REVIEW ARTICLE A Review of Long QT Syndrome: Everything a Hospitalist Should Know Nandita Sharma, MD,a Daniel Cortez, MD,b,c Kristin Disori, MD,d Jason R. Imundo, MD,a Michael Beck, MDd

ABSTRACT In this article, we will review various aspects of long QT syndrome (LQTS) necessary for hospitalists who care for children, adolescents, and young adults who have known LQTS and also review presenting features that should make one consider LQTS as a cause of hospitalization. Pediatric hospitalists care for patients who have suffered near-drowning, unexplained motor vehicular accidents, brief resolved unexpected events, sudden infant death syndrome, recurrent miscarriages, syncope, or . These common conditions can be clinical clues in patients harboring 1 of 16 LQTS genetic mutations. LQTS is commonly caused by a that can cause sudden cardiac death. Over the years, guidelines on management and recommendations for sports participation have evolved with our understanding of the disease and the burden of manifested in the pediatric age group. This review will include the genetic causes of LQTS, clinical features, and important historical information to obtain when these presentations are encountered. We will review medical and surgical treatments available to patients with LQTS and long-term care recommendations and prognosis for those diagnosed with LQTS.

a Divisions of Pediatric www.hospitalpediatrics.org d and Pediatric DOI:https://doi.org/10.1542/hpeds.2019-0139 Hospital Medicine, Copyright © 2020 by the American Academy of Pediatrics Department of Pediatrics, Penn State Children’s Address correspondence to Michael Beck, MD, Division of Pediatric Hospital Medicine, Department of Pediatrics, Penn State Children’s Hospital, Hershey, Hospital, 500 University Dr, Hershey, PA 17033-0850. E-mail: [email protected] Pennsylvania; bDivision of Adult Electrophysiology, HOSPITAL PEDIATRICS (ISSN Numbers: Print, 2154-1663; Online, 2154-1671). Department of FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose. Cardiology, Penn State Medical Center, Hershey, FUNDING: No external funding. Pennsylvania; and POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose. cDepartment of Cardiology, University of Dr Sharma conceptualized and drafted the initial manuscript; Drs Cortez, Disori, Imundo, and Beck reviewed and revised the Lund, Lund, Sweden manuscript; and all authors approved the final manuscript as submitted.

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Downloaded from www.aappublications.org/news by guest on September 29, 2021 Long QT syndrome (LQTS) is more than a BACKGROUND effect of drugs or electrolyte abnormalities, prolongation of the QT segment of the Although a less common etiology of LQTS which can interact with the gene related to electrocardiogram (ECG). As the name compared with acquired causes, congenital LQTS2 (hERG).10,11 “syndrome” implies, a patient should have a LQTS is most commonly caused by an prolonged QTc, plus other ECG abnormalities underlying cardiac channelopathy. LQTS is GENETICS per Schwartz criteria (reviewed later), plus estimated to affect 1 in 2000 people and is Congenital LQTS results from mutations fi responsible for ∼4000 deaths per year in speci c clinical and family history. Failure to involving 1 of the many genes coding for ion the United States.1,2,3 Its clinical include these elements in medical decision- channels that facilitate the transport of manifestations are estimated to be less making to commonly encountered clinical potassium, sodium, and calcium. These ion scenarios frequently seen by pediatric common (1 in 5000) because most mutation carriers remain asymptomatic.4 channels play critical roles in maintaining hospitalists can lead to missed the ’s normal rhythm. Despite having In 1957, Jervell and Lange-Nielsen5 were the opportunities to diagnosis this treatable at least 16 genetically distinct types of LQTS, and potentially fatal disease. The diagnosis first to document this syndrome in Norway at least 75% of the mutations are found in typically receives consideration when a in a family with children who were deaf and 3 genes: KCNQ1 (potassium channel), KCNH2 screening ECG demonstrates QT segment had QT prolongation, syncope, and death at a young age. This association came to be (potassium channel), and SCN5A (sodium prolongation or polymorphic ventricular known as Jervell and Lange-Nielsen channel) causing long QT (LQT) type 1, LQT2, known as torsade-de-pointes 1 syndrome and has an autosomal recessive and LQT3, respectively. (Tdp). This rhythm can degenerate into pattern of inheritance. More commonly, Often Romano-Ward syndrome is used ventricular fibrillation and cause sudden LQTS is inherited in an autosomal dominant interchangeably with LQTS, but it is cardiac death and present as syncope and/ pattern and is associated with normal becoming increasingly common to or collapse. LQTS can result from congenital hearing, described as Romano-Ward reference the subtype according to the or acquired causes. Congenital causes syndrome in 1964.6,7 Although initially underlying genetic mutation (LQT1 to LQT16). occur less frequently than acquired and are described in 1957, much of the research The Jervell and Lange-Nielsen syndrome is due to the presence of genetic mutation(s) contributing to a better understanding caused by mutations in either KCNQ1/LQT1 that affect 1 of the several channels involved (90%) or KCNE1/LQT5 (10%). These genes of the disease has occurred only in with ventricular repolarization. Acquired encode components of the potassium the past 2 decades. As of 2016, causes can be secondary to electrolyte channel, which are critical for function of .500 different mutations have been abnormalities like hypocalcemia, both inner ear and cardiac conduction.9 identified in the 16 genes currently known hypokalemia, hypomagnesemia, drug side LQT1 is the most common of the 3 subtypes 1,8,9 effect, or drug–drug interaction. Both to cause LQTS. and has the highest incidence of cardiac causes of LQTS and familiarization of its Acquired causes of LQTS are far more events or symptomatic patients at 63%, protean manifestations are important for prevalent then congenital causes of LQTS. followed by 46% in LQT2 and 18% in LQT3. any hospitalist to understand. Most acquired causes result from adverse However, the likelihood of dying during a

