Long QT syndrome - Mark Dayer
Long QT syndromeDefinitionLong QT syndrome (LQTS) can be defined asan inheritedcondition associated with a prolongation of theQT interval on the ECG characterized by syncope,seizures, and sudden death secondary to ventricular arrhythmia,specifically torsade de pointes ADDIN EN.CITE <EndNote><Cite><Author>Schwartz</Author><Year>1987</Year><RecNum>4967</RecNum><record><rec-number>4967</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">4967</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schwartz, P. J.</author></authors></contributors><titles><title>[From clinical medicine to electrophysiology. The case of the long QT syndrome]</title><secondary-title>Cardiologia</secondary-title></titles><periodical><full-title>Cardiologia</full-title></periodical><pages>1685-7</pages><volume>32</volume><number>12</number><edition>1987/12/01</edition><keywords><keyword>Adolescent</keyword><keyword>Arrhythmias, Cardiac/*diagnosis</keyword><keyword>Cardiac Pacing, Artificial</keyword><keyword>Child</keyword><keyword>Child, Preschool</keyword><keyword>Electrophysiology</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/*diagnosis/physiopathology</keyword><keyword>Prognosis</keyword></keywords><dates><year>1987</year><pub-dates><date>Dec</date></pub-dates></dates><orig-pub>Dalla clinica all'elettrofisiologia. Il caso della sindrome del QT lungo.</orig-pub><isbn>0393-1978 (Print)</isbn><accession-num>3447719</accession-num><urls><related-urls><url>. It may be congenital or acquired.Prevalence of congenital LQTSA recent study of 43 080 white infants 15 to 25 days old identified 17 who were affected by LQTS, demonstrating a prevalence of at least 1:2534 apparently healthy live births (95% confidence interval, 1:1583 to 1:4350) ADDIN EN.CITE <EndNote><Cite><Author>Schwartz</Author><Year>2009</Year><RecNum>16</RecNum><record><rec-number>16</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">16</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schwartz, P. J.</author><author>Stramba-Badiale, M.</author><author>Crotti, L.</author><author>Pedrazzini, M.</author><author>Besana, A.</author><author>Bosi, G.</author><author>Gabbarini, F.</author><author>Goulene, K.</author><author>Insolia, R.</author><author>Mannarino, S.</author><author>Mosca, F.</author><author>Nespoli, L.</author><author>Rimini, A.</author><author>Rosati, E.</author><author>Salice, P.</author><author>Spazzolini, C.</author></authors></contributors><auth-address>Department of Lung, Blood, and Heart, University of Pavia, Pavia, Italy. peter.schwartz@unipv.it</auth-address><titles><title>Prevalence of the congenital long-QT syndrome</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1761-7</pages><volume>120</volume><number>18</number><edition>2009/10/21</edition><dates><year>2009</year><pub-dates><date>Nov 3</date></pub-dates></dates><isbn>1524-4539 (Electronic)</isbn><accession-num>19841298</accession-num><urls><related-urls><url> [pii]
10.1161/CIRCULATIONAHA.109.863209</electronic-resource-num><language>eng</language></record></Cite></EndNote>2. This is now considered to be the most authoritative estimate of the prevalence of this condition.DiagnosisThe ECGThe ECG is the key to diagnosis. Generally, at rest, in men at QTc of > 450ms or in women > 470ms is considered abnormal (Table 1). There are often associated T-wave abnormlities, which may give a clue as to the genotype. However, interpreting the QT interval is by no means straight-forward and there remains controversyPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5SYXV0YWhhcmp1PC9BdXRob3I+PFllYXI+MjAwOTwvWWVh
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ADDIN EN.CITE.DATA 3, 4. There is considerable variability in QTc duration during serial follow-upPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Hb2xkZW5iZXJnPC9BdXRob3I+PFllYXI+MjAwNjwvWWVh
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ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Hb2xkZW5iZXJnPC9BdXRob3I+PFllYXI+MjAwNjwvWWVh
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ADDIN EN.CITE.DATA 5. Furthermore, in 12-30% of patients with LQTS the resting ECG may have a normal QTc interval at restPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WaW5jZW50PC9BdXRob3I+PFllYXI+MTk5MjwvWWVhcj48
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ADDIN EN.CITE.DATA 6, 7. Conversely a proportion of the normal population may have a modestly prolonged QT interval ADDIN EN.CITE <EndNote><Cite><Author>Vetter</Author><Year>2007</Year><RecNum>997</RecNum><record><rec-number>997</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">997</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vetter, V. L.</author></authors></contributors><titles><title>Clues or miscues? How to make the right interpretation and correctly diagnose long-QT syndrome</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>2595-8</pages><volume>115</volume><number>20</number><edition>2007/05/23</edition><keywords><keyword>Child</keyword><keyword>Diagnostic Errors/prevention & control</keyword><keyword>Electrocardiography/*methods</keyword><keyword>Genetic Screening</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/congenital/*diagnosis/genetics</keyword><keyword>Medical History Taking</keyword></keywords><dates><year>2007</year><pub-dates><date>May 22</date></pub-dates></dates><isbn>1524-4539 (Electronic)</isbn><accession-num>17515476</accession-num><urls><related-urls><url> [pii]
