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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/19452
Title: Congenital long QT syndrome
Authors: Michael J. Ackerman
Anant Khositseth
David J. Tester
Peter J. Schwartz
Mayo Medical School
Mahidol University
Universita degli Studi di Pavia
Keywords: Medicine
Issue Date: 1-Dec-2008
Citation: Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention. (2008), 462-482
Abstract: Once considered an extremely rare yet lethal arrhythmogenic peculiarity, congenital long QT syndrome (LQTS) is understood today as a primary cardiac arrhythmia syndrome (cardiac channelopathy) that is both far more common and, overall, much less lethal than previously recognized. Clinically, LQTS is often characterized by prolongation of the heart rate corrected QT interval (QTc) on a 12-lead surface electrocardiogram (ECG) and is associated with syncope, seizures, and sudden cardiac death due to ventricular arrhythmias (Torsade des pointes, TdP) usually following a precipitating event such as exertion, extreme emotion, or auditory stimulation. The molecular breakthroughs of the 1990s, led in large measure by the research laboratories of Drs. Mark Keating and Jeffrey Towbin in conjunction with LQTS registries containing meticulously phenotyped patients directed by Drs. Arthur Moss and Peter Schwartz, revealed the fundamental molecular underpinnings of LQTS- namely, defective cardiac channels.1 © 2008 Springer-Verlag London Limited.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84890172651&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/19452
Appears in Collections:Scopus 2006-2010

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