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Therapeutic inhibition of the late Na current (INa,late) is reviewed as a potential strategy to address contractile dysfunction and proarrhythmic substrates in ischemia and heart failure.
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This review summarizes the role of the late Na current in myocardial pathology and the potential of its therapeutic inhibition.
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".
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Maier et al. (2013) conducted a review in Ischemia and heart failure. Therapeutic inhibition of late Na current (INa,late) was evaluated. Therapeutic inhibition of the late Na current (INa,late) is reviewed as a potential strategy to address contractile dysfunction and proarrhythmic substrates in ischemia and heart failure.
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