10.1161/CIRCULATIONAHA.107.700195</electronic-resource-num><language>eng</language></record></Cite></EndNote>8. Table 1:. Suggested Bazett Corrected QTc values for diagnosing QT prolongation ADDIN EN.CITE <EndNote><Cite><Author>Goldenberg</Author><Year>2006</Year><RecNum>5288</RecNum><record><rec-number>5288</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5288</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Goldenberg, I.</author><author>Moss, A. J.</author><author>Zareba, W.</author></authors></contributors><auth-address>Cardiology Division, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA. Ilan.Goldenberg@heart.rochester.edu</auth-address><titles><title>QT interval: how to measure it and what is "normal"</title><secondary-title>J Cardiovasc Electrophysiol</secondary-title></titles><periodical><full-title>J Cardiovasc Electrophysiol</full-title></periodical><pages>333-6</pages><volume>17</volume><number>3</number><edition>2006/04/29</edition><keywords><keyword>Arrhythmias, Cardiac/*physiopathology</keyword><keyword>Electrocardiography/*methods</keyword><keyword>Heart Conduction System/*physiopathology</keyword><keyword>Heart Rate/physiology</keyword><keyword>Humans</keyword><keyword>Reference Values</keyword></keywords><dates><year>2006</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1045-3873 (Print)</isbn><accession-num>16643414</accession-num><urls><related-urls><url> [pii]
10.1111/j.1540-8167.2006.00408.x</electronic-resource-num><language>eng</language></record></Cite></EndNote>9QT Interval1-15 YearsAdult MaleAdult FemaleNormal (ms)< 440< 430< 450Borderline (ms)440–460430–450450–470Prolonged (ms)> 460> 450> 470Reversible causes and other conditions must be excluded. In brief, drugs are probably the most common cause. A list of drugs which can prolong the QT interval can be found here: . Electrolyte disturbances must also be considered – particularly hypokalaemia, hypomagnesaemia and hypocalcaemia. Intracranial events may also cause QT prolongation, particularly intracranial haemorrhage. Following resuscitation from cardiac arrest the QT interval may remain prolonged for several months (Moss A J, personal communication). Elite athletes may have modest prolongations in their QT interval without having LQTS ADDIN EN.CITE <EndNote><Cite><Author>Basavarajaiah</Author><Year>2007</Year><RecNum>830</RecNum><record><rec-number>830</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">830</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Basavarajaiah, S.</author><author>Wilson, M.</author><author>Whyte, G.</author><author>Shah, A.</author><author>Behr, E.</author><author>Sharma, S.</author></authors></contributors><auth-address>University Hospital Lewisham/King's College Hospital, London SE5 9RS, UK.</auth-address><titles><title>Prevalence and significance of an isolated long QT interval in elite athletes</title><secondary-title>Eur Heart J</secondary-title></titles><periodical><full-title>Eur Heart J</full-title></periodical><pages>2944-9</pages><volume>28</volume><number>23</number><edition>2007/10/20</edition><keywords><keyword>Adolescent</keyword><keyword>Adult</keyword><keyword>Electrocardiography/methods</keyword><keyword>Exercise Test</keyword><keyword>Female</keyword><keyword>Heart Rate/*physiology</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/*diagnosis/epidemiology/genetics</keyword><keyword>Male</keyword><keyword>Prevalence</keyword><keyword>Sports/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>0195-668X (Print)</isbn><accession-num>17947213</accession-num><urls><related-urls><url> [pii]
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ADDIN EN.CITE.DATA 11, 12. In catecholaminergic polymorphic ventricular tachycardia (CPVT) the QT interval may be modestly prolonged ADDIN EN.CITE <EndNote><Cite><Author>Viitasalo</Author><Year>2008</Year><RecNum>5170</RecNum><record><rec-number>5170</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5170</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Viitasalo, M.</author><author>Oikarinen, L.</author><author>Vaananen, H.</author><author>Kontula, K.</author><author>Toivonen, L.</author><author>Swan, H.</author></authors></contributors><titles><title>U-waves and T-wave peak to T-wave end intervals in patients with catecholaminergic polymorphic ventricular tachycardia, effects of beta-blockers</title><secondary-title>Heart Rhythm</secondary-title></titles><periodical><full-title>Heart Rhythm</full-title></periodical><pages>1382-1388</pages><volume>5</volume><number>10</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>13 and, for interest, it should be remembered that LQT7 (Andersen-Tawil syndrome) can present with bidirectional VT ADDIN EN.CITE <EndNote><Cite><Author>Peters</Author><Year>2007</Year><RecNum>5192</RecNum><record><rec-number>5192</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5192</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Peters, S.</author><author>Schulze-Bahr, E.</author><author>Etheridge, S. P.</author><author>Tristani-Firouzi, M.