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      Acquired Long QT Syndrome and Electrophysiology of Torsade de Pointes

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          Abstract

          Congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS remains the domain of cardiologists, cardiac electrophysiologists and specialised centres, the much more frequently acquired LQTS is the domain of physicians and other members of healthcare teams required to make therapeutic decisions. This paper reviews the electrophysiological mechanisms of acquired LQTS, its ECG characteristics, clinical presentation, and management. The paper concludes with a comprehensive review of the electrophysiological mechanisms of torsade de pointes.

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          SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome.

          Q. Wang, J. Shen, I Splawski … (1995)
          Long QT syndrome (LQT) is an inherited disorder that causes sudden death from cardiac arrhythmias, specifically torsade de pointes and ventricular fibrillation. We previously mapped three LQT loci: LQT1 on chromosome 11p15.5, LQT2 on 7q35-36, and LQT3 on 3p21-24. Here we report genetic linkage between LQT3 and polymorphisms within SCN5A, the cardiac sodium channel gene. Single strand conformation polymorphism and DNA sequence analyses reveal identical intragenic deletions of SCN5A in affected members of two unrelated LQT families. The deleted sequences reside in a region that is important for channel inactivation. These data suggest that mutations in SCN5A cause chromosome 3-linked LQT and indicate a likely cellular mechanism for this disorder.
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            Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation.

            Barbara Drew, Michael J Ackerman, Marjorie Funk … (2010)
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              Drug-induced long QT syndrome.

              Dan Roden, Prince J. Kannankeril, Dawood Darbar (2010)
              The drug-induced long QT syndrome is a distinct clinical entity that has evolved from an electrophysiologic curiosity to a centerpiece in drug regulation and development. This evolution reflects an increasing recognition that a rare adverse drug effect can profoundly upset the balance between benefit and risk that goes into the prescription of a drug by an individual practitioner as well as the approval of a new drug entity by a regulatory agency. This review will outline how defining the central mechanism, block of the cardiac delayed-rectifier potassium current I(Kr), has contributed to defining risk in patients and in populations. Models for studying risk, and understanding the way in which clinical risk factors modulate cardiac repolarization at the molecular level are discussed. Finally, the role of genetic variants in modulating risk is described.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arrhythm Electrophysiol Rev
                Journal ID (iso-abbrev): Arrhythm Electrophysiol Rev
                Journal ID (publisher-id): AER
                Title: Arrhythmia & Electrophysiology Review
                Publisher: Radcliffe Cardiology
                ISSN (Print): 2050-3369
                ISSN (Electronic): 2050-3377
                Publication date (Print): March 2019
                Volume: 8
                Issue: 2
                Pages: 122-130
                Affiliations
                [1. ] SUNY Downstate Medical Center NY, US
                [2. ] VA NY Harbor Healthcare System NY, US
                [3. ] NYU School of Medicine New York NY, US
                [4. ] Weill Cornell Medical College, NewYork-Presbyterian Brooklyn Methodist Hospital NY, US
                Author notes

                Disclosure: The authors have no conflicts of interest to declare.

                Correspondence: Nabil El-Sherif, VA NY Harbor Healthcare System, 800 Poly Place, 10th Floor, Brooklyn, NY 11209, US. E: nelsherif@ 123456aol.com
                Article
                DOI: 10.15420/aer.2019.8.3
                PMC ID: 6528034
                PubMed ID: 31114687
                SO-VID: acb81015-02fe-4695-a3d4-a0f226cca1ec
                Copyright © Copyright © 2019, Radcliffe Cardiology
                License:

                This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

                History
                Date received : 28 November 2018
                Date accepted : 04 April 2019
                Page count
                Pages: 9
                Categories
                Subject: Electrophysiology & Ablation

                Keywords: long qt syndrome,torsade de pointes,electrophysiology
                Data availability:
                Keywords: long qt syndrome, torsade de pointes, electrophysiology

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