Electrical remodeling and arrhythmias in long-QT syndrome: lessons from genetic models in mice.
Mutations in cardiac voltage-gated K+ channels cause long-QT syndrome (LQTS) and sudden death. We have created a mouse with a long-QT phenotype by overexpression of truncated K+ channels in the heart and have investigated the phenotype of these mice. These mice have long-QT phenotype, and spontaneous and inducible arrhythmias. Optical mapping of Kv1DN mice revealed spatial and temporal dispersion of repolarization that underlies the arrhythmias. Here I review our attempts to abolish arrhythmias in this model by crossbreeding with Kv4DN and Kv2DN mice or direct injection of adenoviral or adeno-associated viral vectors expressing wild-type Kv1.5 (AV-Kv1.5) into the myocardium. Our published work suggests that the viral vectors rescue the phenotype at the cellular level, while crossbreeding with Kv4DN mice attenuates the spontaneous and inducible arrhythmias.[1]References
- Electrical remodeling and arrhythmias in long-QT syndrome: lessons from genetic models in mice. Koren, G. Ann. Med. (2004) [Pubmed]
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