</author></authors></contributors><auth-address>Klinikum Dorothea Christiane Erxleben Quedlinburg, Academic Teaching Hospital of the University Hospital Magdeburg, Innere Medizin II-Kardiologie, Ditfurter Weg 24, 06484 Quedlinburg, Germany. s.peters@klinikum-quedlinburg.de</auth-address><titles><title>Sudden cardiac death in Andersen-Tawil syndrome</title><secondary-title>Europace</secondary-title></titles><periodical><full-title>Europace</full-title></periodical><pages>162-6</pages><volume>9</volume><number>3</number><edition>2007/02/03</edition><keywords><keyword>Andersen Syndrome/*complications/genetics/therapy</keyword><keyword>Death, Sudden, Cardiac/*etiology</keyword><keyword>Defibrillators, Implantable</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Potassium Channels, Inwardly Rectifying/genetics</keyword></keywords><dates><year>2007</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1099-5129 (Print)</isbn><accession-num>17272325</accession-num><urls><related-urls><url> [pii]
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ADDIN EN.CITE.DATA 15, 16. The QTc is prolonged in patients withcardiac amyloid, but this does not seem to correlate withlife-threatening arrhythmias ADDIN EN.CITE <EndNote><Cite><Author>Parthenakis</Author><Year>1996</Year><RecNum>5424</RecNum><record><rec-number>5424</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5424</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Parthenakis, F. I.</author><author>Vardas, P. E.</author><author>Ralidis, L.</author><author>Dritsas, A.</author><author>Nihoyannopoulos, P.</author></authors></contributors><titles><title>QT Interval in Cardiac Amyloidosis</title><secondary-title>Clin Cardiol</secondary-title></titles><periodical><full-title>Clin Cardiol</full-title></periodical><pages>A 22, 442</pages><volume>19</volume><number>1</number><dates><year>1996</year></dates><urls></urls></record></Cite></EndNote>17.The Schwartz scoring systemThe Schwartz scoring system ADDIN EN.CITE <EndNote><Cite><Author>Schwartz</Author><Year>1993</Year><RecNum>4575</RecNum><record><rec-number>4575</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">4575</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schwartz, P. J.</author><author>Moss, A. J.</author><author>Vincent, G. M.</author><author>Crampton, R. S.</author></authors></contributors><auth-address>Istituto di Clinica Medica II, University of Milan, Italy.</auth-address><titles><title>Diagnostic criteria for the long QT syndrome. An update</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>782-4</pages><volume>88</volume><number>2</number><edition>1993/08/01</edition><keywords><keyword>Electrocardiography</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/*diagnosis</keyword></keywords><dates><year>1993</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>0009-7322 (Print)</isbn><accession-num>8339437</accession-num><urls><related-urls><url> is widely used but does not take into account additional genetic information. It is reproduced below in table 2.Table 2 – Schwartz scoring system for diagnosis of LQTSPointsECG Findings1AQTc2≥ 480ms3460-470ms2450-460ms (in males)1BTorsades de pointes32CT-Wave alternans1DNotched T wave in 3 leads1ELow heart rate for age40.5Clinical HistoryASyncope3With stress2Without stress1BCongenital deafnessFamily History5AFamily members with definite LQTS1BUnexplained sudden cardiac death below age 30 among immediate family members0.5Notes1In the absence of medications or disorders known to affect these ECG features2QTc calculated by Bazett’s formula, where QTc=QT/√RR3Mutually exclusive4Resting heart rate below the 2nd percentile for age ADDIN EN.CITE <EndNote><Cite><Author>Davignon</Author><Year>1980</Year><RecNum>5168</RecNum><record><rec-number>5168</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5168</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Davignon, A.</author><author>Rautaharju, B.</author><author>Boisselle, E.</author><author>Soumis, F.</author><author>Megelas, M.</author><author>Choquette, A.</author></authors></contributors><titles><title>Normal ECG standards for infants and children</title><secondary-title>Paediatric Cardiology</secondary-title></titles><periodical><full-title>Paediatric Cardiology</full-title></periodical><pages>123-130</pages><volume>1</volume><dates><year>1980</year></dates><urls></urls></record></Cite></EndNote>195The same family member cannot be counted in A and BScoringDefinite≥ 4Intermediate probability2-3Low probability≤1HistoryThe history can point to a diagnosis of LQTS. In particular patients should be asked if they have:fainted or become dizzy with exercise, fear or strong emotionsdeveloped palpitations with exercise, fear or strong emotionsbeen treated for a seizure disorder ADDIN EN.CITE <EndNote><Cite><Author>Vetter</Author><Year>2007</Year><RecNum>997</RecNum><record><rec-number>997</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">997</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vetter, V. L.</author></authors></contributors><titles><title>Clues or miscues? How to make the right interpretation and correctly diagnose long-QT syndrome</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>2595-8</pages><volume>115</volume><number>20</number><edition>2007/05/23</edition><keywords><keyword>Child</keyword><keyword>Diagnostic Errors/prevention & control</keyword><keyword>Electrocardiography/*methods</keyword><keyword>Genetic Screening</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/congenital/*diagnosis/genetics</keyword><keyword>Medical History Taking</keyword></keywords><dates><year>2007</year><pub-dates><date>May 22</date></pub-dates></dates><isbn>1524-4539 (Electronic)</isbn><accession-num>17515476</accession-num><urls><related-urls><url> [pii]
