Oita International Electrocardiology Symposium 2000 “Electrophysiology and Management of Lethal Arrhythmias in the New Millennium: From Genes to Bedside”
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Key result
In vivo adenovirus-mediated dominant-negative suppression of Ito1 in rat cardiocytes prolonged action potential duration at 90% repolarization (p=0.0001) and prolonged the QT interval by approximately 30%.
Population
Adult guinea-pigs and rats
Design
Preclinical
Follow-up
72 hours
Authors
Discussion
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Implication
Provides rat model of Ito1-mediated long QT; leaves open translation to human repolarization disorders or therapies.
Structured PICO
P
Population
Adult guinea-pigs and rats subjected to intramyocardial injection of adenoviral constructs to study cardiac repolarization.
I
Intervention
In vivo direct intramyocardial injection of adenovirus vectors to overexpress (wild-type Kv4.3) or suppress (dominant-negative Kv4.3W362F) the Ca2+-independent transient outward current (Ito1)
O
Outcome
Electrophysiological properties including transient outward current (Ito1) density, action potential duration (APD), plateau potential, and QT interval measured 72 hours after injectionsurrogate
Main Result
p-value: p=0.0001
Somatic gene transfer of Kv4.3 constructs in vivo demonstrates that Ito1 plays a crucial role in setting action potential duration and can be used to create gene-specific animal models of long QT syndrome.
Cite This Study
Eduardo Marbán (2000) studied Long QT syndrome and heart failure models. Adenovirus-mediated in vivo gene transfer (Kv4.3 or dominant-negative Kv4.3W362F) vs. Uninfected/baseline state was evaluated on Action potential duration and QT interval (p=0.0001). In vivo adenovirus-mediated dominant-negative suppression of Ito1 in rat cardiocytes prolonged action potential duration at 90% repolarization (p=0.0001) and prolonged the QT interval by approximately 30%.
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