ArticleThe pharmacogenomics journal2014
A rare loss-of-function SCN5A variant is associated with lidocaine-induced ventricular fibrillation.
Article in The pharmacogenomics journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Contemporary local anaesthetic-associated adverse events and mortality: a pharmacovigilance analysis of a US reporting system.British journal of anaesthesia · 2025Article
- Voltage-Gated Sodium Channels: A Therapeutic Target in Ischemic Heart Disease.Reviews in cardiovascular medicine · 2025Review
- Biophysical mechanisms of myocardium sodium channelopathies.Pflugers Archiv : European journal of physiology · 2024Review
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Identification of Novel SCN5A Single Nucleotide Variants in Brugada Syndrome: A Territory-Wide Study From Hong Kong.Frontiers in physiology · 2020Article
- Predicting cardiac electrical response to sodium-channel blockade and Brugada syndrome using polygenic risk scores.European heart journal · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The human genome contains over 4 million variant sites, as compared with the reference genome, including rare sequence variants, which have the potential to exert large phenotypic effects, such as susceptibility to drug toxicity. We report identification and functional characterization of a rare non-synonymous (p.A1427S) variant in the SCN5A gene that was associated with incessant and lethal ventricular tachycardia and fibrillation after administration of lidocaine to a patient with acute myocardial infarction. The variant, located in a highly conserved domain distinct from the predicted lidocaine-binding site, decreased peak current density of the sodium channel. With the increasing availability of the whole exome and whole genome sequencing data, it would be possible to identify and characterize rare variants in SCN5A that might predispose to lethal ventricular arrhythmias.
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Registered trials
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