Connexin gene transfer preserves conduction velocity and prevents atrial fibrillation.

ABSTRACT:

Background

Several lines of evidence have suggested that maintenance of atrial fibrillation (AF) depends on reentrant mechanisms. Maintenance of reentry necessitates a sufficiently short refractory period and/or delayed conduction, and AF has been associated with both alterations. Fibrosis, cellular dysfunction, and gap junction protein alterations occur in AF and cause conduction delay. We performed this study to test the hypothesis that gap junction protein overexpression would improve conduction and prevent AF.

Methods and results

Thirty Yorkshire swine were randomized into 2 groups (sinus rhythm and AF), and each group into 3 subgroups: sham-operated control, gene therapy with adenovirus expressing connexin (Cx) 40, and gene therapy with adenovirus expressing Cx43 (n=5 p

SUBMITTER: Igarashi T 

PROVIDER: S-EPMC3260348 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature