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Atypical Presentation of Right Ventricular Outflow Tract Ventricular Tachycardia
The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–4, 2014 Copyright Ó 2014 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2014.06.033
Clinical Communications: Pediatric ATYPICAL PRESENTATION OF RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA Jeffrey M. Landreville, BSC,* Gary I. Joubert, MD,*†‡ Eva Welisch, MD,*† Krista Helleman, MD,*†‡ and Naveen P. Poonai, MSC, MD*†‡ *Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada, †Department of Pediatrics, Western University, London, Ontario, Canada, and ‡Division of Emergency Medicine, Western University, London, Ontario, Canada Reprint Address: Naveen P. Poonai, MSC, MD, London Health Sciences Victoria Hospital, Room E1-105, 800 Commissioners Road East, London, Ontario, N6A 2V5
, Abstract—Background: Ventricular tachycardia (VT) in the pediatric population is rare, has a wide differential diagnosis, and can present in numerous ways. In the absence of underlying heart disease, VT is considered idiopathic and is associated with an excellent prognosis. Right ventricular outflow tract ventricular tachycardia (RVOT-VT) represents the most common form of idiopathic VT. The differential diagnosis, mechanism, presentation, management, and prognosis of RVOT-VT in the pediatric population will be discussed. Case Report: We report a case of RVOT-VT that was incidentally discovered in an 11-year-old girl during an emergency department workup for severe headache. Why Should an Emergency Physician Be Aware of This?: It is essential for emergency physicians to have an approach to pediatric VT and appreciate the wide range of potential presentations. Differentiating idiopathic VT, such as RVOT-VT, from more malignant forms of VT can be challenging and requires expert consultation for further diagnostic workup and management. Ó 2014 Elsevier Inc.
INTRODUCTION Ventricular tachycardia (VT) is rare in the pediatric population, with a reported incidence of 1.1 episodes per 100,000 childhood years (1). The initial presentation of pediatric VT is highly variable and, once identified, requires a thorough diagnostic evaluation, as the management and prognosis differs widely according to the underlying etiology (2). In contrast to adults, in whom VT is most often associated with myocardial pathology, the majority of pediatric VT is idiopathic, with no underlying heart disease identified (3). Approximately 70% of pediatric idiopathic VT is believed to originate from a region known as the right ventricular outflow tract (RVOT) (4). Here, we report a case of RVOT-VT that was incidentally discovered during an emergency department (ED) workup for severe headache.
, Keywords—ventricular tachycardia; right ventricular outflow tract; idiopathic; headache; pediatrics
CASE REPORT A previously well 11-year-old girl presented to the ED with a sudden onset, severe, left occipital headache that began while she was eating a snack at home. Emergency Medical Services were called and found the patient to be alert and responsive but in discomfort and extremely anxious. While in transit to the ED, the patient’s electrocardiogram (ECG) demonstrated frequent premature
This article was exempted from our institutions Health Sciences Ethics Review Board.
RECEIVED: 10 October 2013; FINAL SUBMISSION RECEIVED: 26 March 2014; ACCEPTED: 30 June 2014 1
2
J. M. Landreville et al.
Figure 1. Initial 12-lead electrocardiogram demonstrating sinus rhythm with frequent and consecutive premature ventricular contractions in couplets and triplets.
ventricular contractions (PVCs). The patient’s initial vital signs on arrival to the ED were temperature of 36.4 C, blood pressure of 122/73 mm Hg, heart rate of 127 beats/min, respiratory rate of 20 breaths/min, and oxygen saturation of 99% on room air. The initial 12-lead ECG showed sinus rhythm with frequent and consecutive PVCs in couplets and triplets (Figure 1). The patient continued to have frequent PVCs and runs of nonsustained ventricular tachycardia (NSVT) at a rate of 140 to 150 beats/min. During this period, she remained hemodynamically stable. Immediate management included oral acetaminophen 650 mg and ibuprofen 600 mg. Magnesium sulfate 500 mg i.v. was given in consultation with the pediatric cardiology service in an attempt to stabilize cardiac neuronal membranes and prevent possible progression to polymorphic VT. Despite these interventions, the patient continued to have a severe headache with frequent PVCs and runs of NSVT in the ED. On history, she denied any palpitations, chest pain, shortness of breath, syncopal episodes, fever, or recent exertion. Her medical history was significant for a 2year history of recurrent frontal tension-type headaches that resolved with ibuprofen. No allergies or current medications were reported. Her immunizations status was up to date. There was a history of migraines in her mother. There was no family history of dysrhythmia or sudden death. On general examination, the patient was appropriately grown and appeared anxious. She was alert and oriented to person, place, and time. Her physical examination, including detailed neurologic and cardiovascular examinations, was unremarkable. Initial laboratory studies, including complete blood count, electrolytes, extended electrolytes, thyroid-stimulating hormone, and high-sensitivity troponin-T were within a normal range. A chest x-ray study and high-resolution computed tomography of the head were also unremarkable.
