© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Cellular electrophysiology of atrial fibrillation
aDepartment of Cardiology, University of Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany
bResearch Center and Department of Medicine, Montreal Heart Institute, Montreal, QC, Canada
cDepartment of Medicine, University of Montreal, Montreal, QC, Canada
dDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada
* Corresponding author. Tel.: +49-7071-298-3196; fax: +49-7071-294-121 ralph.bosch@uni-tuebingen.de
Received 28 August 2001; accepted 29 October 2001
KEYWORDS Arrhythmia (mechanisms); Ion channels; Membrane currents; Remodeling; Supraventr. arrhythmia
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1. Introduction |
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Atrial fibrillation (AF) is presently the most common cardiac arrhythmia in clinical practice. Its treatment is inadequate. Maintenance of normal sinus rhythm (SR) is obviously the optimal approach, but is difficult to achieve without drugs that have the potential to cause ventricular proarrhythmia and increase mortality. Non-pharmacological therapy is attractive, but to date has not reached the same level of efficacy as in the treatment of arrhythmias other than AF. In order to improve therapeutic approaches, it is important to understand the detailed pathophysiology of the arrhythmia. A key component to the pathophysiology of any cardiac arrhythmia is the cellular milieu in which it occurs. Changes in ion transport processes, including pumps, channels and exchangers, are central to alterations in action potential properties that govern the occurrence of arrhythmias like AF. Action potential duration (APD) determines the refractory period and is therefore a key determinant of the likelihood of reentry.
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2. How can cellular electrophysiology be altered to produce AF? |
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3. Cellular and molecular electrophysiology of atrial fibrillation — experimental considerations |
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3.1 Cellular abnormalities in conditions associated with AF
3.1.1 Congestive heart failure (CHF)
3.1.2 Hyperthyroidism
3.1.3 Thoracic surgery
3.2 Significance and cellular mechanisms of atrial tachycardia-induced remodeling
3.3 Cellular and molecular mechanisms of atrial tachycardia/AF induced remodeling in experimental models
3.4 Cellular and molecular remodeling in human AF
3.5 Cellular changes in early phases of remodeling
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4. Functional consequences and clinical implications of electrical remodeling |
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5. Conclusions |
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