February 1, 2002Cardiovascular ResearchOpen Access

A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease

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Population

Mammalian cells expressing mutant S1710L cardiac sodium channels

Comparison

Expression of S1710L mutant channel vs Wild-type and Brugada syndrome mutant channel…

Design

Preclinical

Authors

NSNaoki ShiraiHokkaido University

Discussion

Member takes

Implication

May link S1710L defects to Brugada-conduction overlap; leaves open in vivo validation and targeted therapies.

Structured PICO

Population

Mammalian cells expressing mutant S1710L cardiac sodium channels

Intervention

Expression of S1710L mutant channel

Comparator

Wild-type (WT) and Brugada syndrome mutant channel T1620M

Outcome

Gating properties (macroscopic current decay, voltage-dependence of fast inactivation, recovery from fast inactivation, slow inactivation, activation shift)surrogate

The S1710L mutation in the cardiac sodium channel exhibits multiple biophysical defects that may explain the overlapping clinical phenotypes of Brugada syndrome and cardiac conduction disease.

Cite This Study

Naoki Shirai (2002) studied this question.

synapsesocial.com/papers/6a85378c64694fc428d97bd9 https://doi.org/10.1016/s0008-6363(01)00494-1

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A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease

Discussion

Member takes

Implication

Structured PICO

Cite This Study

A mutant cardiac sodium channel with multiple biophysical defects associated with overlapping clinical features of Brugada syndrome and cardiac conduction disease

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider