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Europace (2008) 10, 998–1003 doi:10.1093/europace/eun121 Natural history of ventricular premature contractions in children with a structurally normal heart: does origin matter? Gertie C.M. Beaufort-Krol, Sebastiaan S.P. Dijkstra, and Margreet Th.E. Bink-Boelkens* Beatrix Children’s Hospital, Division of Pediatric Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, The Netherlands Received 10 November 2007; accepted after revision 15 April 2008; online publish-ahead-of-print 6 May 2008 KEYWORDS Aims Premature ventricular contractions (PVCs) are thought to be innocent in children with normal hearts, especially if they disappear during exercise. The aim of our study was to study the natural history of PVCs in childhood and whether there is a difference between PVCs originating from the right [premature ventricular contraction with left bundle branch block (PVC-LBBB)] or the left ventricle [premature ventricular contraction with right bundle branch block (PVC-RBBB)]. Methods and results We evaluated children with frequent PVCs and anatomically normal hearts (n ¼ 59; 35M/24F) by 12-lead ECG, echocardiography, Holter recording, and an exercise test. Age at the first visit was 7.1 + 4.3 years (mean + SD), and follow-up was 3.1 + 3.1 years. We could evaluate each child for 2.5 + 1.5 times. Premature ventricular contraction with left bundle branch block was seen in 41% of the children; PVC-RBBB in 36%; and undetermined in 23%. Mean percentage PVCs in the Holter recording decreased (14.3 + 13.7% in the age group 1–3 years to 4.8 + 7.2% in the age group 16 years; P ¼ 0.08). Mean percentage PVC-LBBB did not change (12.3 + 21.4 vs. 11.7 + 5.5%), whereas PVC-RBBB decreased (16.3 + 4.2 to 0.6 + 1.4%; P , 0.02). Conclusion We conclude that there is a difference in the natural history between PVC-LBBB and PVCRBBB in children with an anatomically normal heart. Premature ventricular contraction with right bundle branch block disappears during childhood. Follow-up of these children seems not necessary. Premature ventricular contraction with left bundle branch block does not disappear and, therefore, it may be necessary to follow these children even during adulthood. Introduction Frequent premature ventricular contractions (PVCs) are rare in healthy children and young adults. They are extremely rare in children below the age of 9 years, but also only 2–6% of older children and young adults have more than 50 PVCs/24 h.1–4 These PVCs are, in general, considered benign, if no underlying cardiac disease is diagnosed and if the PVCs are suppressed by exercise. Although probably true, this benign influence of suppression by exercise is never proved by prospective studies. The opposite, induction of ventricular arrhythmias by exercise is of course a sign of structural or electrical heart disease, although it was occasionally found in otherwise healthy children.5 The natural history of PVCs in children with a structurally normal heart seems favourable as many studies, although * Corresponding author. Tel: þ31 50 3612800; fax: þ31 50 3614235. E-mail address: [email protected] with small patient numbers, show a decrease in numbers of PVCs during follow-up and no morbidity or mortality. The only study with a larger number of patients (n ¼ 78) found that PVCs disappeared in 28% of the patients after a follow-up of 72 + 32 months.6 Although probably benign, there are two reasons to hesitate to discharge children with frequent PVCs from follow-up. First, a prolonged period of very frequent PVCs may lead to left ventricular (LV) dilatation7 and, secondly, PVCs originating from the right ventricle (RV) might be the first symptom of arrhythmogenic right ventricular cardiomyopathy (ARVC). Therefore, it is advised to follow these children at 1–2 year intervals.8 The natural history studies in children considered PVCs, irrespective of the origin from RV or LV. However, the origin might be of importance, especially in view of the presence of ARVC. Therefore, we retrospectively studied the natural history of PVCs in relation to their origin in Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email: [email protected]. Downloaded from by guest on October 24, 2016 Natural history; Paediatrics; Premature ventricular contractions; Structurally normal heart PVCs in children with normal hearts children with a structurally normal heart. The aim of our study was to judge if the natural history was different for PVCs originating from the RV or LV and if this might have consequences for the follow-up policy. Methods Patients Fifty-nine children (35 M/24 F) with PVCs were admitted to our hospital since 1975. All parents provided informed consent for clinical