The patient was admitted to the Pediatric Critical Care Unit (PCCU) for further workup and monitoring. While in the PCCU, the patient’s headache resolved with repeat administration of acetaminophen 650 mg and ibuprofen 600 mg. During this time, she continued to have frequent PVCs and NSVT. An i.v. infusion of esmolol 100 mg/kg/ min was started but was discontinued shortly afterwards due to development of hypotension. Additional cardiac evaluation included a transthoracic echocardiogram, which was normal. An exercise stress test following the modified Bruce protocol demonstrated NSVT at rest, a moderately decreased functional capacity, and the absence of VT at maximal exercise (heart rate >160 beats/min). The patient was fitted with a Holter monitor that confirmed the presence of frequent monomorphic PVCs, partially in runs, and again it was demonstrated that the dysrhythmia disappeared at rates >160 beats/ min. A signal-averaged electrocardiography (SAECG) was normal and ruled out delayed after depolarizations. Based on the findings of a structurally normal heart, classic ECG pattern, and absence of delayed after depolarizations on SAECG, the diagnosis of benign RVOTVT was made. The pediatric neurology service was also consulted and magnetic resonance imaging (MRI) of the head and neck with angiography and spectroscopy were completed with no significant abnormalities identified. The patient’s severe headache at presentation was attributed to occipital neuralgia and she was discharged after a 2-day admission. At 6 months post discharge, repeat echocardiogram showed no evidence of cardiomyopathy. A repeat Holter study demonstrated a moderate PVC load and runs of NSVT. The patient has remained asymptomatic from a cardiac perspective and her headaches have returned to baseline. She will continue to be followed by the pediatric cardiology service every 6 months for routine surveillance.
Atypical Case of RVOT-VT
DISCUSSION The differential diagnosis for pediatric VT is wide and includes idiopathic VT, surgically corrected congenital heart disease, myocarditis, cardiac tumor, electrolyte/ metabolic disturbances, primary electric disturbances, and cardiomyopathies (5). In the absence of underlying heart disease, VT is defined as idiopathic. Idiopathic VT is classified anatomically based on the site of origin of the dysrhythmia and includes right and left outflow tract VT, fascicular VT, papillary muscle VT, annular VT, and miscellaneous (VT originating from the body of the right ventricle and crux of the heart) (6). The clinical presentation of RVOT-VT is highly variable and often patients are entirely asymptomatic. Potential presenting complaints include palpitations, chest pain, presyncope, syncope, and, less commonly, abdominal pain, fatigue, asthma-related symptoms, and limb pain (7,8). Identified triggers include stress, exercise, and hormonal fluxes in females (9). To our knowledge, headache has not previously been reported as an antecedent complaint of RVOT-VT and it remains unclear as to whether any causal relationship exists between the headache and the episode of RVOT-VT. In order to appropriately diagnose and manage patients with VT, accurate interpretation of the initial ECG is crucial. RVOT-VT is typically monomorphic with frequent PVCs, and NSVT in the presence of a left bundle branch block (LBBB) QRS morphology and an inferior QRS axis (Figure 1) (10). Patients with an ECG pattern characteristic of RVOT-VT require a cardiology referral and thorough evaluation to rule out structural heart disease. Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), an inherited cardiomyopathy, can also present as LBBB-type VT with an inferior axis, and is associated with increased risk of sudden death (11). Differentiating between RVOT-VT and ARVD/C is challenging and involves SAECG analysis as well as advanced cardiac imaging, such as echocardiogram, MRI, or RV angiogram. Additional investigations in patients presenting with VT may include a Holter monitor, exercise stress testing, and electrophysiologic cardiac mapping to better characterize the dysrhythmia and identify potential triggers. In the acute setting, management of RVOT-VT is based on the severity and frequency of the patient’s symptoms. Asymptomatic patients with monomorphic PVCs and NSVT on ECG can be observed and referred to cardiology for further investigation (3). In symptomatic patients requiring acute RVOT-VT termination, adenosine, verapamil, lidocaine, and carotid sinus massage have all been shown to suppress triggered rhythms (12). bblockers and non-dihydropyridine calcium channel
