In this article we review the late Na current which functionally can be measured using patch-clamp electrophysiology (INa,late). This current is largely enhanced under pathological myocardial conditions such as ischemia and heart failure. In addition, INa,late can cause systolic and diastolic contractile dysfunction via a Na-dependent Ca-overload of the myocyte. Moreover, INa,late plays a crucial role as ventricular and atrial proarrhythmic substrate in myocardial pathology by changing cellular electrophysiology. We summarize recent experimental and clinical studies that investigate therapeutic inhibition of this current and discuss the significance of the available data and try to answer not only the question, where we currently are but also where we may go in the near future. This article is part of a Special Issue entitled “Na+ Regulation in Cardiac Myocytes”.