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Cardiovascular Research 2000 48(2):188-190; doi:10.1016/S0008-6363(00)00181-4
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Acquired delayed rectifier channelopathies: how heart disease and antiarrhythmic drugs mimic potentially-lethal congenital cardiac disorders

Stanley Nattel*

Research Center and Department of Medicine, Montreal Heart Institute, 5000 Belanger Street E., Montreal, Quebec H1T 1C8; and University of Montreal, Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada

* Tel.: +1-514-376-3330; fax: +1-514-593-2521 nattel@icm.umontreal.ca

Received 28 June 2000; accepted 28 June 2000

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

See article by Tsuji et al. [10] (pages 300–309) in this issue.

The discovery of the molecular bases of the congenital long QT syndromes (LQTSs) [1–5] has created an explosion of insight, not only into these relatively rare congenital abnormalities, but also into the broader function of delayed rectifier channels in the heart. Recent reviews have covered the pathophysiology of these syndromes in detail [6,7] with arrhythmogenesis due to defects at the level of the density of repolarizing current and/or abnormal kinetics. The evolving knowledge has highlighted the role of the rapid component (IKr) of delayed rectifier current (IK) as a primary repolarizing current in ventricular tissue (including the human heart) and of the slower component (IKs) as an important ‘safety factor’ in the presence of adrenergic stimulation [8] or prolonged action potentials (APs) [9].

The article by Tsuji et . . . [Full Text of this Article]


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