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Background  Congestive heart failure ( CHF ) is a common cardiovascular disease that is often accompanied by ventricular arrhythmias. The decrease of the slow component of the delayed rectifier potassium current ( I K   s ) in  CHF  leads to action potential ( AP ) prolongation, and the  I K   s  is an important contributor to the development of ventricular arrhythmias. However, the molecular mechanisms underlying ventricular arrhythmias are still unknown.    Methods and Results  Kcna2 and Kcna2 antisense RNA (Kcna2  AS)  transcript expression was measured in rat cardiac tissues using quantitative real‐time reverse transcription–polymerase chain reaction and Western blotting. There was a 43% reduction in Kcna2  mRNA  in the left ventricular myocardium of rats with  CHF . Kcna2 knockdown in the heart decreased the I Ks  and prolonged  AP s in cardiomyocytes, consistent with the changes observed in heart failure. Conversely, Kcna2 overexpression in the heart significantly attenuated the  CHF ‐induced decreases in the I Ks ,  AP  prolongation, and ventricular arrhythmias. Kcna2  AS  was upregulated ≈1.7‐fold in rats with  CHF  and with phenylephrine‐induced cardiomyocyte hypertrophy. Kcna2  AS  inhibition increased the  CHF ‐induced downregulation of Kcna2. Consequently, Kcna2 AS mitigated the decrease in the I Ks  and the prolongation of  AP s in vivo and in vitro and reduced ventricular arrhythmias, as detected using electrocardiography.    Conclusions  Ventricular Kcna2  AS  expression increases in rats with  CHF  and contributes to reduced  I K   s , prolonged  AP s, and the occurrence of ventricular arrhythmias by silencing Kcna2. Thus, Kcna2  AS  may be a new target for the prevention and treatment of ventricular arrhythmias in patients with  CHF .

Long Noncoding RNA Kcna2 Antisense RNA Contributes to Ventricular Arrhythmias via Silencing Kcna2 in Rats With Congestive Heart Failure