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Concise Guide to Pediatric Arrhythmias
Written by one of the foremost pediatric cardiologists in the UK, this essential new book is a clear, practical, highly visual guide to the recognition of arrhythmias and their management. This innovative new reference:
In addition, the book discusses arrhythmias encountered in various clinical settings – early and late after operation, and in congenital heart disease or cardiomyopathy – as well as brief overview of the use of invasive EP studies, catheter ablation, pacemakers and defibrillators.
Whereas other books on this important topic are aimed and tailored for the needs of experts in pediatric cardiology, this book is ideal for pediatricians, pediatric intensivists, trainees in pediatrics, pediatric cardiology and pediatric intensive care, as well as for clinical support staff involved in the cardiac care of children.
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Seitenzahl: 265
Veröffentlichungsjahr: 2011
Contents
Cover
Title Page
Copyright
Foreword
Preface
Abbreviations
1: Anatomy, physiology, and epidemiology of arrhythmias
Electrical anatomy of the normal heart
Basic mechanisms of tachycardias
Basic mechanisms of bradycardias
Epidemiology of arrhythmias
Key references
2: ECGs and other recording devices
The 12-lead ECG
Rhythm strips
Ambulatory ECG recording
ECG event recorders
Exercise ECG
Key references
3: Other diagnostic techniques
Implanted loop recorder
Transesophageal electrophysiology study
Tilt test
Invasive electrophysiology study
Key references
4: The normal ECG and variants
Sinus rhythm
Heart rate
QRS duration
Respiratory sinus arrhythmia
Variations in rhythm on ambulatory monitoring
Notched T waves
Key references
5: Interpretation of the ECG in tachycardia
Regular tachycardia with a normal QRS and 1:1 AV relationship
Regular tachycardia with a normal QRS and AV block
Irregular tachycardia with a normal QRS
Regular tachycardia with a wide QRS with right bundle branch block morphology
Regular tachycardia with a wide QRS with left bundle branch block morphology
Regular tachycardia with a wide QRS and neither RBBB nor LBBB morphology
Irregular tachycardia with a wide QRS
Changing QRS morphology in tachycardia
Key references
6: Adenosine in the diagnosis of tachycardias
Diagnostic use of adenosine
Other findings
Key references
7: Atrial tachycardia
Presentation and natural history of atrial tachycardia
ECG diagnosis of atrial tachycardia
Treatment of atrial tachycardia
Key references
8: Multifocal atrial tachycardia
ECG diagnosis
Treatment
Key references
9: Atrial flutter
Treatment
Key references
10: Atrial fibrillation
ECG diagnosis
Treatment
Key references
11: Atrial premature beats
Key references
12: Atrioventricular re-entry tachycardia
ECG diagnosis
Differential diagnosis
Treatment of AVRT
Key references
13: Wolff–Parkinson–White syndrome
ECG diagnosis
Treatment
Key references
14: Permanent junctional reciprocating tachycardia
ECG diagnosis
Treatment
Key references
15: Atriofascicular re-entry tachycardia
ECG diagnosis
Treatment
Key references
16: Atrioventricular nodal re-entry tachycardia
Key references
17: Junctional ectopic tachycardia
ECG diagnosis
Treatment
Key references
18: Ventricular tachycardia
ECG diagnosis
Differential diagnosis
The role of electrophysiology study
Presentation and causes
Acute treatment
Longer-term management
Ventricular tachycardia and a normal heart
Ventricular tachycardia in poisoning
Key references
19: Neonatal ventricular tachycardia
ECG diagnosis
Treatment
Key references
20: Incessant idiopathic infant ventricular tachycardia
ECG diagnosis
Treatment
Key references
21: Idiopathic left ventricular tachycardia
ECG diagnosis
Treatment
Key references
22: Idiopathic right ventricular tachycardia
ECG diagnosis
Treatment
Key references
23: Ventricular premature beats
ECG diagnosis
Treatment
Key references
24: Ventricular fibrillation
The causes of ventricular fibrillation
Treatment
Key references
25: Long QT syndrome
Measurement of the QT interval
Diagnosis
Risk stratification
Management
Acquired long QT syndrome
Key references
26: Catecholaminergic polymorphic ventricular tachycardia
ECG diagnosis
Treatment
Key references
27: Brugada syndrome
Diagnosis
Treatment
Key references
28: First- and second-degree atrioventricular block
First-degree atrioventricular block
Second-degree atrioventricular block
Key references