3
blockers are considered first line for long-term suppression in symptomatic patients (13). The majority of RVOT-VT is benign and 46% to 65% of pediatric patients have spontaneous resolution with no evidence of VT after several years of follow-up (3,4,14). Expert initial evaluation and management is important, as a minority of patients exhibit a short-coupled variant of RVOT-VT that has been associated with malignant polymorphic VT (15). In addition, patients with a PVC burden >10% are at increased risk for PVC-mediated cardiomyopathy (16,17). These two populations, as well as those patients who remain symptomatic despite medical therapy, should be considered for radiofrequency catheter ablation (18). WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? VT is a rare but important presentation in the pediatric population. It is essential for emergency physicians to have an approach to pediatric VT and appreciate the wide range of potential presentations. Differentiating idiopathic VT, such as RVOT-VT, from more malignant forms of VT can be challenging and often requires advanced diagnostic investigations. Therefore, pediatric patients presenting with VT should be referred for expert consultation and further diagnostic workup.
REFERENCES 1. Roggen A, Pavlovic M, Pfammatter JP. Frequency of spontaneous ventricular tachycardia in a pediatric population. Am J Cardiol 2008;101:852–854. 2. Song MK, Baek JS, Kwon BS, et al. Clinical spectrum and prognostic factors of pediatric ventricular tachycardia. Circ J 2010;74: 1951–1958. 3. Iwamoto M, Niimura I, Shibata T, et al. Long-term course and clinical characteristics of ventricular tachycardia detected in children by school-based heart disease screening. Circ J 2005;69: 273–276. 4. Pfammatter JP, Paul T. Idiopathic ventricular tachycardia in infancy and childhood: a multicenter study on clinical profile and outcome. J Am Coll Cardiol 1999;33:2067–2072. 5. Iwamoto M. Idiopathic ventricular tachycardia in children. Circ J 2011;75:544–545. 6. Hoffmayer KS, Gerstenfeld EP. Diagnosis and management of idiopathic ventricular tachycardia. Curr Probl Cardiol 2013;38: 131–158. 7. Harris KC, Potts JE, Fournier A, et al. Right ventricular outflow tract tachycardia in children. J Pediatr 2006;149:822–826. 8. Kilic E, Celiker A, Karago¨z T, Alehan D, Ozkutlu S, Ozer S. Analysis of idiopathic ventricular tachycardia in childhood. Turk J Pediatr 2011;54:269–272. 9. Marchlinski FE, Deely MP, Zado ES. Sex-specific triggers for right ventricular outflow tract tachycardia. Am Heart J 2000;139: 1009–1013. 10. Shimizu W. Arrhythmias originating from the right ventricular outflow tract: how to distinguish ‘‘malignant’’ from ‘‘benign’’? Heart Rhythm 2009;6:1507–1511.
4 11. Calkins H. Arrhythmogenic right ventricular dysplasia. Curr Probl Cardiol 2013;38:103–123. 12. Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol 2010;35:453–504. 13. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death). J Am Coll Cardiol 2006; 48:e247–346. 14. Tsuji A, Nagashima M, Hasegawa S, et al. Long-term follow-up of idiopathic ventricular arrhythmias in otherwise normal children. Circ J 1995;59:654–662.
J. M. Landreville et al. 15. Viskin S, Rosso R, Rogowski O, Belhassen B. The ‘‘short-coupled’’ variant of right ventricular outflow ventricular tachycardia: a notso-benign form of benign ventricular tachycardia? J Cardiovasc Electrophysiol 2005;16:912–916. 16. Chugh SS, Shen WK, Luria DM, Smith HC. First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart failure. J Cardiovasc Electrophysiol 2000; 11:328–329. 17. Sternick EB, Correa F, Negri R, Scarpelli RB, Gerken LM. Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle. J Interv Card Electrophysiol 2009;25:67–72. 18. O’Connor BK, Case CL, Sokoloski MC, Blair H, Cooper K, Gillette PC. Radiofrequency catheter ablation of right ventricular outflow tachycardia in children and adolescents. J Am Coll Cardiol 1996;27:869–874.
