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