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Publication : Optical mapping of ventricular arrhythmias in LQTS mice with SCN5A mutation N1325S.

First Author  Tian XL Year  2007
Journal  Biochem Biophys Res Commun Volume  352
Issue  4 Pages  879-83
PubMed ID  17157817 Mgi Jnum  J:116505
Mgi Id  MGI:3694390 Doi  10.1016/j.bbrc.2006.11.106
Citation  Tian XL, et al. (2007) Optical mapping of ventricular arrhythmias in LQTS mice with SCN5A mutation N1325S. Biochem Biophys Res Commun 352(4):879-83
abstractText  Transgenic expression of SCN5A mutation N1325S creates a mouse model for type-3 long QT syndrome (LQT3), TG-NS/LQT3. Optical mapping is a high temporal and spatial resolution fluorescence mapping system that records 256 action potentials simultaneously in a Langendorff-perfused heart. Here for the first-time, we provide a spatial view of VT in a genetic LQT3 model using optical mapping. Spontaneous VT was detected in TG-NS/LQT3 hearts, but not in littermate control hearts. VT was initiated primarily by activation of a new firing focus as well as functional conduction block of new activation waves. New firing was initiated at many different Loci in the heart, suggesting that 'increased automaticity' is a key mechanism for initiation of VT. The sustained VT was maintained by a reentry mechanism. Nifedipine, an L-type calcium channel blocker, decreased the frequency of VT, indicating the involvement of abnormalities of the calcium homeostasis in the genesis of VT in TG-NS/LQT3 mice.
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