http://dx.doi.org/10.1016/j.jemermed.2014.06.033
Clinical Communications: Pediatric ATYPICAL PRESENTATION OF RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA Jeffrey M. Landreville, BSC,* Gary I. Joubert, MD,*†‡ Eva Welisch, MD,*† Krista Helleman, MD,*†‡ and Naveen P. Poonai, MSC, MD*†‡ *Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada, †Department of Pediatrics, Western University, London, Ontario, Canada, and ‡Division of Emergency Medicine, Western University, London, Ontario, Canada Reprint Address: Naveen P. Poonai, MSC, MD, London Health Sciences Victoria Hospital, Room E1-105, 800 Commissioners Road East, London, Ontario, N6A 2V5
, Abstract—Background: Ventricular tachycardia (VT) in the pediatric population is rare, has a wide differential diagnosis, and can present in numerous ways. In the absence of underlying heart disease, VT is considered idiopathic and is associated with an excellent prognosis. Right ventricular outflow tract ventricular tachycardia (RVOT-VT) represents the most common form of idiopathic VT. The differential diagnosis, mechanism, presentation, management, and prognosis of RVOT-VT in the pediatric population will be discussed. Case Report: We report a case of RVOT-VT that was incidentally discovered in an 11-year-old girl during an emergency department workup for severe headache. Why Should an Emergency Physician Be Aware of This?: It is essential for emergency physicians to have an approach to pediatric VT and appreciate the wide range of potential presentations. Differentiating idiopathic VT, such as RVOT-VT, from more malignant forms of VT can be challenging and requires expert consultation for further diagnostic workup and management. Ó 2014 Elsevier Inc.
INTRODUCTION Ventricular tachycardia (VT) is rare in the pediatric population, with a reported incidence of 1.1 episodes per 100,000 childhood years (1). The initial presentation of pediatric VT is highly variable and, once identified, requires a thorough diagnostic evaluation, as the management and prognosis differs widely according to the underlying etiology (2). In contrast to adults, in whom VT is most often associated with myocardial pathology, the majority of pediatric VT is idiopathic, with no underlying heart disease identified (3). Approximately 70% of pediatric idiopathic VT is believed to originate from a region known as the right ventricular outflow tract (RVOT) (4). Here, we report a case of RVOT-VT that was incidentally discovered during an emergency department (ED) workup for severe headache.
, Keywords—ventricular tachycardia; right ventricular outflow tract; idiopathic; headache; pediatrics
CASE REPORT A previously well 11-year-old girl presented to the ED with a sudden onset, severe, left occipital headache that began while she was eating a snack at home. Emergency Medical Services were called and found the patient to be alert and responsive but in discomfort and extremely anxious. While in transit to the ED, the patient’s electrocardiogram (ECG) demonstrated frequent premature
This article was exempted from our institutions Health Sciences Ethics Review Board.
RECEIVED: 10 October 2013; FINAL SUBMISSION RECEIVED: 26 March 2014; ACCEPTED: 30 June 2014 1
2
J. M. Landreville et al.
Figure 1. Initial 12-lead electrocardiogram demonstrating sinus rhythm with frequent and consecutive premature ventricular contractions in couplets and triplets.
ventricular contractions (PVCs). The patient’s initial vital signs on arrival to the ED were temperature of 36.4 C, blood pressure of 122/73 mm Hg, heart rate of 127 beats/min, respiratory rate of 20 breaths/min, and oxygen saturation of 99% on room air. The initial 12-lead ECG showed sinus rhythm with frequent and consecutive PVCs in couplets and triplets (Figure 1). The patient continued to have frequent PVCs and runs of nonsustained ventricular tachycardia (NSVT) at a rate of 140 to 150 beats/min. During this period, she remained hemodynamically stable. Immediate management included oral acetaminophen 650 mg and ibuprofen 600 mg. Magnesium sulfate 500 mg i.v. was given in consultation with the pediatric cardiology service in an attempt to stabilize cardiac neuronal membranes and prevent possible progression to polymorphic VT. Despite these interventions, the patient continued to have a severe headache with frequent PVCs and runs of NSVT in the ED. On history, she denied any palpitations, chest pain, shortness of breath, syncopal episodes, fever, or recent exertion. Her medical history was significant for a 2year history of recurrent frontal tension-type headaches that resolved with ibuprofen. No allergies or current medications were reported. Her immunizations status was up to date. There was a history of migraines in her mother. There was no family history of dysrhythmia or sudden death. On general examination, the patient was appropriately grown and appeared anxious. She was alert and oriented to person, place, and time. Her physical examination, including detailed neurologic and cardiovascular examinations, was unremarkable. Initial laboratory studies, including complete blood count, electrolytes, extended electrolytes, thyroid-stimulating hormone, and high-sensitivity troponin-T were within a normal range. A chest x-ray study and high-resolution computed tomography of the head were also unremarkable.
