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(Circulation Research. 2007;101:1073.)
© 2007 American Heart Association, Inc.

Editorials

Fading Sodium Channels in Failing Hearts

John R. Bankston, Robert S. Kass

From the Department of Pharmacology, College of Physicians & Surgeons, Columbia University, NY.

Correspondence to Robert S. Kass, PhD, Department of Pharmacology, College of Physicians & Surgeons, Columbia University, 630 W 168th St, New York, NY 10032. E-mail rsk20@columbia.edu

See related article, pages 1146–1154

Key Words: arrhythmia • transcription • ventricular tachycardia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Heart failure (HF) affects over 5 million Americans with 550 000 new cases diagnosed each year. Despite advances in understanding and treatment the mortality rate remains extremely high with up to 50% of the patients dying suddenly.¹ Ventricular arrhythmias are frequently the cause of sudden death in these heart failure patients. The mechanisms for these arrhythmias remain the focus of fervent research, but ion channel remodeling in the heart with prolongation of the action potential is one of the best documented changes in heart failure that lead to these fatal arrhythmias.² Prolongation of the cardiac action potential can occur through a decrease in outward current or an increase in inward current during the plateau phase of the action potential. Reduction in outwardly conducting potassium channels during heart failure has been well documented.^2,3 The role of the inwardly conducting cardiac sodium channel (Na_V1.5) in sudden death in heart failure patients is much less clear. In this issue of Circulation Research, Shang et al⁴ report a novel contribution of altered gene transcription in failing hearts to the expression of potentially arrhythmogenic dysfunctional sodium channels expressed in the heart.

	Sodium Channels and Channelopathies

 
During excitation, opening of the cardiac sodium channel produces a large and rapid inward current that underlies membrane depolarization and conduction of electrical impulses in the heart. The precise timing of ion channel opening and closing can be altered under pathological conditions or during drug treatment, resulting in changes in cellular action potentials that can eventually affect heart function. Dysfunctional sodium channel . . . [Full Text of this Article]

Related Article:

Human Heart Failure Is Associated With Abnormal C-Terminal Splicing Variants in the Cardiac Sodium Channel

Lijuan L. Shang, Arnold E. Pfahnl, Shamarendra Sanyal, Zhe Jiao, Jon Allen, Kathrin Banach, John Fahrenbach, Daiana Weiss, W. Robert Taylor, A. Maziar Zafari, and Samuel C. Dudley, Jr
Circ. Res. 2007 101: 1146-1154. [Abstract] [Full Text] [PDF]