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      The Measurement of the QT Interval

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          Abstract

          The evaluation of every electrocardiogram should also include an effort to interpret the QT interval to assess the risk of malignant arrhythmias and sudden death associated with an aberrant QT interval. The QT interval is measured from the beginning of the QRS complex to the end of the T-wave, and should be corrected for heart rate to enable comparison with reference values. However, the correct determination of the QT interval, and its value, appears to be a daunting task. Although computerized analysis and interpretation of the QT interval are widely available, these might well over- or underestimate the QT interval and may thus either result in unnecessary treatment or preclude appropriate measures to be taken. This is particularly evident with difficult T-wave morphologies and technically suboptimal ECGs. Similarly, also accurate manual assessment of the QT interval appears to be difficult for many physicians worldwide. In this review we delineate the history of the measurement of the QT interval, its underlying pathophysiological mechanisms and the current standards of the measurement of the QT interval, we provide a glimpse into the future and we discuss several issues troubling accurate measurement of the QT interval. These issues include the lead choice, U-waves, determination of the end of the T-wave, different heart rate correction formulas, arrhythmias and the definition of normal and aberrant QT intervals. Furthermore, we provide recommendations that may serve as guidance to address these complexities and which support accurate assessment of the QT interval and its interpretation.

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          Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2.

          J. E. M. Robinson, Margaret M. Lehmann, Alexander Towbin … (2000)
          Long-QT Syndrome (LQTS) is a cardiovascular disorder characterized by prolongation of the QT interval on ECG and presence of syncope, seizures, and sudden death. Five genes have been implicated in Romano-Ward syndrome, the autosomal dominant form of LQTS: KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Mutations in KVLQT1 and KCNE1 also cause the Jervell and Lange-Nielsen syndrome, a form of LQTS associated with deafness, a phenotypic abnormality inherited in an autosomal recessive fashion. We used mutational analyses to screen a pool of 262 unrelated individuals with LQTS for mutations in the 5 defined genes. We identified 134 mutations in addition to the 43 that we previously reported. Eighty of the mutations were novel. The total number of mutations in this population is now 177 (68% of individuals). KVLQT1 (42%) and HERG (45%) accounted for 87% of identified mutations, and SCN5A (8%), KCNE1 (3%), and KCNE2 (2%) accounted for the other 13%. Missense mutations were most common (72%), followed by frameshift mutations (10%), in-frame deletions, and nonsense and splice-site mutations (5% to 7% each). Most mutations resided in intracellular (52%) and transmembrane (30%) domains; 12% were found in pore and 6% in extracellular segments. In most cases (78%), a mutation was found in a single family or an individual.
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            AN ANALYSIS OF THE TIME-RELATIONS OF ELECTROCARDIOGRAMS.

            H C Bazett (1997)
            Article 0 comments Cited 146 times – based on 0 reviews     Review now
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              Sudden death associated with short-QT syndrome linked to mutations in HERG.

              Ramon Brugada, Guido Pollevick, M Menéndez … (2004)
              Sudden cardiac death takes the lives of more than 300 000 Americans annually. Malignant ventricular arrhythmias occurring in individuals with structurally normal hearts account for a subgroup of these sudden deaths. The present study describes the genetic basis for a new clinical entity characterized by sudden death and short-QT intervals in the ECG. Three families with hereditary short-QT syndrome and a high incidence of ventricular arrhythmias and sudden cardiac death were studied. In 2 of them, we identified 2 different missense mutations resulting in the same amino acid change (N588K) in the S5-P loop region of the cardiac IKr channel HERG (KCNH2). The mutations dramatically increase IKr, leading to heterogeneous abbreviation of action potential duration and refractoriness, and reduce the affinity of the channels to IKr blockers. We demonstrate a novel genetic and biophysical mechanism responsible for sudden death in infants, children, and young adults caused by mutations in KCNH2. The occurrence of sudden cardiac death in the first 12 months of life in 2 patients suggests the possibility of a link between KCNH2 gain of function mutations and sudden infant death syndrome. KCNH2 is the binding target for a wide spectrum of cardiac and noncardiac pharmacological compounds. Our findings may provide better understanding of drug interaction with KCNH2 and have implications for diagnosis and therapy of this and other arrhythmogenic diseases.
              Article 0 comments Cited 125 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Cardiol Rev
                Journal ID (iso-abbrev): Curr Cardiol Rev
                Journal ID (publisher-id): CCR
                Title: Current Cardiology Reviews
                Publisher: Bentham Science Publishers
                ISSN (Print): 1573-403X
                ISSN (Electronic): 1875-6557
                Publication date (Print): August 2014
                Publication date (Electronic): August 2014
                Volume: 10
                Issue: 3
                Pages: 287-294
                Affiliations
                Heart Center, Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands
                Author notes
                [* ] Address correspondence to this author at the Department of Cardiology, Academic Medical Center, P.O. box 22660, 1100 DD Amsterdam, The Netherlands; Tel: +31-20-5663072; Fax: +31-20-6971385; E-mail: P.G.Postema@ 123456cardiologie-amc.nl
                Article
                Publisher ID: CCR-10-287
                DOI: 10.2174/1573403X10666140514103612
                PMC ID: 4040880
                PubMed ID: 24827793
                SO-VID: 5e446e0d-5313-4d03-9c5e-2e541869a534
                Copyright © © 2014 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 10 June 2013
                Date revision received : 10 June 2013
                Date accepted : 28 January 2014
                Categories
                Subject: Article

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: qt interval,long qt syndrome,arrhythmias,sudden death.
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: qt interval, long qt syndrome, arrhythmias, sudden death.

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