29: Complete atrioventricular block
Etiology of isolated complete AV block
ECG diagnosis of complete AV block
Indications for pacing
Key references
30: Sinus node dysfunction and sinoatrial disease
Treatment
Key references
31: Early postoperative arrhythmias
Tachycardias
Atrial tachycardia and atrial flutter
Bradycardias
Key references
32: Late postoperative arrhythmias
Arrhythmias after the Senning and Mustard operations
Arrhythmias after repair of a tetralogy of Fallot
Arrhythmias after the Fontan operation
Other diagnoses
Key references
33: Arrhythmias in congenital heart defects
Congenitally corrected transposition of the great arteries
Ebstein's anomaly of the tricuspid valve
Atrial isomerism
Atrial septal defect
Key references
34: Arrhythmias in cardiomyopathies
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Restrictive cardiomyopathy
Kearns–Sayre syndrome
Duchenne muscular dystrophy
Friedreich's ataxia
Emery–Dreifuss muscular dystrophy
Becker muscular dystrophy
Myotonic dystrophy
Barth's syndrome
Key references
35: Syncope
Vasovagal syncope
Reflex asystolic syncope
Orthostatic hypotension
Postural orthostatic tachycardia syndrome
Psychogenic syncope
Structural cardiac abnormalities
Cardiomyopathies
Arrhythmias
Investigation of syncope
Management of syncope
Conclusion
Key references
36: Sudden death
Family screening in the event of sudden death
Population screening
Key references
37: Antiarrhythmic drug treatment
Adenosine
Amiodarone
β-Blockers
Digoxin
Flecainide
Propafenone
Verapamil
Conclusions
Key references
38: Pacemakers and implantable defibrillators
Pacemaker leads
Pacemaker generators
Indications for pacemaker implantation
Outcome
Resynchronization
Implantable defibrillators
Key references
39: Catheter ablation
Success rates and complications
Key references
40: Artifacts
Key references
Appendix
Index
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Library of Congress Cataloging-in-Publication Data
Wren, C. (Christopher) Concise guide to pediatric arrhythmias / Christopher Wren. p. cm. Includes bibliographical references and index. ISBN-13: 978-0-470-65855-0 (pbk. alk. paper) ISBN-10: 0-470-65855-X (pbk.: alk. paper) 1. Arrhythmia in children–Handbooks, manuals, etc. I. Title. [DNLM: 1. Arrhythmias, Cardiac–diagnosis–Handbooks. 2. Arrhythmias, Cardiac–therapy–Handbooks. 3. Child. 4. Infant. WS 39] RJ426.A7W74 2012 618.92′128–dc23
2011015325
A catalogue record for this book is available from the British Library.
This book is published in the following electronic formats: ePDF 9781119979456; Wiley Online Library 9781119979487; ePub 9781119979463; Mobi 9781119979470
Foreword
I was particularly honored when Dr. Wren asked me to write this brief foreword to his monograph, “A Concise Guide to Pediatric Arrhythmias”. However, when I reflected on this opportunity, I wondered whether there was a deeper motivation to Dr. Wren's request. Not noted for my prowess in electrophysiology, I wonder whether he felt it long overdue that I be educated in the causes, identification and treatment of electrical disturbances of the heart!
While primarily aimed at the non-specialist, and trainee, Dr. Wren's book will provide an important resource to anyone caring for children with heart disease. Anyone that knows Dr. Wren will attest to his simple, pragmatic, and insightful approach to problems, his huge wealth of clinical experience, and his scholarly and critical approach to his own written works, and those of others. This book is a perfect reflection of those attributes, providing the reader with a beautifully written, easily assimilated, and clinically oriented approach to electrophysiology. While every illustration has an important message, and every paragraph is rich in content, the message never becomes overwhelming. Complex basic concepts are handled with a light touch, and the reader is guided through potentially complicated diagnostic and management algorithms with a logical, sequential, and thoughtfully outlined rationale. As such, it is the perfect text for those in training, a go-to resource for the generalist, or handy aide memoire to those of us who are more senior.
So, whether intended or not, I have indeed been educated by reading Dr. Wren's “Concise Guide to Pediatric Arrhythmias”. I am certain that those likewise exposed to this book will be similarly enlightened. Indeed, I am sure it will rapidly become required reading and a staple text in our field.
