Chronic heart failure (CHF) has a high incidence rate and mortality rate, seriously affecting the quality of life of patients with heart failure. Prolonged action potential duration (APD) resulting from abnormal ion channels and consequent abnormal triggering activity constitutes the main mechanism of arrhythmia in heart failure. Transient outward potassium current (I_to) is mainly involved in the repolarization of AP in cardiomyocytes and plays an important role in prolonging APD in heart failure. Potassium channel interacting protein 2 (KChIP₂) is an important functional subunit of I_to channel and plays a key role in regulating I_to. I_to almost completely disappears in cardiomyocytes in KChIP₂-knockout rats, and the susceptibility to arrhythmia increases significantly. This article reviews the progress in potassium channel mechanism of arrhythmia in chronic heart failure with a view to providing new pathways for the treatment targets of arrhythmia in heart failure.