Key result
Altered intracellular sodium homeostasis and the slow inactivating sodium current play a key role in the pathophysiology of heart failure and the propensity for cardiac arrhythmias.
This review highlights the pathophysiological importance of intracellular sodium homeostasis and the late sodium current in heart failure and arrhythmogenesis.
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Supports late sodium current research in heart failure; leaves open clinical benefits of targeted inhibitors pending trials.
In recent years, it has become increasingly clear that, as well as abnormal intracellular calcium handling, changes in intracellular sodium homeostasis play an important role in the pathophysiology of heart failure. One key source of altered sodium homeostasis may be the slow inactivating sodium current. Altered intracellular sodium promotes alterations in intracellular calcium mainly through the sarcolemmal Na+/Ca2+ exchanger that can transport Ca2+ vs. Na+ in both directions. Changes in both calcium and sodium handling are the main factors associated with cardiac dysfunction and the propensity for cardiac arrhythmias. This article gives insight into the mechanisms involved in the pathophysiology of sodium homeostasis in heart failure.
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Maier et al. (2006) conducted a review in Heart failure. Altered intracellular sodium homeostasis and late sodium current was evaluated. Altered intracellular sodium homeostasis and the slow inactivating sodium current play a key role in the pathophysiology of heart failure and the propensity for cardiac arrhythmias.
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