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Previous studies indicated that E23K variant of the Kir6.2 subunit of ATP sensitive potassium (KATP) channel was implicated in cardiac remodeling. The present study aimed to evaluate the effects of E23K variant on ventricular electrophysiology and arrhythmogenesis.
Transgenic rats were generated to express human wild type or E23K variant genomic DNA in the heart under α-myosin heavy chain promoter. Electrophysiological parameters including electrocardiograph, ventricular action potential duration (APD), and effective refractory period (ERP) were recorded at baseline and 30 min after acute ischemia. Acute ischemia was induced through occlusion of left anterior descending branch (LAD).
No difference was found for electrophysiological parameters between wild type and E23K variant rats at baseline. However, after acute ischemia stress, shortened QT intervals were further aggravated in E23K variant rats. Also, E23K variant exacerbated the decrease of APD70, APD90 and ERP. Ventricular arrhythmia and alternant threshold was significantly decreased, and duration of ventricular arrhythmia induced by electrical stimulation was significantly prolonged in E23K variant rats.
E23K variant of the KATP channel increased the susceptibility of ventricular arrhythmia induced by acute ischemia.