10.1161/CIRCULATIONAHA.107.700195</electronic-resource-num><language>eng</language></record></Cite></EndNote>8Syncope with exercise, particularly swimming tends to point towards a diagnosis of LQT1. Symptoms following emotional stimulation, particularly fear, or strong auditory stimuli seem more common in patients with LQT2. LQT3 syndrome tends to be associated with problems that occur during sleep. Of note LQT1 tends to present before the age of 9, whereas LQT2 and 3 tend to present in teenagers, although cases can remain undiagnosed until adulthood.A full drug history should be taken, including a history of over-the-counter medications and herbal remedies ADDIN EN.CITE <EndNote><Cite><Author>Agarwal</Author><Year>2005</Year><RecNum>5296</RecNum><record><rec-number>5296</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5296</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Agarwal, S. C.</author><author>Crook, J. R.</author><author>Pepper, C. B.</author></authors></contributors><titles><title>Herbal remedies - how safe are they? A case report of polymorphic ventricular tachycardia/ventricular fibrillation induced by herbal medication used for obesity.</title><secondary-title>Int J Cardiol</secondary-title></titles><periodical><full-title>Int J Cardiol</full-title></periodical><pages>260-261</pages><volume>106</volume><number>2</number><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>20.A history of deafness is important. The Jervell-Lange-Nielsen syndrome – the combination of a long QT interval and congenital deafness was the first of the Long QT syndromes to be described in 1957 ADDIN EN.CITE <EndNote><Cite><Author>Jervell</Author><Year>1957</Year><RecNum>5294</RecNum><record><rec-number>5294</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5294</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jervell, A.</author><author>Lange-Nielsen, F.</author></authors></contributors><titles><title>Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval and sudden death</title><secondary-title>Am Heart J</secondary-title></titles><periodical><full-title>Am Heart J</full-title></periodical><pages>59-68</pages><volume>54</volume><number>1</number><edition>1957/07/01</edition><keywords><keyword>*Deafness</keyword><keyword>Heart Diseases/*complications</keyword></keywords><dates><year>1957</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0002-8703 (Print)</isbn><accession-num>13435203</accession-num><urls><related-urls><url> a comprehensive family history should be taken. A family history of LQTS or unexplained sudden cardiac death raises the likelihood of the index case having LQTS.ExaminationTypically findings on examination will not reveal the diagnosis of LQTS. Some patients may have excessive bradycardia or deafness. Scoliosis and short stature may be seen in LQTS type 7PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Zb29uPC9BdXRob3I+PFllYXI+MjAwNjwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA 23 (Timothy syndrome) is characterised by co-existent congenital heart disease, cognitive dysfucntion, musculoskeletal problems and immune dysfunction. Examination may suggest an alternative diagnosis – for example a murmur may be heard from underlying hypertrophic cardiomyopathy. Routine investigationsEchocardiographyEchocardiography should be normal in patients with LQTS. It would seem sensible, however, when investigating patients for LQTS to perform echocardiography routinely given the nature of the conditions outlines above which can incidentally prolong the QT interval.Holter monitoringIn patients where the diagnosis of LQTS is in doubt holter monitoring may reveal the diagnosis as the QT interval and QTc are variable over time.Exercise testingIn patients with borderline QT intervals, the dynamic behaviour of the QT interval during exercise testing may suggest the diagnosis. Exercise testing may also suggest an alternate diagnosis, particularly CPVT ADDIN EN.CITE <EndNote><Cite><Author>Horner</Author><Year>2008</Year><RecNum>314</RecNum><record><rec-number>314</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">314</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Horner, J. M.</author><author>Ackerman, M. J.</author></authors></contributors><auth-address>Department of Pediatric and Adolescent Medicine, Division of Pediatric Cardiology, Mayo Clinic, Rochester, Minnesota 55905, USA.</auth-address><titles><title>Ventricular ectopy during treadmill exercise stress testing in the evaluation of long QT syndrome</title><secondary-title>Heart Rhythm</secondary-title></titles><periodical><full-title>Heart Rhythm</full-title></periodical><pages>1690-4</pages><volume>5</volume><number>12</number><edition>2008/12/17</edition><keywords><keyword>Diagnosis, Differential</keyword><keyword>*Electrocardiography</keyword><keyword>Exercise Test/*adverse effects</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Heart Rate/physiology</keyword><keyword>Humans</keyword><keyword>Long QT Syndrome/*diagnosis/physiopathology</keyword><keyword>Male</keyword><keyword>Prognosis</keyword><keyword>Retrospective Studies</keyword><keyword>Ventricular Premature Complexes/diagnosis/*etiology/physiopathology</keyword><keyword>Young Adult</keyword></keywords><dates><year>2008</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>1556-3871 (Electronic)</isbn><accession-num>19084807</accession-num><urls><related-urls><url>(08)00869-2 [pii]
