In 1992, Brugada et al 1 suggested that the presence of right bundle-branch block and ST-segment elevation in leads V1 to V3 in the absence of structural heart disease is a marker of susceptibility to ventricular fibrillation and represents the diagnostic feature of a novel syndrome that rapidly became known as “Brugada syndrome.” A few years later, mutations in the human cardiac sodium channel gene (SCN5A) were identified in 3 families affected by the syndrome and was therefore classified among the inherited arrhythmogenic diseases.2 In the past 12 years, Brugada syndrome has become the focus of active investigations, and it has generated strong scientific debate concerning its diagnosis, risk stratification, and treatment. In this article, we present our view on the diagnosis and management of Brugada syndrome, with a specific focus on asymptomatic patients.
Should patients with an asymptomatic Brugada electrocardiogram undergo pharmacological and electrophysiological testing?
PRIORI, SILVIA GIULIANA;NAPOLITANO C.
2005-01-01
Abstract
In 1992, Brugada et al 1 suggested that the presence of right bundle-branch block and ST-segment elevation in leads V1 to V3 in the absence of structural heart disease is a marker of susceptibility to ventricular fibrillation and represents the diagnostic feature of a novel syndrome that rapidly became known as “Brugada syndrome.” A few years later, mutations in the human cardiac sodium channel gene (SCN5A) were identified in 3 families affected by the syndrome and was therefore classified among the inherited arrhythmogenic diseases.2 In the past 12 years, Brugada syndrome has become the focus of active investigations, and it has generated strong scientific debate concerning its diagnosis, risk stratification, and treatment. In this article, we present our view on the diagnosis and management of Brugada syndrome, with a specific focus on asymptomatic patients.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
