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December 22, 2008CirculationOpen Access

Epicardial Border Zone Overexpression of Skeletal Muscle Sodium Channel SkM1 Normalizes Activation, Preserves Conduction, and Suppresses Ventricular Arrhythmia

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Why the study?

Does SkM1 gene therapy reduce inducible ventricular tachyarrhythmia in canine myocardial infarct models?

Population

Canine myocardial infarct models created by coronary ligation and computer simulations using a modified…

Comparison

Adenovirus expressing skeletal muscle sodium… vs Adenovirus expressing green fluorescent protein…

Design

Preclinical

Follow-up

5 to 7 days

Authors

DLDavid H. LauCCChris ClausenESEugene A. Sosunov

Discussion

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Overview

Attenuates inducible VT/VF in canine post-MI models; leaves open translation of SkM1 gene therapy to human arrhythmia prevention.

Structured PICO

Does SkM1 gene therapy reduce inducible ventricular tachyarrhythmia in canine myocardial infarct models?

P
Population
Canine myocardial infarct models created by coronary ligation (n=20) and computer simulations using a modified Hund-Rudy model.
I
Intervention
Adenovirus expressing skeletal muscle sodium channel (SkM1) and green fluorescent protein injected into epicardial border zones.
C
Comparator
Adenovirus expressing green fluorescent protein alone (sham) injected into epicardial border zones.
O
Outcome
Incidence of inducible sustained ventricular tachyarrhythmia/fibrillation >60 seconds.surrogate

Overexpression of the skeletal muscle sodium channel SkM1 in the epicardial border zone of canine infarcts normalizes activation and significantly reduces inducible ventricular tachyarrhythmia.

Cite This Study

Lau et al. (2008) studied this question.

synapsesocial.com/papers/6a70a2eeac440176ef294d8dhttps://doi.org/10.1161/circulationaha.108.809301
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