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HIV protease inhibitors induced prolongation of the QT Interval: electrophysiology and clinical implications.
MedLine Citation:
PMID:  19636247     Owner:  NLM     Status:  In-Process    
In recent years, there have been considerable advancements in our understanding of the role of ionic channels in mediating cardiac repolarization. Advances in ion channel cloning have generated great interest in the diagnosis and understanding of electrophysiological processes involved in ventricular repolarization, particularly the QT interval prolongation and abnormal T- and T/U-wave morphology associated with torsades de pointes. Unfortunately, a number of drugs are being increasingly recognized to alter the repolarization and, thus, increase the propensity for various cardiac arrhythmias, especially polymorphic ventricular tachycardia, syncope, and even ventricular fibrillation and sudden death. Recently, HIV protease inhibitors have been shown to cause prolongation of ventricular repolarization. This review focuses on electrophysiological mechanisms underlying drug-induced QTc prolongation in relation to protease inhibitors and its clinical implications.
Mukesh Singh; Rohit Arora; Evyan Jawad
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American journal of therapeutics     Volume:  17     ISSN:  1536-3686     ISO Abbreviation:  Am J Ther     Publication Date:    2010 Nov-Dec
Date Detail:
Created Date:  2010-11-09     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9441347     Medline TA:  Am J Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e193-201     Citation Subset:  IM    
Section of Cardiology, Department of Medicine, Rosalind Franklin University of Medicine & Science/The Chicago Medical School, North Chicago, and Mount Sinai Hospital, Chicago, IL, USA.
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