterdepolarizations. The voltage gradient results in phase 2 re-entry. In Brugada syndrome re-entry occurs because of the voltage gradient caused by the shortening of the duration of the action potential.		PICTURE 14 Effects of ajmaline in a patient with Chagas' disease. Ajmaline produces ST segment elevation in the right precordial leads (arrows). It is not clear whether this patient suffered from two diseases at the same time or whether Chagas' disease causes the same abnormalities as Brugada.
PICTURE 15 Electrocardiogram of a patient with Steinert's disease.Some disease may result in electrocardiographic patterns resembling Brugada syndrome. However, the differences are usually evident,both clinically and electrocardiographically. On this electrocardiogram we do not observe the typical ST segment elevation in leads V1 to V3 although the right bundle branch block is evident.		PICTURE 16 Survival of symptomatic and asymptomatic patients with Brugada syndrome and survival of patients with Brugada syndrome according to treatment. Only the implantable cardioverter-defibrillator protects against sudden cardiac death.