10.1016/j.hrthm.2008.08.038</electronic-resource-num><language>eng</language></record></Cite></EndNote>24. Other investigationsEP testing has not proved useful in risk stratification in patients with LQTS (See ACC/AHA/ESC 2006 guidelines, section 5.3.3.1PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5aaXBlczwvQXV0aG9yPjxZZWFyPjIwMDY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 25). Genetic testingLQTS is inherited in an autosomal dominant fashion.Genetic testing is of value in LQTS, particularly as the QT interval may appear normal. In patients with LQTS genetic testing may be abnormal in up to ? of patients. It can be used to confirm the diagnosis of LQTS. It may also suggest appropriate therapy and it is beginning to help with risk stratification in quite a sophisticated way. It may facilitate the screening of relatives. If genetic testing for LQTS is negative it may be reasonable to screen for RyR2 mutations which are found in CPVT. Genetic testing for LQTS is recommended as part of a genetic autopsy.It is important to remember that clinical screening alone cannot identify relatives of patients with LQTS who carry identical genetic mutations. Part of this may be due to erroneous computer-generated ECG diagnostic interpretation. The genetics of LQTS are complex, and becoming increasingly so, and are summarised in table 3.LQT1, 2 and 3 comprise the majority of clinical cases.Importantly around 10% of patients have more than one mutation. It has been suggested that because double heterozygosity appears to be more common than expected, molecular diagnosis should be performed on all LQTS-related genes, notwithstanding the identification of a single mutation.Table 3. The genetics of LQTS LINK Excel.Sheet.12 "C:\\Users\\Mark\\Desktop\\LQT syndrome\\Genetics of LQTs.xlsx" Acr4E73!R1C1:R13C5 \a \f 5 \h \* MERGEFORMAT Type of LQTS Chromosomal LocusMutated GeneIon Current Affected PrevalenceLQT1 (Romano-Ward syndrome)11p15.5 KCNQ1Potassium (IKs) 42%LQT2 7q35-36 KCNH2 Potassium (IKr) 45%LQT3 3p21-24 SCN5A Sodium (INa) 8%LQT4 4q25-27 ANK2Sodium, potassium and calcium RareLQT5 (Jervell and Lange-Nielsen syndrome)21q22.1-22.2 KCNE1Potassium (IKs) 3%LQT6 21q22.1-22.2 KNCE2 Potassium (IKr) 2%LQT7 (Anderson syndrome) 17q23.1-q24.2 KCNJ2 Potassium (IK1) RareLQT8 (Timothy syndrome) 12q13.3 CACNA1C CalciumRareLQT9 3p25.3 CAV3 Sodium (INa) 0.66%LQT10 11q23.3 SCN4B Sodium (INa) Single familyLQT11 7q21-q22 AKAP9 Potassium (IKs) Single familyLQT12 SNTA1Sodium (INa) Single familyRisk prediction is complex. Although events in LQT1 are more common than in LQT2 and LQT3, events which do occur in these latter two conditions carry a higher risk of death. For patients with LQT1 and LQT2 syndrome the genetic locus and the QTc are independent predictors of risk. For patients with LQT3 the QTc is not an independent predictor, but male patients were noted to be at higher risk, even when their QTc was < 500msPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Qcmlvcmk8L0F1dGhvcj48WWVhcj4yMDAzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA 26. Patients with more than one mutation tend to have a longer QTc and a significantly higher risk of death.The current UK stance recommends genetic testing for confirmed clinical cases of LQTS only ADDIN EN.CITE <EndNote><Cite><Year>2008</Year><RecNum>6841</RecNum><record><rec-number>6841</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">6841</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors></contributors><auth-address>Manchester Heart Centre, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK. clifford.garratt@cmmc.nhs.uk</auth-address><titles><title>Clinical indications for genetic testing in familial sudden cardiac death syndromes: an HRUK position statement</title><secondary-title>Heart</secondary-title></titles><periodical><full-title>Heart</full-title></periodical><pages>502-7</pages><volume>94</volume><number>4</number><edition>2007/08/01</edition><keywords><keyword>Adult</keyword><keyword>Age Factors</keyword><keyword>Cost-Benefit Analysis</keyword><keyword>Death, Sudden, Cardiac/*etiology/prevention & control</keyword><keyword>Evidence-Based Medicine</keyword><keyword>Genetic Counseling/methods</keyword><keyword>Genetic Diseases, Inborn/diagnosis</keyword><keyword>*Genetic Predisposition to Disease</keyword><keyword>Genetic Testing/economics/*methods</keyword><keyword>Heart Diseases/diagnosis/genetics</keyword><keyword>Humans</keyword><keyword>Patient Selection</keyword><keyword>Sensitivity and Specificity</keyword></keywords><dates><year>2008</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>1468-201X (Electronic)
1355-6037 (Linking)</isbn><accession-num>17664186</accession-num><urls><related-urls><url> [pii]
