Syncope in pharmacologically unmasked Brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

A 30-year-old Caucasian male was referred for evaluation of a 2-year histor y of recurrent post-exertion lightheadedness and near syncopal spells in th e setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of Brugada syndrome. An exercise stre ss test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family histor y and EGG, pharmacological testing with procainamide, isoprenaline and meto prolol, as well as programmed ventricular stimulation, were undertaken. Pha rmacological provocation further supported a diagnosis of Brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic r egarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of Brugada syndrome, there appe ared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyar rhythmias. The patient was treated with midodrine, and has remained symptom -free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as Brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic Brugada sy ndrome, the identification of other causes of syncope in such patients pose s an uncomfortable, and currently unsettled dilemma. (Europace 2001; 3: 159 -163) (C) 2001 The European Society of Cardiology.