TABLE 1 Distinguishing Features of LQTS For the 3 Most Common Genetic Mutations Genotype LQT1 LQT2 LQT3 Genetics KCNQ1 KCNH2 SCNA5 Frequency, % 35–45 30–35 8–10 Function Loss Loss Gain

Ion current affected ↓ IKs ↓ IKr ↑ INa Incidence of cardiac events22,% 63 46 18 Likelihood of dying during a 4420 cardiac event22,% Triggers21 Swimming, exercise, Loud noises, emotion, adrenergic stimuli peripartum period ECG Broad-based Low-amplitude bifid T wave Long isoelectric ST segment Response to b-blockade21,33 111 11 1 Response to mexilitine21 1111 Exercise restriction 111 11 Uncertain Exercise-triggered events22,% 68 29 4 1, low likelihood; 11, moderate likelihood; 111, high likelihood.

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Downloaded from www.aappublications.org/news by guest on September 29, 2021 LQT3 event is 5 times more compared with TABLE 2 Differentiating Characteristics of Presenting Symptoms of LQTS and Vasovagal others.12 (Table 1) Syncope LQTS Vasovagal Syncope CLINICAL PRESENTATION Sudden onset syncope Aura first, followed by or Now that we have reviewed the genetics of During exercise During cooldown after exercise LQTS, hospitalists need to be made aware of Swimming, exercise, emotionally, loud noise Typically orthostatic or emotionally induced what information to seek when obtaining a induced family history on patients who they take May present as convulsive event May present as convulsive event care of and the conditions that mimic LQTS. LQTS has a variety of clinical manifestations, many of which can find their way to syncope. In patients who experience unexplained sudden cardiac death in the hospitalist services. Patients with LQTS vasovagal syncope, typically an aura occurs young, 10% to 15% of sudden infant death typically present with syncope, fainting before syncope. In contrast, - syndrome (SIDS), and 9% of miscarried spells, brief resolved unexplained events, mediated syncope may have sudden loss of fetuses may be attributable to mutations in sudden cardiac death, near-drowning or occur after a brief either LQTS or catecholaminergic events, aborted , recurrent of .15 Syncope that polymorphic – syncopal episodes, drop attacks, , occurs during exertion (not during the susceptibility genes.16 20 or .13 Although the cardiac events cooldown phase of exercise) should always may occur at any age from infancy through Family History be concerning and should alert the middle age, they are most common from the We would like to emphasize to hospitalists hospitalist to consider LQTS as an etiology preteen years through the 20s. Of the the importance of obtaining a family history and thus consider involving a pediatric individuals who do become symptomatic, that covers 3 generations when called to cardiologist. 50% experience their first cardiac event by evaluate patients who present with any of the age of 12 years and 90% present by the Because seizures have been mentioned in the aforementioned presentations. age of 40 years.14 Given that patients with the differential, a history of syncope or Exploration of family history should seek to LQTS frequently present in the pediatric age collapse before a witnessed may determine if any of the following are range, increasing awareness of its indicate the presence of an arrhythmia that present: sudden cardiac death or cardiac diagnosis is necessary. causes a hypoxic seizure. It is also arrest in young individuals ,50 years of estimated that ∼25% of autopsy-negative or age, history of recurrent syncope or Syncope Evaluation Because LQTS can present to hospitalists as syncope, its evaluation should include a detailed clinical and family history. The history obtained (discussed later) should parse out if the event is due to benign vasovagal syncope or a potentially fatal arrhythmia due to LQTS. Vasovagal syncope is typically associated with a prodrome of , sweating, cold extremities, nausea, and abdominal pain. It is usually associated with abrupt postural changes (laying or sitting to standing). Vasovagal events can result from standing for prolonged periods in hot weather and are exacerbated by hypovolemic states causing ( and diarrhea). Palpitations usually occur after the onset of dizziness, and if ever related to exercise, vasovagal syncope occurs once the patient begins to cool down and after a period of physical exertion (Table 2). Situational- FIGURE 1 A, Demonstrates prolongation of the ventricular action potential with phase 0, phase specific triggers such as pain, , laugh, 1, phase 2, phase 3, and phase 4 of the action potential and a phase 3 depolarization micturition, defecation, and deglutition have (early afterdepolarization [EAD]) causing Tdp. B, Demonstrates how to measure the also been associated with vasovagal end of the T wave on the basis of the T wave tangent.

