Abstract:
INTRODUCTION:Since the recognition of inherited sodium (Na(+)) channel disease, the cardiac Na(+) channel has been extensively studied. Both loss-of-function and gain-of-function mutations of the cardiac Na(+) channel are associated with cardiac arrhythmia and sudden cardiac death. Pathophysiological mechanisms that may induce arrhythmia are unravelled and include alterations in biophysical properties due to the mutation in SCN5A, drug use and circumstantial factors. Insights into the mechanisms of inherited Na(+) channel disease may result in tailored therapy. However, due to the complexity of cardiac electrical activity and pathophysiological mechanisms, pharmacotherapy in cardiac Na(+) channel disease remains challenging. AREAS COVERED:This review discusses various mechanisms involved in inherited Na(+) channel disorders, focussing on Brugada syndrome (Brs) and long QT syndrome type 3 (LQTS3). It aims to provide an overview of developments in pharmacotherapy, discussing both treatment and which drugs to avoid to prevent arrhythmia. EXPERT OPINION:Altered biophysical properties of cardiac Na(+) channels are the basis of arrhythmias in patients with inherited Na(+) channel diseases such as BrS and LQTS3. The effects of such biophysical derangements are strongly modulated by concomitant factors. Tailored drug therapy is required to prevent arrhythmia and is best achieved by educating patients affected by Na(+) channel disorders.
journal_name
Expert Opin Pharmacotherjournal_title
Expert opinion on pharmacotherapyauthors
van Hoeijen DA,Blom MT,Tan HLdoi
10.1517/14656566.2014.936380subject
Has Abstractpub_date
2014-09-01 00:00:00pages
1875-87issue
13eissn
1465-6566issn
1744-7666journal_volume
15pub_type
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