Andrew RedingtonHead of CardiologyThe Hospital for Sick ChildrenToronto, ONCanada
Preface
Most infants and children with arrhythmias present to a pediatrician before being referred to a pediatric cardiologist for assessment and management. Thus, the pediatrician has to be able to recognize the arrhythmia and in some cases to provide the acute treatment. Other arrhythmias arise in children who are already under the care of a cardiologist – either as part of the natural history of their heart problem or as a consequence of its treatment. This book is intended to be useful to pediatric trainees and pediatricians with an interest in cardiology as well as to trainees in and practitioners of pediatric cardiology and pediatric intensive care. It aims to provide a guide to the recognition of arrhythmias and their management. It is not written for the specialist because there are already plenty of advanced works written by experts for experts. It contains no invasive electrophysiological images but does give a brief guide to how and when invasive study might be indicated as well as an introductory guide to the use of catheter ablation and pacemakers and defibrillators.
I am indebted to many colleagues who have referred patients or who have helped to source some of the ECG examples. They include John O’Sullivan, Richard Kirk, and Milind Chaudhari in Freeman Hospital, Newcastle upon Tyne and Philip Rees and Martin Lowe in Great Ormond Street Hospital, London. I am also grateful to Andrew Sands, Satish Adwani, Kevin Walsh, Paul Oslizlok, Desmond Duff, Frank Casey, and Karen McLeod, and I am sure there are others, who have given permission to use images from patients who they have referred.
The quality of the ECGs that we have available for analysis varies and is sometimes less than ideal. However, if the only traces we have are from a paramedic recording or from a Holter recording or arrive via fax, they may still provide valuable information. I have chosen the best examples I have of all the various arrhythmias but they are all real ECGs so their quality also varies. They do represent the situations that we are faced with in real life and are preferable to redrawn idealized images.
The layout of the book is perhaps a little different from a traditional textbook with a great emphasis on ECG examples. Many of the individual arrhythmias are discussed in a small number of pages so that all the key features are available almost at a glance.
I have tried to limit the number of abbreviations in the text because they may be confusing for readers whose first language is not English. However, some are inevitable and most will be fairly familiar, such as AV, BBB, and WPW. A list of abbreviations is provided.
The opinions on antiarrhythmic drug treatment discussed throughout the book are my own and represent a fairly Eurocentric view. I recognize that practice varies in other parts of the world and other approaches to drug treatment are adopted. It is not possible to present all options for treatment but it is probably true to say that almost all antiarrhythmic drugs have been used for the treatment of almost all arrhythmias at some stage.
Over the past few years I have given many lectures, talks, seminars, and courses on the subjects of ECG interpretation and cardiac arrhythmias in infants and children, and in young adults with congenital heart disease. I have been consistently impressed by the interest and enthusiasm of those whom I have met, many of whom have asked for a monograph such as this. I hope that this will meet the need.
Christopher Wren2011
Abbreviations
AAVRT antidromic atrioventricular re-entry tachycardia
AET atrial ectopic tachycardia
AF atrial fibrillation
AFL atrial flutter
AFRT atriofascicular re-entry tachycardia
AT atrial tachycardia
AV atrioventricular
AVB atrioventricular block
AVNRT atrioventricular nodal re-entry tachycardia
AVRT atrioventricular re-entry tachycardia
BBB bundle branch block
CAT chaotic atrial tachycardia
CAVB complete atrioventricular block
CPVT catecholaminergic polymorphic ventricular tachycardia
FAT focal atrial tachycardia
HBT His bundle tachycardia
JET junctional ectopic tachycardia
LBBB left bundle branch block
LQTS long QT syndrome
MAT multifocal atrial tachycardia
OAVRT orthodromic atrioventricular re-entry tachycardia
PJRT permanent junctional reciprocating tachycardia
RBBB right bundle branch block
SR sinus rhythm
ST sinus tachycardia
SVT supraventricular tachycardia
VT ventricular tachycardia
WPW Wolff–Parkinson–White
1
Anatomy, physiology, and epidemiology of arrhythmias
An arrhythmia is an abnormality of cardiac rhythm. Arrhythmias differ in their population frequency, anatomical substrate, physiological mechanism, etiology, natural history, prognostic significance, and response to treatment. As is emphasized throughout this book, it is important to gain as much information as possible about the substrate and mechanism of an arrhythmia to be able to predict the natural history and to define the prognosis and response to treatment.
