Population
Caucasian family with prolonged QT interval, intermittent bundle-branch block, sudden cardiac death, and…
Comparison
Lidocaine in patients; T1620K mutation in… vs Wild-type hNav1.5 channels in vitro
Design
Preclinical
Authors
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May link SCN5A variants to mixed conduction-LQTS phenotypes; leaves open human validation from animal models.
The T1620K mutation in the SCN5A gene leads to both loss-of-function and gain-of-function properties in cardiac sodium channels, explaining the concomitant occurrence of cardiac conduction disease and long QT syndrome.
Surber et al. (2007) studied this question.
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