evaluation. Monitoring parameters We evaluated the children three-yearly during follow-up by history, physical examination, ECG, 24-h Holter recording, echocardiography, and an exercise test. The data of the children were analysed in different age groups (1–3, 3–5, 5–8, 8–12, 12–16, and 16 years). Electrocardiogram Results Patients Age at the first visit was 7.1 + 4.3 years (mean + SD) and follow-up was 3.1 + 3.1 years. There was no difference in follow-up duration in the LBBB and RBBB group (4.6 + 2.6 vs. 6.2 + 3.7 years; NS). We could evaluate each child for 2.5 + 1.5 times. Most children had no complaints at all and were referred because of an accidentally found irregular heart rate. Eight children had complaints of chest pain or irregular heart beat. Family history was negative for cardiac diseases. There were two first or second degree family members with complaints of irregular heart beat. No morbidity or mortality occurred during follow-up. Electrocardiogram Heart rate, frontal axis, PQ interval, QRS width, and QTc interval were normal. Representative ECGs demonstrating the PVC morphology (BBB and frontal axis) to illustrate the specific type of ventricular ectopy are shown in Figure 1. Premature ventricular contraction with left bundle branch block was seen in 41% of the children, PVC-RBBB in 36%, and in 23%, the origin of the PVC could not be determined. Of the children with PVC-LBBB, 83% had an inferior axis and 17% had a superior axis. Holter recording Holter recording In the Holter recording, lowest, mean, and highest heart rates were evaluated. Premature ventricular contractions were expressed as a percentage of the total number of QRS complexes per 24 h. It was determined whether the PVCs were uniform or multiform, and whether there were couplets or ventricular tachycardias (VTs). Furthermore, the heart rate above which no PVCs were present was determined. Lowest, mean, and highest heart rates were within normal values. For the total group, the mean percentage PVCs decreased from 14.3 + 13.7% in the age group 1–3 years to 4.8 + 7.2% in the age group 16 years (P ¼ 0.08). Mean percentage PVC-LBBB did not change (Figure 2; 12.3 + 21.4 vs. 11.7 + 5.5%). Mean percentage PVC-RBBB decreased from 16.3 + 4.2 to 0.6 + 1.4% (Figure 3; P , 0.02). Most children had uniform PVCs (uniform 69%, multiform 26%, and undetermined 5%). Couplets were found in 47% of the total group of children and consisted mostly of PVC with a fusion beat. The group of children with couplets had a higher percentage of PVCs than the group without couplets (15.6 + 12.4 vs. 9.8 + 9.8%; P , 0.05). Ventricular tachycardia (maximum three beats; most PVC/fusion beat/PVC) mostly once per 24 h was found in 20% of the children. There was no difference in the occurrence of couplets or VT between the PVC-LBBB and PVC-RBBB groups. Mean heart rate at which the PVCs disappeared was not different between the PVC-LBBB and PVC-RBBB groups. For the total group, this heart rate was higher in the age groups 8 years than in the age groups 8 years (Figure 4; e.g. 5–8 years: 163 + 24 vs. 16 years: 130 + 36 b.p.m.; P , 0.02). None of the children developed repetitive monomorphic VT or sustained VT of either the right ventricular or the LV origin during follow-up. Echocardiography Echocardiography was performed to exclude anatomical abnormalities and cardiomyopathy. Measurements of LV dimensions and walls were made by two-dimensional and M-mode echocardiography on a parasternal short-axis view using standard techniques. All measurements were performed in triplicate and averaged. Left ventricular end-diastolic diameter (LVEDD) was measured between the endocardium of the intraventricular septum and the posterior LV wall at the chordal level, expressed in millimeters and plotted on percentile curves adjusted for weight.9 Left ventricular end-systolic diameter (LVESD) was measured likewise. Shortening fraction (SF) was calculated as (LVEDD 2 LVESD)/LVEDD. Repetitive echocardiograms were performed when the children still had .10% PVCs in the Holter recording. Exercise test During ergometry (7 years; bicycle test), heart rate at rest and during exercise was measured. Furthermore, the heart rate above which no PVCs were found was determined. The exercise test was finished when complaints of fatigue or ventricular arrhythmias (couplets or VT) occurred. Statistical analysis Data are expressed as mean + SD. Statistical analysis was performed with a two-tailed Student’s t-test or x2 test. A P-value ,0.05 was considered to be statistically significant. Echocardiography All children had a normal anatomy of the heart with LV dimensions that were within normal limits. No signs of cardiomyopathy or abnormalities of the RV were found. The echocardiograms at last follow-up (4.6 + 3.9 years; n ¼ 15) showed normal LV function (SF 0.35 + 0.04). Downloaded from by guest on October 24, 2016 In a 12-lead ECG (rest; supine position), heart rate (b.p.m.), frontal axis, PQ interval (ms), QRS width, and QTc interval were evaluated. If PVCs were present, it was determined whether they originated from the RV [premature ventricular contraction with left bundle branch block (PVC-LBBB)] or from the LV [premature ventricular contraction with right bundle branch block (PVC-RBBB)]. If possible, the axis of the PVCs was also determined. 