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- W2034222799 abstract "This editorial refers to ‘Role of common and rare variants in SCN10A : results from the Brugada syndrome QRS locus gene discovery collaborative study’ by E.R. Behr et al ., doi:10.1093/cvr/cvv042. Everything must be taken into account. If the fact will not fit the theory—let the theory go. ―Agatha Christie, The Mysterious Affair at Styles Brugada syndrome (BrS) has been named after the description of the disease made by the Brugada brothers in 1992.1 BrS is clinically characterized by arrhythmic events, in particular ventricular fibrillation, resulting in syncope and sudden cardiac arrest mainly in middle-aged men. The ECG shows a peculiar down-sloping elevation of the ST segment in the right pre-cordial ECG leads with inversion of T-waves.2 Since 1998, a genetic component to BrS has been demonstrated.3 Over the past years, at least 20 genes have been proposed either to cause BrS or to be BrS-susceptibility genes.4For several years, SCN5A , which encodes the ‘cardiac sodium channel’ Nav1.5, was presented as a gene ‘causing’ BrS in ∼20% of the patients; however, this concept had to be revised due to recent findings. First, in some families where the probands were found to carry SCN5A rare variants, other family members diagnosed with BrS did not carry the supposedly …" @default.
- W2034222799 created "2016-06-24" @default.
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- W2034222799 date "2015-04-29" @default.
- W2034222799 modified "2023-09-27" @default.
- W2034222799 title "Genetic background of Brugada syndrome is more complex than what we would like it to be!" @default.
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- W2034222799 doi "https://doi.org/10.1093/cvr/cvv135" @default.
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