10.1136/hrt.2007.127761</electronic-resource-num><language>eng</language></record></Cite></EndNote>27. A confirmed clinical case would correspond with a Schwartz score of ≥ 4. Genetic testing of 1st degree relatives of an index case in whom the mutation has been identified is also recommended. Genetic testing for borderline cases to confirm or refute the diagnosis is not recommended routinely. The current approach is to target the most commonly involved genes, often in a sequential manner, although these guidelines will almost certainly change in the future as new sequencing techniques become available and costs reduce.ManagementThe fact that this is a disease which has a genetic basis should be discussed with the patient and the potential need to screen relatives for the same condition should be broached. A more complete discussion of the implications is probably not practical in the cardiology out-patient setting and referral to a clinical genetics service is recommended. Genetic testing for the individual and relatives may be appropriate and a decision should be made by the cardiologist, geneticist and affected (or potentially affected) individual. A combination of phenotype and genotype can inform management.It is reasonable to give lifestyle advice. In particular for LQT1 strenuous exercise should be avoided, particularly swimming, although avoidance of strenuous exercise is recommended for all forms of LQTSPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5aaXBlczwvQXV0aG9yPjxZZWFyPjIwMDY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 25. It may be appropriate to teach behavioural techniques to deal with stressful situations and avoid alarm clocks and phones by the bedside in patients with LQT2. All patients with LQTS should avoide drugs which prolong the QT interval or drugs which may result in electrolyte disturbance.Beta-blockers are the mainstay of therapy in patients with LQTS and have been recommended for many years ADDIN EN.CITE <EndNote><Cite><Author>Schwartz</Author><Year>1975</Year><RecNum>5166</RecNum><record><rec-number>5166</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5166</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schwartz, P. J.</author><author>Periti, M.</author><author>Malliani, A.</author></authors></contributors><titles><title>The long Q-T syndrome</title><secondary-title>Am Heart J</secondary-title></titles><periodical><full-title>Am Heart J</full-title></periodical><pages>378-390</pages><volume>89</volume><dates><year>1975</year></dates><urls></urls></record></Cite></EndNote>28. They should be given to patients with a genetic diagnosis of LQTS even if their QTc is normal. They are variably effective depending upon the type of LQTSPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Nb3NzPC9BdXRob3I+PFllYXI+MjAwMDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA 32.Beta-blockers tend to be ineffective in LQT3. This is unsurprising given that arrhythmias tend to occur after exercise in LQT1, whereas they tend to occur at rest in LQT3. LQT3 is characterised by a gain of function of the sodium channel SCN5A; mexiletene, a sodium channel blocker, appears to be effective in LQT3 ADDIN EN.CITE <EndNote><Cite><Author>Nademanee</Author><Year>2009</Year><RecNum>5425</RecNum><record><rec-number>5425</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5425</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nademanee, K.</author></authors></contributors><titles><title> Genotype-Phenotype Relationship in the Long QT Syndrome: Brimming with Knowledge but Thirsting for a Therapeutic Solution.</title><secondary-title>J Am Coll Cardiol</secondary-title></titles><periodical><full-title>J Am Coll Cardiol</full-title></periodical><pages>2063-4.</pages><volume>54</volume><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>33. In the USA over-the-counter sales of AEDs (Automatic external defibrillators) are approved for home use in patients with high risk inherited arrhythmias such as LQTSPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5aaXBlczwvQXV0aG9yPjxZZWFyPjIwMDY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 25, 34. The ESC/AHA guidelines include a long and detailed section on the management of LQTS, part of which is reproduced here; The NICE guidelines do not.An ICD may be indicated for some patients with LQTS for primary prevention. The indications are not clearly defined and the decision must be individualised and will depend in part on the clinical presentation, the genotype and the fears and beliefs of the patient. Family history does not necessarily have any bearing on riskPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Nb3NzPC9BdXRob3I+PFllYXI+MjAwMDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA 29, 35. A QTc ≥ 500ms and syncope or a history of aborted sudden cardiac death appear to be the best predictors of future events ADDIN EN.CITE <EndNote><Cite><Author>Nademanee</Author><Year>2009</Year><RecNum>5425</RecNum><record><rec-number>5425</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5425</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nademanee, K.</author></authors></contributors><titles><title> Genotype-Phenotype Relationship in the Long QT Syndrome: Brimming with Knowledge but Thirsting for a Therapeutic Solution.