© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Atrial fibrillation: from cells to computers
aCardiac Electrophysiology Section, Division of Cardiology, Department of Medicine, University of Iowa Hospitals and Clinics, 4426 B, JCP, 200 Hawkins Drive, Iowa City, IA 52242-1081, USA
bUCLA Cardiovascular Research Laboratory, Departments of Medicine (Cardiology) and Physiology, UCLA School of Medicine, Los Angeles, CA 90095, USA
* Corresponding author. Tel.: +1-319-384-6105; fax: +1-319-384-6247 kalyanam-shivkumar@uiowa.edu
accepted 6 September 2001
| The first 150 words of the full text of this article appear below. |
See article by Workman et al. [11] (pages 226–235) in this issue.
Atrial fibrillation is one of the commonest arrhythmias encountered in clinical practice. The incidence of this arrhythmia increases with age and it is responsible for substantial morbidity, mortality [1]. Numerous studies have been performed to elucidate the cellular and molecular events associated with this rhythm. Our conceptual framework for understanding this rhythm disturbance is based on the pioneering work of Gordon Moe [2]. Atrial fibrillation is thought to be due to repetitive activation of the atria by multiple reentrant wavelets. Subsequent experimental work confirmed the key elements of the hypothesis of Moe [1]. The exact origin and the behavior of such wavelets is a source of intense ongoing investigation utilizing experimental and computational approaches.
| 1. Cellular electrophysiological changes due to AF |
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The cellular ionic changes that allow repetitive activation of the atria at such high rates have been the focus of several
| 2. The present study |
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| 3. Intra-atrial and inter-atrial heterogeneity in action potential characteristics |
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| 4. What are the implications of such studies? |
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| 5. Future questions |
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