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Downloaded from www.aappublications.org/news by guest on September 29, 2021 having significant prolongation of the action TABLE 3 The Modified Schwartz Criteria for Determining Probability of LQTS potentialdurationcomparedwiththe 1993–2011 LQTS Diagnostic Criteria epicardial or endocardial cells. The Points prolongation represents delayed cardiac Electrocardiographic findings repolarization and differential repolarization QTc between parts of the ventricles as well as $480 ms 3 between the epicardium, midmyocardium, 460–479 ms 2 and endocardium. This differential 450–459 ms (males) 1 repolarization then allows differential signal QTc fourth minute of recovery from exercise 1 propagation during phase 3 of the action stress test potential for parts of the heart, while other $480 ms partswaittofollowsuitandallowthis Tdp 2 depolarization-repolarization difference to T wave alternans 1 continue and propagate as Tdp (Fig 1A). This Notched T wave in 3 leads 1 transmural dispersion of repolarization between the myocardial layers can result in a Low heart rate for age 0.5 predisposition of having multiple reentrant Clinical history circuits that can cause Tdp, which can Syncope degenerate to ventricular fibrillation.10 This With stress 2 phenomenon occurs in LQTS when cardiac Without stress 1 action potential duration is prolonged. Action Congenital deafness 0.5 potential prolongation can lead to early Family history afterdepolarizations, in which the preceding Family members with definite LQTS 1 action potential triggers a series of abnormal Unexplained sudden cardiac death below age 0.5 impulses in phase 2 or 3 and may degenerate 30 among intermediate family members to Tdp and ventricular fibrillation10 (Fig 1A). In 2011, QTc at fourth minute of recovery from exercise stress was added (ref 26). QTc was calculated by Early after depolarizations are more prone to Bazett’s formula, in which QTc 5 QT√RR. Score of 1 or less equals less probability of LQTS. 1.5 to 3 points occur with , which is more typical equals intermediate probability of LQTS. 3.5 points equals high probability. in patients who have sodium channel mutations characteristic of LQTS3. seizures, narcolepsy, sleep-related deaths, with narcolepsy. As a result, the peripartum Finally, R-on-T phenomenon can occur and pacemaker or defibrillator implantation in period is a high-risk period for patients who result in Tdp. This scenario is seen when young, congenital deafness, SIDS, carry LQT2 mutation or with acquired LQTS. the R wave of an ectopic beat or premature unexplained deaths associated with Finally, sleep-induced bradycardia appears ventricular contraction falls on the drowning, or motor vehicle accidents. to be the main trigger in LQT3.21 upslope of a T wave of a preceding wave, thus Thus, for any hospitalist who cares for triggering Tdp and ventricular fibrillation.11 Genetic Insight From Event patients with particular LQT types (with the Sometimes the triggers for the syncopal above-noted histories and range of clinical DIAGNOSIS event can provide a clue to the type of presentations), these arrhythmic triggers Diagnosing LQTS is challenging because as genetic defect present. For instance, LQTS should be considered and raise suspicion many as 25% to 33% of patients with genetic can occur in patients who are exposed to an for the presence of undiagnosed LQTS. LQTS have a concealed QT (normal QT adrenergic stimulus (eg, swimming, diving). interval).22–25 Once the diagnosis of LQTS is This is why patients who carry PATHOPHYSIOLOGY OF considered, published criteria, by Schwartz LQT1 mutations can present as drowning TORSADES et al26 in 1993, can be used to help clinicians events or with exertional syncope. Patients Mutations in any of the 16 genes mentioned weigh the likelihood of having LQTS. It later who carry mutations for LQT2 are at a can alter the structure or function of the came to be known as the “Schwartz higher risk for lethal events during arousal respective channels affecting the flow of criteria.” In 2011, the Schwartz criteria was and auditory stimulation (loud noises or ions. Altered flow of ions, under the right updated with the addition of a prolonged alarms). Female adolescents with LQT2 have inherited and acquired circumstances (ie, QTc .480 ms at 4 minutes of recovery in a ninefold increase in risk of experiencing electrolyte derangements or medications), exercise stress test. (Table 3)27 arousal-triggered cardiac events compared can result in prolonged and heterogeneous with male adolescents in the same age cardiac repolarization. In patients with LQTS, POINTERS FOR MEASURING QTC group. This presentation can mimic the layers of the myocardium repolarize at a When using a standard 12-lead ECG, a rule , a finding that is often associated different rates, with the midmyocardial cells of thumb is that a normal QTc is a QT