Electrical anatomy of the normal heart
The diagram in Figure 1.1 shows a sketch of the electrically active parts of the normal heart. The atrial muscle and ventricular muscle are separated by insulation of the fibrous mitral and tricuspid valve rings, and normally the only connection between them is via the His bundle.
Figure 1.1
All cardiac myocytes are capable of electrical conduction and have intrinsic pacemaker activity. Each tissue has a conduction velocity and a refractory period, both of which vary with changes in heart rate and influences such as autonomic tone, circulating catecholamines, etc. The conduction velocities of various parts of the heart vary as shown in Figure 1.1.
Basic mechanisms of tachycardias
Although it is not necessary to have a deep understanding of cardiac electrophysiology to diagnose and treat a cardiac arrhythmia, some knowledge of the basics is helpful. Tachycardias are mostly caused by re-entry or abnormal automaticity. Some common examples are shown in Figure 1.2. A few rare types of tachycardia are probably caused by a third mechanism, triggered activity.
Figure 1.2
Many common tachycardias are caused by re-entry. This means that there is a self-propagating wave of electrical excitation which maintains the arrhythmia. The fundamental requirements for re-entry are that there should be: (1) an anatomical circuit, (2) a zone of slow conduction in the circuit, and (3) a region of unidirectional block. The best model of re-entry is an orthodromic atrioventricular (AV) re-entry, e.g. Wolff–Parkinson–White syndrome (see Chapter 13). The circuit comprises the accessory pathway, atrium, AV node, and ventricle. The slow conduction is in the AV node and functional unidirectional block can occur in the accessory pathway. Tachycardia is interrupted if one part of the circuit has a refractory period longer than the cycle length of the tachycardia. In practice this is most easily achieved by prolonging AV node refractoriness with adenosine. Tachycardia will restart only if the requirements for reinitiation are met. These include a trigger (often an atrial or ventricular premature beat) and an appropriate balance of electrical behavior of the various parts of the circuit. Re-entry tachycardias can be started and stopped by pacing and stopped by cardioversion. Other examples of re-entry include AV nodal re-entry tachycardia (see Chapter 16), atrial flutter (see Chapter 9), and some types of ventricular tachycardia (see Chapter 18).
Fewer tachycardias are caused by abnormal automaticity. The best model of automaticity is sinus rhythm. Similar to sinus rhythm, automatic (also known as ectopic) tachycardias cannot be started or stopped by pacing and cannot be interrupted by cardioversion. In the normal heart the sinus node has the highest spontaneous rate and, therefore, determines the rhythm. If the sinus node fails another part of the heart with a lower pacemaker rate, usually the AV node, will provide an escape rhythm. Sometimes an area of the heart other than the sinus node will have an abnormally high spontaneous rate and will produce an automatic (or ectopic) tachycardia, overriding the sinus node. Examples of tachycardias caused by enhanced automaticity include atrial ectopic tachycardia (a type of focal atrial tachycardia – see Chapter 7), junctional ectopic tachycardia (see Chapter 17), and some types of ventricular tachycardia (see Chapter 18).
Triggered activity is the least common tachycardia mechanism. Depolarization is caused by a trigger – either an early after-depolarization or a delayed after-depolarization. Triggered activity causes ventricular arrhythmias in long QT syndrome, some electrolyte disturbances, and in some postoperative ventricular tachycardia with myocardial injury.
Basic mechanisms of bradycardias
Bradycardias are due to either failure of impulse generation or failure of conduction. The most common example of failure of impulse generation is sinoatrial disease (see Chapter 30). Abnormal sinus node function may be due extrinsic effects (high vagal tone) or to depressed automaticity. Significant bradycardias are more commonly due to second- or third-degree AV block (see Chapters 28 and 29).
Epidemiology of arrhythmias
Some arrhythmias are more common than others but there are almost no data on the population prevalence of these conditions. However, we recognize that the prevalence and spectrum of arrhythmias change with age. Faced with a new patient with an arrhythmia, our diagnosis is based mainly on the child's age, the age of onset of arrhythmia, the history (palpitations, heart failure, syncope, etc.), and the ECG findings. but should also take into account the prevalence of different arrhythmias (in other words, a common arrhythmia is often a more likely diagnosis than a rare one).