999 1000 G.C.M. Beaufort-Krol et al. Downloaded from by guest on October 24, 2016 Figure 1 Examples of representative electrocardiograms (leads I, AVF, V1, and V6) demonstrating the premature ventricular contraction morphology to illustrate the specific type of ventricular ectopy. (A) Premature ventricular contraction with left bundle branch block inferior axis; (B) premature ventricular contraction with left bundle branch block superior axis; and (C ) premature ventricular contraction with right bundle branch block. Exercise test Discussion All children had a normal exercise performance. Rise in heart rate during exercise was normal. Premature ventricular contractions were suppressed by exercise in most patients. In eight children, the PVCs did not disappear but decreased in percentage at the highest heart rates. In all children, PVCs disappeared at about the same heart rate as during the Holter recording. Ventricular tachycardias during exercise were not found. Exercise tests at last follow-up (5.2 + 3.9 years; n ¼ 24) showed a normal maximal exercise capacity (97 + 14% of the normal value for age and length).10 Our study showed that indeed the percentage of PVCs in children with a structurally normal heart decreases spontaneously with age. However, if the origin of the premature beats is taken into account, this is only true for premature beats originating from the LV (PVC-RBBB). The percentage of premature beats originating from the RV (PVC-LBBB) did not change over time. This is a new finding with consequences for the follow-up of these children. Like others we found that PVCs in children with a structurally normal heart were well tolerated, without morbidity or mortality. All children had a normal LV function and exercise capacity PVCs in children with normal hearts 1001 Figure 3 Percentage (mean + SD) premature ventricular contraction with right bundle branch block of total number of QRS complexes per 24 h in the Holter recording per age group. *P , 0.02; #P , 0.01. at last follow-up. None of the children needed pharmacological treatment during follow-up. Are there reasons to follow these children? There are indications from studies in adults with structurally normal hearts that frequent premature ventricular beats may influence LV function. Facchini et al.7 found a subclinical but significant increase of LV dimensions in patients with frequent PVCs compared with the control group. A recent study of Bogun et al.11 found a decreased LV ejection fraction in 37% of the patients with frequent premature beats, which normalized after radiofrequency ablation of the premature beats. In both studies, the majority of the premature beats originated from the RV. We do not know the response of the PVCs to exercise in these patients, and it is not known whether the PVCs were already present in the childhood or developed later in the adulthood. Downloaded from by guest on October 24, 2016 Figure 2 Percentage (mean + SD) premature ventricular contraction with left bundle branch block of total number of QRS complexes per 24 h in the Holter recording per age group. 1002 G.C.M. Beaufort-Krol et al. Figure 4 Heart rate (mean + SD) in the Holter recording at which premature ventricular contractions disappeared. *P , 0.01; #P , 0.06. Limitations of the study To study the natural history it was necessary to analyse the data in different age groups, which unfortunately resulted in small numbers of children in some age group. To determine the natural history of PVCs, a much longer follow-up, in which the data are collected prospectively, would have been desirable. Conclusion We conclude that the natural history of PVCs in children with an anatomically normal heart differs depending on the origin of the PVCs. Premature ventricular contractions originating from the LV disappear during childhood. Follow-up of these children seems not necessary. In contrast, PVCs from the RV do not disappear. Left ventricular dysfunction found in adults with frequent PVCs may be an argument to continue to follow these children, as well as the potential, but small risk of developing ARVC. We advise that follow-up of children consists of Holter recording, echocardiogram, and exercise testing. Conflict of interest: none declared. References 1. Nagashima M, Matsushima M, Ogawa A, Ohsuga A, Kaneko T, Yazaki T et al. Cardiac arrhythmias in healthy children revealed by 24-hour ambulatory ECG monitoring. Pediatr Cardiol 1987;8:103–8. 