Vol 14, No 1 (2007)
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Published online: 2006-12-01
The management of Brugada syndrome patients
Cardiol J 2007;14(1):97-106.
Abstract
Brugada syndrome is a congenital electrical disorder characterised by the appearance of distinctive
QRST-T patterns in the right precordial leads and an increased risk of sudden death
(SCD) in young healthy adults. Although chamber enlargement is not apparent in most cases,
autopsy and histological investigations have revealed structural abnormalities. The typical
Brugada ECG manifestation is often concealed and may be revealed by Class IC anti-arrhythmic
agents with the effect of blocking the fast component of sodium channel currents. The
syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, α-adrenergic
agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of
glucose and insulin and hypokalaemia, as well as by alcohol and cocaine toxicity. Since the
typical Brugada ECG pattern can be normalised by Class IA agents to block transient outward
currents (Ito) or by isoproterenol and cilostazol to boost calcium channel currents, they have
been considered pharmacological therapies aimed at rebalancing the ion channel currents
during cardiac depolarisation and repolarisation. Case studies by intra-cardiac mappingguided
ablation in the right ventricular outflow tract and Purkinje network have shown
evidence of eliminating the substrate of ventricular tachycardia/fibrillation (VT/VF) in
Brugada syndrome, which may be used as an adjunct to device therapy to abort electrical
storms. At present the most effective therapy to prevent sudden cardiac death in Brugada
syndrome is an implantable cardioverter defibrillator. (Cardiol J 2007; 14: 97–106)
Keywords: Brugada syndromequinidineisoproterenolimplantable cardioverter defibrillatorradiofrequency ablation