Literature DB >> 17111025

Clinical aspects and physiopathology of Brugada syndrome: review of current concepts.

E Herbert1, M Chahine.   

Abstract

Brugada syndrome (BS) is an inherited cardiac disorder characterized by typical electrocardiographic patterns of ST segment elevation in the precordial leads, right bundle branch block, fast polymorphic ventricular tachycardia in patients without any structural heart disease, and a high risk of sudden cardiac death. The incidence of BS is high in male vs. female (i.e., 8-10/1: male/female). The disorder is caused by mutations in the SCN5A gene encoding Nav1.5, the cardiac sodium channel, which is the only gene in which mutations were found to cause the disease. Mutations in SCN5A associated with the BS phenotype usually result in a loss of channel function by a reduction in Na+ currents. We review the clinical aspects, risk stratification, and therapeutic management of this important syndrome.

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Year:  2006        PMID: 17111025     DOI: 10.1139/y06-038

Source DB:  PubMed          Journal:  Can J Physiol Pharmacol        ISSN: 0008-4212            Impact factor:   2.273


  2 in total

1.  Fluoxetine blocks Nav1.5 channels via a mechanism similar to that of class 1 antiarrhythmics.

Authors:  Hugo Poulin; Iva Bruhova; Quadiri Timour; Olivier Theriault; Jean-Martin Beaulieu; Dominique Frassati; Mohamed Chahine
Journal:  Mol Pharmacol       Date:  2014-07-15       Impact factor: 4.436

Review 2.  A New Cardiac Channelopathy: From Clinical Phenotypes to Molecular Mechanisms Associated With Nav1.5 Gating Pores.

Authors:  Adrien Moreau; Mohamed Chahine
Journal:  Front Cardiovasc Med       Date:  2018-10-09
  2 in total

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