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- W2080574385 abstract "Atrial fibrillation (AF) is associated with atrial conduction disturbances caused by electrical and structural remodeling. We hypothesized that expression of the gap junction protein connexin 43 is reduced during AF, and that atrial Cx43 gene transfer would prevent persistent atrial fibrillation. The first aim of this study was to assess whether atrial fibrillation (AF) is associated with connexin remodeling in a porcine model. Second, a strategy to suppress persistent AF by gene therapy was developed and evaluated in vivo.AF was inducedin domestic pigs via atrial burst pacing, causing a 62.4% reduction of atrial Cx43 protein. Adenoviruses encoding for connexin 43 (Ad-Cx43) or green fluorescent protein (Ad-GFP) were injected into both atria, followed by epicardial electroporation to enhance transgene expression. Ad-Cx43 treated animals did not exhibit persistent AF during the observation period of 14 days. In contrast, control animals developed persistent AF within 7.4 ± 0.5 days. Rapid ventricular heart rates during AF led to deterioration of cardiac function in control pigs but not in animals treated with Ad-Cx43.In conclusion, our results highlight the contribution of connexin 43 to atrial fibrillation and demonstrate the viability of electrophysiological gene therapy for prevention of atrial arrhythmias." @default.
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- W2080574385 date "2012-01-01" @default.
- W2080574385 modified "2023-09-28" @default.
- W2080574385 title "Suppression of Atrial Fibrillation by Over-Expression of Connexin 43 in a Porcine Model" @default.
- W2080574385 doi "https://doi.org/10.1016/j.bpj.2011.11.3671" @default.
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