The patient was admitted to the Pediatric Critical Care Unit (PCCU) for further workup and monitoring. While in the PCCU, the patient’s headache resolved with repeat administration of acetaminophen 650 mg and ibuprofen 600 mg. During this time, she continued to have frequent PVCs and NSVT. An i.v. infusion of esmolol 100 mg/kg/ min was started but was discontinued shortly afterwards due to development of hypotension. Additional cardiac evaluation included a transthoracic echocardiogram, which was normal. An exercise stress test following the modified Bruce protocol demonstrated NSVT at rest, a moderately decreased functional capacity, and the absence of VT at maximal exercise (heart rate >160 beats/min). The patient was fitted with a Holter monitor that confirmed the presence of frequent monomorphic PVCs, partially in runs, and again it was demonstrated that the dysrhythmia disappeared at rates >160 beats/ min. A signal-averaged electrocardiography (SAECG) was normal and ruled out delayed after depolarizations. Based on the findings of a structurally normal heart, classic ECG pattern, and absence of delayed after depolarizations on SAECG, the diagnosis of benign RVOTVT was made. The pediatric neurology service was also consulted and magnetic resonance imaging (MRI) of the head and neck with angiography and spectroscopy were completed with no significant abnormalities identified. The patient’s severe headache at presentation was attributed to occipital neuralgia and she was discharged after a 2-day admission. At 6 months post discharge, repeat echocardiogram showed no evidence of cardiomyopathy. A repeat Holter study demonstrated a moderate PVC load and runs of NSVT. The patient has remained asymptomatic from a cardiac perspective and her headaches have returned to baseline. She will continue to be followed by the pediatric cardiology service every 6 months for routine surveillance.
Atypical Case of RVOT-VT
DISCUSSION The differential diagnosis for pediatric VT is wide and includes idiopathic VT, surgically corrected congenital heart disease, myocarditis, cardiac tumor, electrolyte/ metabolic disturbances, primary electric disturbances, and cardiomyopathies (5). In the absence of underlying heart disease, VT is defined as idiopathic. Idiopathic VT is classified anatomically based on the site of origin of the dysrhythmia and includes right and left outflow tract VT, fascicular VT, papillary muscle VT, annular VT, and miscellaneous (VT originating from the body of the right ventricle and crux of the heart) (6). The clinical presentation of RVOT-VT is highly variable and often patients are entirely asymptomatic. Potential presenting complaints include palpitations, chest pain, presyncope, syncope, and, less commonly, abdominal pain, fatigue, asthma-related symptoms, and limb pain (7,8). Identified triggers include stress, exercise, and hormonal fluxes in females (9). To our knowledge, headache has not previously been reported as an antecedent complaint of RVOT-VT and it remains unclear as to whether any causal relationship exists between the headache and the episode of RVOT-VT. In order to appropriately diagnose and manage patients with VT, accurate interpretation of the initial ECG is crucial. RVOT-VT is typically monomorphic with frequent PVCs, and NSVT in the presence of a left bundle branch block (LBBB) QRS morphology and an inferior QRS axis (Figure 1) (10). Patients with an ECG pattern characteristic of RVOT-VT require a cardiology referral and thorough evaluation to rule out structural heart disease. Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), an inherited cardiomyopathy, can also present as LBBB-type VT with an inferior axis, and is associated with increased risk of sudden death (11). Differentiating between RVOT-VT and ARVD/C is challenging and involves SAECG analysis as well as advanced cardiac imaging, such as echocardiogram, MRI, or RV angiogram. Additional investigations in patients presenting with VT may include a Holter monitor, exercise stress testing, and electrophysiologic cardiac mapping to better characterize the dysrhythmia and identify potential triggers. In the acute setting, management of RVOT-VT is based on the severity and frequency of the patient’s symptoms. Asymptomatic patients with monomorphic PVCs and NSVT on ECG can be observed and referred to cardiology for further investigation (3). In symptomatic patients requiring acute RVOT-VT termination, adenosine, verapamil, lidocaine, and carotid sinus massage have all been shown to suppress triggered rhythms (12). bblockers and non-dihydropyridine calcium channel
3
blockers are considered first line for long-term suppression in symptomatic patients (13). The majority of RVOT-VT is benign and 46% to 65% of pediatric patients have spontaneous resolution with no evidence of VT after several years of follow-up (3,4,14). Expert initial evaluation and management is important, as a minority of patients exhibit a short-coupled variant of RVOT-VT that has been associated with malignant polymorphic VT (15). In addition, patients with a PVC burden >10% are at increased risk for PVC-mediated cardiomyopathy (16,17). These two populations, as well as those patients who remain symptomatic despite medical therapy, should be considered for radiofrequency catheter ablation (18). WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS? VT is a rare but important presentation in the pediatric population. It is essential for emergency physicians to have an approach to pediatric VT and appreciate the wide range of potential presentations. Differentiating idiopathic VT, such as RVOT-VT, from more malignant forms of VT can be challenging and often requires advanced diagnostic investigations. Therefore, pediatric patients presenting with VT should be referred for expert consultation and further diagnostic workup.
