Three different repolarisation patterns can be distinguished in the right precordial ECG leads. Type 1 is diagnostic for Brugada syndrome. In this case, the ECG shows ST-elevation of a least 2 mm with a typical coved shape in at least two of the three right precordial leads (V1 – V3), followed by a negative T-wave (fig 1a and 1b). In addition, there is a complete or incomplete right bundle branch block. The diagnosis Brugada syndrome is definite when the ECG shows a type 1 ST-abnormality and when one of the following criteria is met: documented ventricular fibrillation (VF), polymorphic ventricular tachycardia (VT), family history of sudden cardiac death under age of 45, family members with type 1 ECG abnormalities, inducible VT by electrical stimulation, syncope, or sleep apnea. There is a clinically important distinction between Brugada syndrome with ECG abnormalities including one of the additional criteria, and patients with Brugada-type ECG patterns without any of the additional criteria. The latter are not diagnosed with Brugada syndrome.
For cases in which the ECG manifestations of Brugada syndrome are concealed, they may be unmasked by sodium channel blockers i.v. (e.g. flecainide 2 mg/kg, up to a maximum of 150 mg). However, it is important to realise that the sensitivity of this test is unknown, but that it is definitely less than 100 % (4). One study showed a sensitivity of 77 % in a subgroup of patients who were carriers of a mutation in the SCN5A gene (5). Asymptomatic patients with an ECG type 1 pattern are usually not subjected to the provocation test, as this provides little additional information. The typical Brugada ECG pattern can also appear under the influence of external factors, such as an overdose of tricyclic antidepressants, fever, cocaine, anaesthetics etc. (6). It is unclear whether these patients are at higher or lower risk of sudden death.
Type 2 ST-segment elevation has a saddleback appearance with ≥ 2 mm elevation at the highest and ≥ 1 mm at the lowest point, and either a positive or a biphasic T-wave. Type 3 shows either a saddleback or upwardly bent ST-segment elevation at < 1 mm (fig 3) (4). All three distinct ECG patterns can be observed in the same patient if ECG is recorded at different points in time, as was the case with our patient (fig 1 and 2). This is an important point to be aware of, as ECG patterns of type 2 and 3 can easily be classified as unspecific and the correct diagnosis may thus be missed.
It is important to realise that a number of other conditions can lead to ECG abnormalities similar to those in the Brugada syndrome (2, 7) and that such ECG abnormalities can appear after cardioversion (8). It should be noted that ST- elevation in the right precordial leads may also be observed with well-trained athletes (fig 4), but these differ from those in the Brugada syndrome as the ST-segment is ascending or horizontal, and is not influenced by sodium channel blockers (2).
Depolarisation disturbances such as prolonged P-wave, PR and QRS intervals are often seen, especially in Brugada patients with the sodium channel (SNC5A) mutation (9). Our patient also had prolongation of these intervals (fig 2).