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Downloaded from www.aappublications.org/news by guest on September 29, 2021 interval that is less than half of the exclude small U waves, which is the most mindful of asthma control and preceding RR interval. An RR interval is the common mistake when calculating the QTc.29 awareness in patients with asthma and time elapsed between 2 successive R-waves Individuals who receive 3.5 points using the diabetes, respectively. Therefore, involving the of the QRS complex. Manual calculation of updated Schwartz criteria should be necessary specialists in patient care with QTc is important because even with the referred to an electrophysiologist or these conditions would be prudent. assistance of ECG software, mistakes can cardiologist with experience in managing Pharmacotherapy in LQT3 can be occur in calculations of QTc. A standard 12- LQTS so that there can be careful challenging. b-blockers remain the first- lead ECG tracing at a paper speed of 25 mm consideration to conduct genetic testing.30,31 line drug; use of a sodium channel blocker per second at 10 mm per mV amplitude is like mexiletine might be considered as generally adequate for accurate MANAGEMENT adjunctive therapy (level of evidence class measurement of QTc. Bazett’s formula Medical IIa).32,35 Drugs that are known to cause ð Þ QTpffiffiffiffiseconds is widely used to calculate the b-blockers are the primary treatment of LQTS prolongation of the QT interval should be RRðsecondsÞ QTc but may give erroneous results at both and are clinically indicated in all individuals avoided (Table 4). A comprehensive list can slow and fast or irregular heart rates. To with QTc .470 (level of evidence class I). They befoundonWebsiteslike calculate QTc, it is best to use QT canalsobeusefulinasymptomaticLQTSwith crediblemeds.org and torsades.net.36,37 , measurements from leads II, or precordial QTc 470 ms (level of evidence class IIa) if Another important consideration when caring fi leads V5 or V6, and it should be determined there is concern for signi cant family history for patients with known LQTS is safe as a mean value derived from at least 3 to of sudden death events or questionable administration of anesthesia when they 32 5 cardiac cycles (heartbeats). history. However, it is important to know require procedural and nonprocedural Electrophysiologists typically use lead II to that LQT1 and LQT2 mutations are more sedation. These interventions should only be b determine the QTc because the interval responsive to -blockers than LQT3. performed by an anesthesiologist who has usually consists of a discrete T wave rather Longitudinal data have demonstrated that up experience and is comfortable caring for than a T and an associated U wave, thus to 90% of LQT1 and 77% of LQT2 patients patients with LQTS or has dedicated training in 28 b making it easy to measure the QT interval. treated with -blockerswerefreefrom cardiac anesthesia because several drugs can QT is measured from the beginning of the syncope and cardiac arrest at 5.2 years of prolong the QTc. Telemetry monitoring during 33 earliest onset of the QRS complex to the end follow-up versus 68% of LQT3. Furthermore, and after the procedure in the recovery phase b of the T wave, determined by drawing a not all -blockers are equally effective. For is recommended for at least 5 half-lives of the b steep slope (closest to vertical line along instance, nadolol, a nonselective -blocker, is QT-prolonging medication administered. A the descending side of the T wave). Despite more effective in reducing sudden cardiac repeat 12-lead ECG should be obtained and some debate, most pediatric death in symptomatic patients compared with evaluated before discharge from the hospital. electrophysiologists agree that if U waves propranolol, , or atenolol.34 .25% of the T wave are present and fused Because pediatric hospitalists treat asthma Tdp Treatment and Prevention with T waves, they should be included in the and diabetes, care should be taken into When a patient with congenital or acquired b fi QT segment. Often this will be labeled as account given -blocker therapy as rst line LQTS develops Tdp, the first-line therapy is QTUc because there is no formal guidelines for prevention of sudden death. Nadalol is magnesium sulfate, 25 to 50 mg per fi for including prominent U waves in QTc considered rst-line therapy even in asthma kilogram per dose, and cardioversion if measurements (Fig 1B). However, and diabetes. However, because dose unstable or sustained Tdp. If a patient has a hospitalists must always be careful to adjustments may be needed, one needs to be prolonged QTc and intermittent ectopy, this is an instance in which isoproterenol or TABLE 4 Common Drugs That Are Known To Cause Prolongation of the QT Interval Should Be atrial pacing at a faster rate can be helpful Avoided to prevent any further Tdp. One also has to Drugs and side effect(s) know the QTc and mechanism of initiation of Antibiotics: macrolides like erythromycin, azithromycin the ventricular tachycardia when treating polymorphic ventricular tachycardia as to Anticongestants: albuterol, ephedrine, pseudoephedrine avoid QTc-prolonging drugs that might Antidepressant: citalopram, fluoxetine, sertraline, escitalopram, clomipramine, amitriptyline, nortriptyline otherwise be harmful in this particular Antiemetic: ondansetron situation. Maintaining serum potassium .4.0 mmol per L, magnesium .2.0 mg per Antifungals: voriconazole, ketoconazole, fluconazole dL, and ionized calcium .1.25 mmol per L is Antihistamine: astemizole, terfenadine, diphenhydramine often recommended. Appetite suppressants: phentermine, fenfluramine, sibutramine Central stimulants: amphetamines, dexmethylphenidate, lisdexmethylphenidate. SURGICAL Opiate agonist: methadone Implantable cardioverter-defibrillators and/ A comprehensive list can be found on Web sites like crediblemeds.org and torsades.net.36,37 or left cardiac sympathetic denervation are

