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ABSTRACT: Background
In cardiac gene therapy to improve contractile function, achieving gene expression in the majority of cardiac myocytes is essential. In preventing cardiac arrhythmias, however, this goal may not be as important since transduction efficiencies as low as 40% suppressed ventricular arrhythmias in genetically modified mice with catecholaminergic polymorphic ventricular tachycardia.Methods
Using computational modeling, we simulated 1-, 2-, and 3-dimensional tissue under a variety of conditions to test the ability of genetically engineered nonarrhythmogenic stabilizer cells to suppress triggered activity due to delayed or early afterdepolarizations.Results
Due to source-sink relationships in cardiac tissue, a minority (20%-50%) of randomly distributed stabilize
SUBMITTER: Liu MB
PROVIDER: S-EPMC7494545 | biostudies-literature | 2020 Sep
REPOSITORIES: biostudies-literature