Probably fewer than half of new tachycardias present in the first year of life. By far the most common tachycardia presenting in early infancy is orthodromic AV re-entry (see Chapter 12). Most of these infants have a normal ECG in sinus rhythm but some show ventricular pre-excitation. Other neonatal tachycardias are much less common and include atrial flutter (see Chapter 9), permanent junctional reciprocating tachycardia (see Chapter 14), atrial tachycardia (see Chapter 7), and ventricular tachycardia (see Chapters 19 and 20).
The most common tachycardia in childhood is also orthodromic AV re-entry tachycardia, although AV nodal re-entry tachycardia (see Chapter 16) becomes progressively more common after the age of 5 years. Less common tachycardias in this age group are antidromic AV re-entry (see Chapter 13), atriofascicular re-entry (see Chapter 15), ventricular tachycardias (see Chapter 18), and atrial tachycardias (see Chapter 7).
Arrhythmias presenting with palpitations include most of the common types of supraventricular tachycardia and a few cases of ventricular tachycardia. Many children with palpitations do not have an arrhythmia and a detailed first-hand history is essential before assessing the likelihood of an arrhythmia and the necessity of further investigation. Similarly very few children with chest pain have arrhythmias (or indeed any cardiac abnormality) and only a few with syncope have an arrhythmia. Again it all depends on the history.
Incessant tachycardias presenting with heart failure or apparent cardiomyopathy include focal atrial tachycardia (see Chapter 7), permanent junctional reciprocating tachycardia (see Chapter 14), incessant idiopathic infant ventricular tachycardia (see Chapter 20), and orthodromic atrioventricular re-entry tachycardia (see Chapter 15).
Arrhythmias presenting with syncope include complete AV block (see Chapter 29), atrial fibrillation in Wolff–Parkinson–White syndrome (see Chapter 13), sinoatrial disease (see Chapter 30), and ventricular tachycardia, especially in long QT syndrome (see Chapter 25), catecholaminergic ventricular tachycardia (see Chapter 26) or late after cardiac surgery (see Chapter 32). Syncope is discussed in detail in Chapter 35.
Some arrhythmias are so common as to be considered as almost normal variants. They include atrial premature beats (see Chapter 11), ventricular premature beats (see Chapter 23), and transient nocturnal Wenckebach AV block (see Chapter 28).
Arrhythmias occurring early or late after cardiac surgery are specific to those situations and are considered in detail in Chapters 31 and 32, respectively.
Key references
Anderson RH, Ho SY. The morphologic substrates for pediatric arrhythmias. Cardiol Young 1991;1:159–76.
Antzelevitch C. Basic mechanisms of reentrant arrhythmias. Curr Opin Cardiol 2001;16:1–7.
Kantoch MJ. Supraventricular tachycardia in children. Indian J Pediatr 2005;72:609–19.
Ko JK, Deal BJ, Strasburger JF, et al. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992;69:1028–32.
Massin MM, Benatar A, Rondia G. Epidemiology and outcome of tachyarrhythmias in tertiary pediatric cardiac centers. Cardiology 2008;111:191–6.
Mazgalev TN, Ho SY, Anderson RH. Anatomic-electrophysiological correlations concerning the pathways for atrio-ventricular conduction. Circulation 2001;103:2660–7.
Paul T, Bertram H, Bökenkamp R, et al. Supraventricular tachycardia in infants, children and adolescents: diagnosis, and pharmacological and interventional therapy. Paediatr Drugs 2000;2:171–81.
Porter MJ, Morton JB, Denman R, et al. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 2004;1:393--6.
Sekar RP. Epidemiology of arrhythmias in children. Indian Pacing Electrophysiol J 2008;8(suppl 1):S8–3.
Tipple MA. Usefulness of the electrocardiogram in diagnosing mechanisms of tachycardia. Pediatr Cardiol 2000;21:516--21.
3
Other diagnostic techniques
Implanted loop recorder
In children with worrying syncope but no proven diagnosis, an implanted loop recorder may be very helpful. The device has a 3-year battery and is inserted subcutaneously in the left axilla or on the left anterior chest wall. It works in loop mode and can be programmed to store recordings of arrhythmias which have rates below or above preset limits. A recording can also be triggered by children or their parents or teachers using an external activating device. The yield from this type of recorder depends on the selectivity of the physician but it can be most useful in children with infrequent major syncope. The recording in Figure 3.1 is from a 4-year-old boy with infrequent syncope. It shows an episode of polymorphic ventricular tachycardia. He was proven to have congenital long QT syndrome.
