Effect of Skeletal Muscle Na+ Channel Delivered Via a Cell Platform on Cardiac Conduction and Arrhythmia Induction

BACKGROUND—In depolarized myocardial infarct epicardial border zones, the cardiac sodium channel is largely inactivated, contributing to slow conduction and reentry. We have demonstrated that adenoviral delivery of the skeletal muscle Na channel (SkM1) to epicardial border zones normalizes conductio...

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Veröffentlicht in:Circulation. Arrhythmia and electrophysiology 2012-08, Vol.5 (4), p.831-840
Hauptverfasser: Boink, Gerard J.J, Lu, Jia, Driessen, Helen E, Duan, Lian, Sosunov, Eugene A, Anyukhovsky, Evgeny P, Shlapakova, Iryna N, Lau, David H, Rosen, Tove S, Danilo, Peter, Jia, Zhiheng, Ozgen, Nazira, Bobkov, Yevgeniy, Guo, Yuanjian, Brink, Peter R, Kryukova, Yelena, Robinson, Richard B, Entcheva, Emilia, Cohen, Ira S, Rosen, Michael R
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Sprache:eng
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Zusammenfassung:BACKGROUND—In depolarized myocardial infarct epicardial border zones, the cardiac sodium channel is largely inactivated, contributing to slow conduction and reentry. We have demonstrated that adenoviral delivery of the skeletal muscle Na channel (SkM1) to epicardial border zones normalizes conduction and reduces induction of ventricular tachycardia/ventricular fibrillation. We now studied the impact of canine mesenchymal stem cells (cMSCs) in delivering SkM1. METHODS AND RESULTS—cMSCs were isolated and transfected with SkM1. Coculture experiments showed cMSC/SkM1 but not cMSC alone and maintained fast conduction at depolarized potentials. We studied 3 groups in the canine 7d infarctsham, cMSC, and cMSC/SkM1. In vivo epicardial border zones electrograms were broad and fragmented in sham, narrower in cMSCs, and narrow and unfragmented in cMSC/SkM1 (P
ISSN:1941-3149
1941-3084
DOI:10.1161/CIRCEP.111.969907