Large and growing body of data suggest that an increased late sodium current (I_Na,late) can have a significant pathophysiological role in heart failure and other heart diseases. The first goal of this article is to describe how I_Na,late functions under physiological circumstances. The second goal is to show the wide range of cellular mechanisms that can increase I_Na,late in cardiac disease, and also to describe how the up‐regulated I_Na,late contributes to the pathophysiology of heart failure. The final section of the article discusses the possible use of I_Na,late‐modifying drugs in heart failure, on the basis of experimental and preclinical data.