</title><secondary-title>J Am Coll Cardiol</secondary-title></titles><periodical><full-title>J Am Coll Cardiol</full-title></periodical><pages>2063-4.</pages><volume>54</volume><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>33. The precise genetic mutation may be a predictor of risk and a number of studies have identified higher risk mutationsPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Nb3NzPC9BdXRob3I+PFllYXI+MjAwNzwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA 36-38. We recommend that cases of LQTS where an ICD may be contemplated for primary prevention should be discussed at a multi-disciplinary meeting, such as quarterly meeting held in our network.The following section on ganglionectomy is taken directly from the ACC/AHA/ESC guidelinesPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5aaXBlczwvQXV0aG9yPjxZZWFyPjIwMDY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA 25. Left cervicothoracic sympathetic ganglionectomy wasintroduced in 1971 for the treatment of adrenergicallytriggered life-threatening ventricular arrhythmias associatedwith the LQTS ADDIN EN.CITE <EndNote><Cite><Author>Moss</Author><Year>1971</Year><RecNum>5161</RecNum><record><rec-number>5161</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">5161</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Moss, A. J.</author><author>McDonald, J.</author></authors></contributors><titles><title>Unilateral cervicothoracic sympathetic ganglionectomy for the treatment of long QT interval syndrome</title><secondary-title>N Engl J Med</secondary-title></titles><periodical><full-title>N Engl J Med</full-title></periodical><pages>903-4</pages><volume>285</volume><number>16</number><edition>1971/10/14</edition><keywords><keyword>Adult</keyword><keyword>Arrhythmias, Cardiac/*surgery</keyword><keyword>Cervical Vertebrae</keyword><keyword>*Electrocardiography</keyword><keyword>Female</keyword><keyword>Ganglia, Autonomic</keyword><keyword>Horner Syndrome/etiology</keyword><keyword>Humans</keyword><keyword>Postoperative Complications</keyword><keyword>Stellate Ganglion/surgery</keyword><keyword>*Sympathectomy</keyword><keyword>Syncope/etiology</keyword><keyword>Thoracic Vertebrae</keyword><keyword>Ventricular Fibrillation/complications/prevention & control</keyword></keywords><dates><year>1971</year><pub-dates><date>Oct 14</date></pub-dates></dates><isbn>0028-4793 (Print)</isbn><accession-num>5112730</accession-num><urls><related-urls><url>. This procedure, performed througha limited supraclavicular approach, involves resection of thelower half of the left stellate ganglion and removal of at leastthe second and third thoracic sympathetic ganglia on theleft side ADDIN EN.CITE <EndNote><Cite><Author>Ouriel</Author><Year>1995</Year><RecNum>4372</RecNum><record><rec-number>4372</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">4372</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ouriel, K.</author><author>Moss, A. J.</author></authors></contributors><auth-address>Department of Surgery, University of Rochester School of Medicine and Dentistry, NY 14642, USA.</auth-address><titles><title>Long QT syndrome: an indication for cervicothoracic sympathectomy</title><secondary-title>Cardiovasc Surg</secondary-title></titles><periodical><full-title>Cardiovasc Surg</full-title></periodical><pages>475-8</pages><volume>3</volume><number>5</number><edition>1995/10/01</edition><keywords><keyword>Adolescent</keyword><keyword>Adult</keyword><keyword>Child</keyword><keyword>Child, Preschool</keyword><keyword>Female</keyword><keyword>Ganglia, Sympathetic/surgery</keyword><keyword>*Ganglionectomy/methods</keyword><keyword>Humans</keyword><keyword>Infant</keyword><keyword>Long QT Syndrome/diagnosis/*surgery</keyword><keyword>Male</keyword><keyword>Postoperative Complications</keyword></keywords><dates><year>1995</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0967-2109 (Print)</isbn><accession-num>8574528</accession-num><urls><related-urls><url> [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>40. This surgical therapy is associated withreduction in the frequency of arrhythmogenic syncope inthis syndrome and may be useful as adjunctive therapy inhigh-risk LQTS patients who have recurrent syncopeand/or aborted cardiac arrest despite combined ICD andbeta-blocker therapy or in LQTS patients who cannottolerate beta blockersPEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TY2h3YXJ0ejwvQXV0aG9yPjxZZWFyPjIwMDQ8L1llYXI+
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ADDIN EN.CITE.DATA 41.A summary of ESC/AHA recommendations for Long QT Syndrome Recommendationsis reproduced from the guidelines below: Class ILifestyle modification is recommended for patients with an LQTS diagnosis (clinical and/or molecular). (Level of Evidence: B)Beta blockers are recommended for patients with an LQTS clinical diagnosis (i.e., in the presence of prolonged QT interval). (Level of Evidence: B)Implantation of an ICD along with use of beta blockers is recommended for LQTS patients with previous cardiac arrest and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: A)Class IIaBeta blockers can be effective to reduce SCD in patients with a molecular LQTS analysis and normal QT interval. (Level of Evidence: B)Implantation of an ICD with continued use of beta blockers can be effective to reduce SCD in LQTS patients