Arrhythmogenic ion-channel remodeling in the heart: heart failure, myocardial infarction, and atrial fibrillation.

Full Abstract

Rhythmic and effective cardiac contraction depends on appropriately timed generation and spread of cardiac electrical activity. The basic cellular unit of such activity is the action potential, which is shaped by specialized proteins (channels and transporters) that control the movement of ions across cardiac cell membranes in a highly regulated fashion. Cardiac disease modifies the operation of ion channels and transporters in a way that promotes the occurrence of cardiac rhythm disturbances, a process called "arrhythmogenic remodeling." Arrhythmogenic remodeling involves alterations in ion channel and transporter expression, regulation and association with important protein partners, and has important pathophysiological implications that contribute in major ways to cardiac morbidity and mortality. We review the changes in ion channel and transporter properties associated with three important clinical and experimental paradigms:
congestive heart failure, myocardial infarction, and atrial fibrillation. We pay particular attention to K+, Na+, and Ca2+ channels; Ca2+ transporters; connexins; and hyperpolarization-activated nonselective cation channels and discuss the mechanisms through which changes in ion handling processes lead to cardiac arrhythmias. We highlight areas of future investigation, as well as important opportunities for improved therapeutic approaches that are being opened by an improved understanding of the mechanisms of arrhythmogenic remodeling.

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Author information

Author/s: Nattel, Stanley (S); Maguy, Ange (A); Le Bouter, Sabrina (S); Yeh, Yung-Hsin (YH);

Affiliation: Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, Quebec, Canada. stanley.nattel(-atsign-)icm-mhi.org

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Physiological reviews (Physiol Rev), published in United States. (Language: eng)

Reference: 2007-Apr; vol 87 (issue 2) : pp 425-56

Dates: Created 2007/04/12; Completed 2007/05/15; Revised 2007/11/15;

PMID: 17429037, status: MEDLINE (last retrieval date: 12/26/2008)

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Arrhythmias, Cardiac - metabolism; physiopathology
Atrial Fibrillation - metabolism; physiopathology
Electrophysiology
Heart - physiopathology

Heart - physiopathology
Heart Failure - metabolism; physiopathology
Humans
Ion Channels - physiology
Myocardial Infarction - metabolism; physiopathology

Associated Chemicals: Ion Channels (0)

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