title: Molecular ablation of ventricular tachycardia after myocardial infarction.
abstract: Ventricular tachycardia is a common and lethal complication after myocardial infarction. Here we show that focal transfer of a gene encoding a dominant-negative version of the KCNH2 potassium channel (KCNH2-G628S) to the infarct scar border eliminated all ventricular arrhythmias in a porcine model. No proarrhythmia or other negative effects were discernable. Our results demonstrate the potential viability of gene therapy for ablation of ventricular arrhythmias.
authors.affiliation: Heart and Vascular Research Center, MetroHealth Hospital, Case Western Reserve University School of Medicine, Rammelkamp 653, 2500 MetroHealth Drive, Cleveland, Ohio 44109, USA.
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Sasano
authors.forename: Amy D
authors.initials: AD
authors.lastname: McDonald
authors.forename: Kan
authors.initials: K
authors.lastname: Kikuchi
authors.forename: J Kevin
authors.initials: JK
authors.lastname: Donahue
mesh_terms: D000818:Animals; D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; D015316:Genetic Therapy; D009203:Myocardial Infarction / Q000503:physiopathology*; D024642:Potassium Channels, Voltage-Gated / Q000235:genetics*; D013552:Swine; D017180:Tachycardia, Ventricular / Q000503:physiopathology / Q000628:therapy*; D014162:Transfection
chemical_list: D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; D024642:Potassium Channels, Voltage-Gated