experiencing syncope and/or VT while receiving beta blockers and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B)Class IIbLeft cardiac sympathetic neural denervation may be considered for LQTS patients with syncope, torsades de pointes, or cardiac arrest while receiving beta blockers. (Level of Evidence: B)Implantation of an ICD with the use of beta blockers may be considered for prophylaxis of SCD for patients in categories possibly associated with higher risk of cardiac arrest such as LQT2 and LQT3 and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B)SummaryLQTS is a rare disorder which can be difficult to diagnose, as the QTc can be normal. Furthermore, risk stratification can be challenging. A genetic mutation can be identified in up to ? of patients and assists with the screening of relative and also potentially with risk stratification and is therefore recommended.Also see: 1: QTc interval noted to be prolongedSituation 2: 1st degree relative of patient (alive or dead) is diagnosed with LQTSSample ECGS()LQT1LQT1 is characterised by prolonged QT intervals associated with a broad-based T wave ADDIN EN.CITE <EndNote><Cite><Author>Moss</Author><Year>2003</Year><RecNum>2672</RecNum><record><rec-number>2672</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">2672</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Moss, A. J.</author></authors></contributors><auth-address>Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA. heartajm@heart.rochester.edu</auth-address><titles><title>Long QT Syndrome</title><secondary-title>JAMA</secondary-title></titles><periodical><full-title>JAMA</full-title></periodical><pages>2041-4</pages><volume>289</volume><number>16</number><edition>2003/04/24</edition><keywords><keyword>Adrenergic beta-Antagonists/therapeutic use</keyword><keyword>Death, Sudden, Cardiac/etiology</keyword><keyword>Defibrillators, Implantable</keyword><keyword>Electrocardiography</keyword><keyword>Genotype</keyword><keyword>Humans</keyword><keyword>*Long QT Syndrome/diagnosis/genetics/physiopathology/therapy</keyword><keyword>Pacemaker, Artificial</keyword><keyword>Sympathectomy</keyword><keyword>Syncope/etiology</keyword></keywords><dates><year>2003</year><pub-dates><date>Apr 23-30</date></pub-dates></dates><isbn>0098-7484 (Print)</isbn><accession-num>12709446</accession-num><urls><related-urls><url> [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>42LQT2LQT2 is characterised by low-amplitude and notched T waves ADDIN EN.CITE <EndNote><Cite><Author>Moss</Author><Year>2003</Year><RecNum>2672</RecNum><record><rec-number>2672</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">2672</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Moss, A. J.</author></authors></contributors><auth-address>Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA. heartajm@heart.rochester.edu</auth-address><titles><title>Long QT Syndrome</title><secondary-title>JAMA</secondary-title></titles><periodical><full-title>JAMA</full-title></periodical><pages>2041-4</pages><volume>289</volume><number>16</number><edition>2003/04/24</edition><keywords><keyword>Adrenergic beta-Antagonists/therapeutic use</keyword><keyword>Death, Sudden, Cardiac/etiology</keyword><keyword>Defibrillators, Implantable</keyword><keyword>Electrocardiography</keyword><keyword>Genotype</keyword><keyword>Humans</keyword><keyword>*Long QT Syndrome/diagnosis/genetics/physiopathology/therapy</keyword><keyword>Pacemaker, Artificial</keyword><keyword>Sympathectomy</keyword><keyword>Syncope/etiology</keyword></keywords><dates><year>2003</year><pub-dates><date>Apr 23-30</date></pub-dates></dates><isbn>0098-7484 (Print)</isbn><accession-num>12709446</accession-num><urls><related-urls><url> [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>42LQT3LQT3 is characterised by long ST segments with a late-appearing T wave resulting in a long QT interval ADDIN EN.CITE <EndNote><Cite><Author>Moss</Author><Year>2003</Year><RecNum>2672</RecNum><record><rec-number>2672</rec-number><foreign-keys><key app="EN" db-id="fr0tzpp2v9xtpoewa52p0evqsz2dvvst9sd0">2672</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Moss, A. J.</author></authors></contributors><auth-address>Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA. heartajm@heart.rochester.edu</auth-address><titles><title>Long QT Syndrome</title><secondary-title>JAMA</secondary-title></titles><periodical><full-title>JAMA</full-title></periodical><pages>2041-4</pages><volume>289</volume><number>16</number><edition>2003/04/24</edition><keywords><keyword>Adrenergic beta-Antagonists/therapeutic use</keyword><keyword>Death, Sudden, Cardiac/etiology</keyword><keyword>Defibrillators, Implantable</keyword><keyword>Electrocardiography</keyword><keyword>Genotype</keyword><keyword>Humans</keyword><keyword>*Long QT Syndrome/diagnosis/genetics/physiopathology/therapy</keyword><keyword>Pacemaker, Artificial</keyword><keyword>Sympathectomy</keyword><keyword>Syncope/etiology</keyword></keywords><dates><year>2003</year><pub-dates><date>Apr 23-30</date></pub-dates></dates><isbn>0098-7484 (Print)</isbn><accession-num>12709446</accession-num><urls><related-urls><url> [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>42References ADDIN EN.REFLIST 1.Schwartz PJ. 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