Mechanisms of Disease: current understanding and future challenges in Brugada syndrome
Wataru Shimizu*, Takeshi Aiba and Shiro Kamakura
Correspondence *Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan
Email wshimizu@hsp.ncvc.go.jp
Mutations in SCN5A, the gene encoding the 
subunit of the cardiac sodium channel, are associated with a number of cardiac rhythm syndromes, including Brugada syndrome. This review discusses the genotypic and phenotypic characteristics, cellular mechanisms, diagnosis and management of Brugada syndrome.
Full text of this article is available with one of the following:
- Personal subscription Purchase your own personal subscription to this journal. Already a subscriber? Please log in for immediate access.
- 7 day single article pass for US$32 In order to purchase this article you must be a registered user. Please register or log in.
- Site licence Learn more about institutional site licences
Current Subscribers
Please log in to access the full text article using the login box at the top of the page.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
RESEARCH
A sodium-channel mutation causes isolated cardiac conduction diseaseNature Letters to Editor (22 Feb 2001)
A calcium sensor in the sodium channel modulates cardiac excitabilityNature Letters to Editor (24 Jan 2002)
Polymorphisms in the cardiac sodium channel promoter displaying variant in vitro expression activityEuropean Journal of Human Genetics Article Response
See all 6 matches for Research