Journal
CARDIOVASCULAR DRUGS AND THERAPY
Volume 27, Issue 1, Pages 91-101Publisher
SPRINGER
DOI: 10.1007/s10557-012-6433-x
Keywords
Late sodium current; Pharmacology; Myocardial ischemia; Heart failure; Arrhythmias; Long QT syndrome
Funding
- InterUniversity Cardiology Institute of the Netherlands (ICIN) [061.02]
- Division for Earth and Life Sciences (ALW)
- Netherlands Organization for Scientific Research (NWO) [836.09.003]
- Gilead Sciences
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The late sodium current has been increasingly recognized for its mechanistic role in various cardiovascular pathologies, including angina pectoris, myocardial ischemia, atrial fibrillation, heart failure and congenital long QT syndrome. Although relatively small in magnitude, the late sodium current (I-NaL) represents a functionally relevant contributor to cardiomyocyte (electro)physiology. Many aspects of I-NaL itself are as yet still unresolved, including its distribution and function in different cell types throughout the heart, and its regulation by sodium channel accessory proteins and intracellular signalling pathways. Its complexity is further increased by a close interrelationship with the peak sodium current and other ion currents, hindering the development of inhibitors with selective and specific properties. Thus, increased knowledge of the intricacies of the complex nature of I-NaL during distinct cardiovascular conditions and its potential as a pharmacological target is essential. Here, we provide an overview of the functional and electrophysiological effects of late sodium current inhibition on the level of the ventricular myocyte, and its potential cardioprotective and anti-arrhythmic efficacy in the setting of acquired and inherited ventricular dysfunction and arrhythmias.
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