Literature DB >> 15030278

Brugada syndrome: clinical, genetic, molecular, cellular and ionic aspects.

Charles Antzelevitch1.   

Abstract

Brugada syndrome, first described as a new clinical entity by Pedro and Josep Brugada in 1992, has attracted great interest because of its high prevalence in many regions of the world and its association with high risk for sudden death. The syndrome has captured the attention of the cardiac electrophysiology community because it serves as a paradigm for our understanding of the role of spatial dispersion of repolarization in the development of cardiac arrhythmias. The past decade has witnessed an exponential rise in the number of reported cases and a striking proliferation of papers serving to define the clinical, genetic, cellular, ionic and molecular aspects of this disease. This brief review summarizes the key clinical and experimental milestones that have brought us to our current understanding and approach to therapy of the Brugada syndrome.

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Year:  2003        PMID: 15030278     DOI: 10.1586/14779072.1.2.177

Source DB:  PubMed          Journal:  Expert Rev Cardiovasc Ther        ISSN: 1477-9072


  5 in total

1.  Genetic and biophysical basis for bupivacaine-induced ST segment elevation and VT/VF. Anesthesia unmasked Brugada syndrome.

Authors:  Kevin Vernooy; Serge Sicouri; Robert Dumaine; Kui Hong; Antonio Oliva; Elena Burashnikov; Carl Timmermans; Tammo Delhaas; Harry J G M Crijns; Charles Antzelevitch; Luz-Maria Rodriguez; Ramon Brugada
Journal:  Heart Rhythm       Date:  2006-07-07       Impact factor: 6.343

2.  Molecular differential expression of voltage-gated sodium channel α and β subunit mRNAs in five different mammalian cell lines.

Authors:  Debora Baroni; Oscar Moran
Journal:  J Bioenerg Biomembr       Date:  2011-11-12       Impact factor: 2.945

Review 3.  Murine Electrophysiological Models of Cardiac Arrhythmogenesis.

Authors:  Christopher L-H Huang
Journal:  Physiol Rev       Date:  2017-01       Impact factor: 37.312

4.  Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.

Authors:  Claire A Martin; Urszula Siedlecka; Kristin Kemmerich; Jason Lawrence; James Cartledge; Laila Guzadhur; Nicola Brice; Andrew A Grace; Christof Schwiening; Cesare M Terracciano; Christopher L-H Huang
Journal:  Open Biol       Date:  2012-06       Impact factor: 6.411

Review 5.  On the multiple roles of the voltage gated sodium channel β1 subunit in genetic diseases.

Authors:  Debora Baroni; Oscar Moran
Journal:  Front Pharmacol       Date:  2015-05-18       Impact factor: 5.810

  5 in total

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