Abstract

Different situations have been involved in the origin of ventricular arrhythmic events in patients with the Brugada syndrome such as bradycardia, alcohol consumption and mental stress. We present a 30 year old male with recurrent ventricular fibrillation due to a febrile illness with intense sweating. He had been previously studied at our Unit in 1995 because of an episode of resuscitated cardiac arrest due to ventricular fibrillation. The twelve-lead electrocardiogram showed the typical characteristics of a patient with the Brugada syndrome. Different invasive and non-invasive tests performed were normal. He received a defibrillator and had no recurrences during 4 years of follow up. In March,1999, after an upper respiratory tract infection he had high fever treated with paracetamol but at down he had sweating and chills, followed by 3 defibrillator shocks. Late interrogation showed 5 episodes of ventricular fibrillation, two of them non-sustained, and the rest adequately treated by the defibrillator. Activation and inactivation kinetics for early INa are twofold faster at higher temperature, and shift activation and steady-state inactivation. This may explain the role of the temperature as a trigger for ventricular arrhythmias in our patient.

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