Arrhythmogenesis in Brugada syndrome: impact and constrains of current concepts
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
23295036
DOI
10.1016/j.ijcard.2012.12.019
PII: S0167-5273(12)01648-8
Knihovny.cz E-resources
- Keywords
- Arrhythmogenesis, Atrial fibrillation, Brugada syndrome, Discontinuous conduction, Dysfunction, Mutation,
- MeSH
- Brugada Syndrome diagnosis genetics physiopathology MeSH
- Atrial Fibrillation diagnosis genetics physiopathology MeSH
- Tachycardia, Ventricular diagnosis genetics physiopathology MeSH
- Humans MeSH
- Mutation genetics MeSH
- Risk Factors MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Brugada syndrome (BrS), an inherited arrhythmogenic disease first described in 1992, is characterized by ST segment elevations on the electrocardiogram in the right precordium and by a high occurrence of arrhythmias including the life-threatening ventricular tachycardia/fibrillation. Knowledge of the underlying mechanisms of formation of arrhythmogenic substrate in BrS is essential, namely for the risk stratification of BrS patients and their therapy which is still restrained almost exclusively to the implantation of cardioverter/defibrillator. In spite of many crucial findings in this field published within recent years, the final consistent view has not been established so far. Hence, BrS described 20 years ago remains an actual topic of both clinical and experimental studies. This review presents an overview of the current knowledge related to the pathogenesis of BrS arrhythmogenic substrate, namely of the genetic basis of BrS, functional consequences of mutations related to BrS, and arrhythmogenic mechanisms in BrS.
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