A36 year old man was admitted after a profound syncopal episode during a hot bath. Examination and investigation findings on admission were unremarkable except for his ECG, which showed ST elevation in V1–V3 (panel A). His ECG gradually returned to normal over three days (panel B). ST elevation then recurred after a flecainide challenge (panel C), thus confirming the diagnosis of Brugada syndrome, and the patient had a defibrillator implanted.
Two weeks after implantation he was readmitted with Staphylococcus aureus septicaemia related to device infection. ECG (panel D) during fever (40°C) again showed pronounced ST elevation in V1–V3.
These ECGs demonstrate the potential temporal variation of the ECG in Brugada syndrome and the effects of sodium channel blocking drugs and body temperature. Brugada syndrome results from a mutation in the SCN5A gene that encodes the α subunit of the sodium channel. Evidence suggests that increasing temperature results in faster decay of the sodium channel, accentuating the effect of the already impaired sodium channel. Recurrent ventricular fibrillation in a Brugada patient during fever has been described. It is postulated that this patient’s index presentation was induced by the hot bath, producing an elevated core temperature and faster decay of sodium channels and arrhythmia. This might be similar to the multiple sclerosis crises precipitated by hot baths that formed the basis of the “hot bath test” of yesteryear
Figure 1.