Figure 3.1
Transesophageal electrophysiology study
The transesophageal electrophysiology study is not widely employed in pediatric practice because of its limited physical acceptability. It involves peroral or pernasal positioning of a pacing wire in the esophagus behind the left atrium. Pacing in this position can usually capture the atria but requires a higher output stimulator than a normal pacing box. Transesophageal pacing can be used in neonates to overdrive atrial flutter or atrioventricular tachycardia, but its use in older children is limited by discomfort and it often requires general anesthesia. It has been advocated for investigation of children with symptoms of palpitation, elucidation of arrhythmia mechanism if tachycardia is documented on ambulatory ECG monitoring, and “risk assessment” in asymptomatic children with a Wolff–Parkinson–White pattern on the ECG. It is perhaps more widely used in some European countries than in the UK, the USA, or elsewhere.
Tilt test
A head-up tilt test is sometimes used for investigation of children older than 6 years with recurrent syncope or presyncope. Protocols vary but all involve the child lying horizontal for 15–20 min before being passively tilted to an angle of 60–80° for up to 45 min or until the development of symptoms. The ECG and blood pressure are recorded continuously. Fainting or a feeling of faintness is usually accompanied by bradycardia and hypotension, and the child is rapidly returned to the horizontal. Less commonly there is a hypotensive response without bradycardia. The most unusual response is cardioinhibitory with bradycardia or asystole before syncope.
A “positive” test response with passive tilting is observed in 40–50% of children with a good history suggesting neurally mediated syncope (see Chapter 35). The sensitivity is increased by infusion of isoprenaline (isoproterenol) but specificity is reduced. The usefulness of the test is limited by false positives and false negatives, but it can be helpful in management of syncope. Figure 3.2 shows the response after a period of tilting in a 14-year-old girl. She became progressively hypotensive and bradycardic at the onset of symptoms. The heart rate and blood pressure recovered quickly after she was restored to a horizontal position.
Figure 3.2
Invasive electrophysiology study
This is a large subject and there is space in this text only for a brief review of the indications for its use. In the past electrophysiology studies were performed for a variety of reasons but are now mainly used as part of a catheter ablation procedure (see Chapter 39). The use of electrophysiology study for diagnosis of arrhythmia, assessment of antiarrhythmic drug efficacy, investigation of syncope, and risk assessment is now very limited. It may be helpful in refining the diagnosis in children with suspected or known ventricular tachycardia (see Chapter 18).
The use of electrophysiology study for risk assessment in asymptomatic children with a Wolff–Parkinson–White pattern on the ECG is controversial. Although advocated by some authors, there is little evidence that measurement of the accessory pathway refractory period, or the shortest RR interval in atrial fibrillation, or the inducibility of tachycardia or atrial fibrillation is of any prognostic value. Its usefulness in risk stratification of patients with hypertrophic cardiomyopathy, postoperative tetralogy of Fallot, etc. is unproven.
Key references
Abrams DJ. Invasive electrophysiology in paediatric and congenital heart disease. Heart 2007;93:383–91.
Brembilla-Perrot B, Groben L, Chometon F, et al. Rapid and low-cost method to prove the nature of no documented tachycardia in children and teenagers without pre-excitation syndrome. Europace 2009;11:1083–9.
Brignole M, Vardas P, Hoffman E,et al. Indications for the use of diagnostic implantable and external ECG loop recorders. Europace 2009;11:671–87.
Campbell RM, Strieper MJ, Frias PA, et al. Survey of current practice of pediatric electrophysiologists for asymptomatic Wolff–Parkinson–White syndrome. Pediatrics 2003;111:e245–7.
Kinlay S, Leitch JW, Neil A, et al. Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter monitoring in patients with palpitations. A controlled clinical trial. Ann Intern Med 1996;124:16–20.
Seifer CM, Kenny RA. Head-up tilt testing in children. Eur Heart J 2001;22:1968–7.
Szili-Torok T, Mikhaylov E, Witsenburg M. Transoesophageal electrophysiology study for children: can we swallow the limitations? Europace 2009;11:987–8.