REFERENCES 1. Roggen A, Pavlovic M, Pfammatter JP. Frequency of spontaneous ventricular tachycardia in a pediatric population. Am J Cardiol 2008;101:852–854. 2. Song MK, Baek JS, Kwon BS, et al. Clinical spectrum and prognostic factors of pediatric ventricular tachycardia. Circ J 2010;74: 1951–1958. 3. Iwamoto M, Niimura I, Shibata T, et al. Long-term course and clinical characteristics of ventricular tachycardia detected in children by school-based heart disease screening. Circ J 2005;69: 273–276. 4. Pfammatter JP, Paul T. Idiopathic ventricular tachycardia in infancy and childhood: a multicenter study on clinical profile and outcome. J Am Coll Cardiol 1999;33:2067–2072. 5. Iwamoto M. Idiopathic ventricular tachycardia in children. Circ J 2011;75:544–545. 6. Hoffmayer KS, Gerstenfeld EP. Diagnosis and management of idiopathic ventricular tachycardia. Curr Probl Cardiol 2013;38: 131–158. 7. Harris KC, Potts JE, Fournier A, et al. Right ventricular outflow tract tachycardia in children. J Pediatr 2006;149:822–826. 8. Kilic E, Celiker A, Karago¨z T, Alehan D, Ozkutlu S, Ozer S. Analysis of idiopathic ventricular tachycardia in childhood. Turk J Pediatr 2011;54:269–272. 9. Marchlinski FE, Deely MP, Zado ES. Sex-specific triggers for right ventricular outflow tract tachycardia. Am Heart J 2000;139: 1009–1013. 10. Shimizu W. Arrhythmias originating from the right ventricular outflow tract: how to distinguish ‘‘malignant’’ from ‘‘benign’’? Heart Rhythm 2009;6:1507–1511.
4 11. Calkins H. Arrhythmogenic right ventricular dysplasia. Curr Probl Cardiol 2013;38:103–123. 12. Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol 2010;35:453–504. 13. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death). J Am Coll Cardiol 2006; 48:e247–346. 14. Tsuji A, Nagashima M, Hasegawa S, et al. Long-term follow-up of idiopathic ventricular arrhythmias in otherwise normal children. Circ J 1995;59:654–662.
J. M. Landreville et al. 15. Viskin S, Rosso R, Rogowski O, Belhassen B. The ‘‘short-coupled’’ variant of right ventricular outflow ventricular tachycardia: a notso-benign form of benign ventricular tachycardia? J Cardiovasc Electrophysiol 2005;16:912–916. 16. Chugh SS, Shen WK, Luria DM, Smith HC. First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart failure. J Cardiovasc Electrophysiol 2000; 11:328–329. 17. Sternick EB, Correa F, Negri R, Scarpelli RB, Gerken LM. Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle. J Interv Card Electrophysiol 2009;25:67–72. 18. O’Connor BK, Case CL, Sokoloski MC, Blair H, Cooper K, Gillette PC. Radiofrequency catheter ablation of right ventricular outflow tachycardia in children and adolescents. J Am Coll Cardiol 1996;27:869–874.