2. Brodsky M, Wu D, Denes P, Kanakis C, Rosen KM. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977; 39:390–5. 3. Sobotka PA, Mayer JH, Bauernfeind RA, Kanakis C, Rosen KM. Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease. Am Heart J 1981;101:753–9. 4. Montague TJ, Taylor PG, Stockton R, Roy DL, Smith ER. The spectrum of cardiac rate and rhythm in normal newborns. Pediatr Cardiol 1982;2: 33–8. Downloaded from by guest on October 24, 2016 Moreover, in adults with frequent premature beats from the RV, although asymptomatic, abnormalities of the RV outflow tract were found on echocardiogram and magnetic resonance.12,13 Despite these anatomical abnormalities, the prognosis of these patients was good and none showed progression to clinical manifestations of ARVC. Knowing that PVCs from the LV nearly disappear during childhood, we are in favour of discharging these children from follow-up, if the (family) history is normal as well as the echocardiogram and if the PVCs disappear with exercise. Because the percentage of PVCs from the RV did not diminish during childhood, we advise to follow these children with 2– 3 year intervals, especially for LV function and the small risk of developing ARVC. Couplets are especially seen in children with a high number of PVCs. The natural history is not different if a child has couplets or only single PVCs, as was found earlier by Paul et al.14 Thus, couplets are not a risk factor for the development of VT. Two studies of children with idiopathic VT showed a spontaneous resolution of VT of +50%. In contrast with our findings in children with frequent PVCs, resolution of idiopathic VT was seen more often in patients with a VT originating from the RV.15,16 The only explanation can be that there is a different electrophysiological substrate for frequent PVCs and idiopathic VT in children with a structurally normal heart. In favour of this hypothesis is that in the group with frequent PVCs, the arrhythmia was suppressed by exercise, whereas in the idiopathic VT group, 70% VT was induced by exercise.16 PVCs in children with normal hearts 5. Bricker JT, Traweek MS, Smith RT, Moak JP, Vargo TA, Garson A. Exercise-related ventricular tachycardia in children. Am Heart J 1986; 112:186–8. 6. Tsuji A, Nagashima M, Hasegawa S, Nagai N, Nishibata K, Goto M et al. Long-term follow-up of idiopathic ventricular arrhythmias in otherwise normal children. Jpn Circulation J 1995;59:654–62. 7. Facchini M, Malfatto G, Ciambeloetti F, Chianca R, Bragato R, Branzi G et al. Increased left ventricular dimensions in patients with frequent nonsustained ventricular arrhythmia and no evidence of underlying heart disease. J Cardiovasc Electrophysiol 1999;10:1433–8. 8. Kugler JD. Benign arrhythmias: neonate throughout childhood. In Current Concepts in Diagnosis and Management of Arrhythmias in Infants and Children. Armonk, New York: Futura Publishing Company 1998 pp. 81–5. 9. Daniels O, Voogd PJ, Gussenhoven WJ, de Knecht S, Rijsterborgh H, van Lier H. Left ventricular inner dimensions in normal children. In Sobotka MA (ed.), Anthracycline Cardiotoxicity in Children an Echocardiographic Study. The Netherlands: Thesis State University Leiden 1991 pp. 97–100. 1003 10. Washington RL, Bricker T, Alpert BS, Daniels SR, Deckelbaum RJ, Fisher EA et al. Guidelines for exercise testing in the pediatric age group. Circulation 1994;90:2166–79. 11. Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E et al. Radiofrequency ablation of frequent idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm 2007;4:863–7. 12. Zweytick B, Pignoni-Mory P, Zweytick G, Steinbach K. Prognostic significance of right ventricular extrasystoles. Europace 2004;6:123–9. 13. Gaita F, Giustetto C, Di Donna P, Richiardi E, Libero L, Rosa Brusin M et al. Long-term follow-up of right ventricular monomorphic extrasystoles. J Am Coll Cardiol 2001;38:364–70. 14. Paul T, Marchal C, Garson A. Ventricular couplets in the young: prognosis related to underlying substrate. Am Heart J 1990;119:577–82. 15. Pfammatter JP, Paul T. Idiopathic ventricular tachycardia in infancy and childhood. J Am Coll Cardiol 1999;33:2067–72. 16. Iwamoto M, Niimura I, Shibata T, Yasui K, Takigiku K, Nishizawa T et al. Long-term course and clinical characteristics of ventricular tachycardia detected in children by school-based heart disease screening. Circ J 2005;69:273–6. 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