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Downloaded from www.aappublications.org/news by guest on September 29, 2021 therapies typically reserved for high-risk resuscitation. This is a deviation from 2. Schwartz PJ, Stramba-Badiale M, Crotti patients. High-risk patients have been earlier recommendations that allowed only L, et al. Prevalence of the congenital defined as those patients who have had class 1A activities (bowling, billiards, long-QT syndrome. Circulation. 2009; cardiac events while on -blocker therapy, curling, cricket, golf, riflery, or yoga). 120(18):1761–1767 history of cardiac arrest, or inability to Current recommendations are that patients 3. Vincent GM. The molecular genetics of tolerate b-blockers (ie, severe asthma) in which LQTS is suspected or has been the long QT syndrome: genes causing (level of evidence class I).32 Regular follow- diagnosed and remain symptomatic should fainting and sudden death. Annu Rev up is necessary for assessment of b-blocker refrain from sports until evaluated by an Med. 1998;49:263–274 dose for efficacy and adverse effects, electrophysiologist. Thus, at time of especially during periods of rapid growth, discharge from the hospital, for newly 4. Crotti L, Stramba-Badiale M, Pedrazzini as is often encountered in pediatric diagnosed LQTS patients, it is reasonable to M, et al. Prevalence of the long QT patients. Implantable cardioverter- ask them to refrain from any competitive syndrome. Circulation. 2005;112:724 fi de brillators are routinely interrogated and sports until evaluated further by cardiology 5. Jervell A, Lange-Nielsen F. Congenital monitored for the occurrence of ventricular and/or electrophysiology. Other lifestyle deaf-mutism, functional heart disease fi arrhythmias, inappropriate shocks, or lead modi cations include no swimming or with prolongation of the Q-T interval and complications. For smaller school-aged diving in LQT1; modifying loud telephone or sudden death. Am Heart J. 1957;54(1): individuals, availability of an automatic cell phone ringtones, alarm clocks, and 59–68 external defibrillator (AED) at home and school or house bells; and encouraging school along with AED and cardiopulmonary fathers or significant others to be the 6. Romano C, Gemme G, Pongiglione R. resuscitation training for caretakers and primary caretaker in peripartum periods Rare cardiac arrythmias of the pediatric school or team officials is also strongly for LQT2. age. II. Syncopal attacks due to fi recommended. paroxysmal ventricular brillation. (Presentation of 1st case in Italian In the past, the diagnosis of LQTS meant CONCLUSIONS pediatric literature). Clin Pediatr restriction from all sports activities. Our knowledge of LQTS has grown (Bologna). 1963;45:656–683 Participation in competitive sports is still a exponentially over the past 2 decades, with matter of debate among the experts. an increased understanding of its genetics, 7. Ward OC. A new familial cardiac However, recent evidence has shown that clinical course, and management. Because syndrome in children. J Ir Med Assoc. some patients with LQTS can safely more than half of LQTS patients present at a 1964;54:103–106 young age, the initial diagnosis may be participate in certain activities (except 8. Reed GJ, Boczek NJ, Etheridge SP, 38,39 made or suspected by the pediatrician or swimming in those with LQT1). To assist Ackerman MJ. CALM3 mutation pediatric hospitalist. All hospitalists, hospitalists and other physicians in associated with long QT syndrome. Heart pediatric and adult, should remain vigilant counseling patients and families who deal Rhythm. 2015;12(2):419–422 with LQTS, the American Heart Association for LQTS when caring for patients who and American College of Cardiology issued experienced near-drowning, unexplained 9. Schwartz PJ, Spazzolini C, Crotti L, et al. an updated recommendation on exercise in motor vehicular accidents, seizures, The Jervell and Lange-Nielsen syndrome: 2015. This most recent statement “Eligibility syncope or SIDS, or who have a concerning natural history, molecular basis, and and disqualification recommendations for family history because these can be clinical outcome. Circulation. 2006; – competitive athletes with cardiovascular markers for patients harboring an LQTS 113(6):783 790 abnormalities: Task Force 10: The cardiac genetic mutation. Hospitalists should be 10. Antzelevitch C, Sicouri S. Clinical ”40 has liberalized familiar with commonly used medications relevance of cardiac arrhythmias restrictions recommended in previous and other acquired causes that are generated by afterdepolarizations. Role statements. It may be reasonable for associated with prolonging the QTc and of M cells in the generation of U waves, patients with low-risk LQTS, who have know how to treat Tdp. Hospitalists should triggered activity and torsade de remained asymptomatic for at least be aware of historical features that might pointes. J Am Coll Cardiol. 1994;23(1): 3 months, to participate in competitive be clues to the presence of congenital LQTS, 259–277 sports (except swimming for those with indications to involve a cardiologist, 11. Smirk FH. R waves interrupting T waves. LQT1).38,40 Patients should continue to take pharmacotherapy options, and sports Br Heart J. 1949;11(1):23–36 the following precautions: avoid QT- participation guidelines. prolonging drugs, electrolyte derangements, 12. 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Downloaded from www.aappublications.org/news by guest on September 29, 2021 A Review of Long QT Syndrome: Everything a Hospitalist Should Know Nandita Sharma, Daniel Cortez, Kristin Disori, Jason R. Imundo and Michael Beck Hospital Pediatrics originally published online March 6, 2020;

