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Cardiovascular Research 2003 58(3):498-500; doi:10.1016/S0008-6363(03)00370-5
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Pharmacological electrical remodelling in human atria induced by chronic β-blockade

Carmen Valenzuela*

Institute of Pharmacology and Toxicology CSIC/UCM, School of Medicine, Universidad Complutense, 28040 Madrid, Spain

carmenva@med.ucm.es

* Tel.: +34-91-384-1474; fax: +34-91-394-1470.

Received 28 March 2003; accepted 1 April 2003

The first 10% of the full text of this article appears below.

See article by Workman et al. [5] (pages 518–525) in this issue.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia found in clinical practice. AF is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activation with consequent deterioration of atrial mechanical function [1]. The ventricular response to AF depends on the electrophysiological properties of the atrio-ventricular (AV) node, the level of vagal or sympathetic tone, and the action of drugs with which the patient is being treated [2]. Very often, AF occurs in conjunction with other cardiovascular diseases, such as hypertension, ischaemic heart disease, valve disease, or cardiac failure. However, in a certain percentage of patients (20–50%) AF is not associated with any underlying pathology [3]. Treatment with β-blockers is considered to be efficacious for controlling the ventricular heart rate during AF, which is likely due . . . [Full Text of this Article]


   1 Electrical remodelling during AF
 

   2 Effects of chronic treatment with β-blockers on atrial human action potentials and ionic currents
 

   3 Conclusions
 

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