Updated Information & including high resolution figures, can be found at: Services http://hosppeds.aappublications.org/content/early/2020/03/04/hpeds. 2019-0139 Supplementary Material Supplementary material can be found at: References This article cites 38 articles, 19 of which you can access for free at: http://hosppeds.aappublications.org/content/early/2020/03/04/hpeds. 2019-0139#BIBL Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): Cardiology http://www.hosppeds.aappublications.org/cgi/collection/cardiology_ sub Hospital Medicine http://www.hosppeds.aappublications.org/cgi/collection/hospital_me dicine_sub Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.hosppeds.aappublications.org/site/misc/Permissions.xht ml Reprints Information about ordering reprints can be found online: http://www.hosppeds.aappublications.org/site/misc/reprints.xhtml

Downloaded from www.aappublications.org/news by guest on September 29, 2021 A Review of Long QT Syndrome: Everything a Hospitalist Should Know Nandita Sharma, Daniel Cortez, Kristin Disori, Jason R. Imundo and Michael Beck Hospital Pediatrics originally published online March 6, 2020;

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://hosppeds.aappublications.org/content/early/2020/03/04/hpeds.2019-0139

Hospital Pediatrics is an official journal of the American Academy of Pediatrics. Hospital Pediatrics is owned, published, and trademarked by the American Academy of Pediatrics, 345 Park Avenue, Itasca, Illinois, 60143. Copyright © 2020 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

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