Short- and Long-Term Outcome of Children With Congenital Complete

Heart Block Diagnosed In Utero or as a Newborn

Marianne Eronen, MD, PhD; Marja-Kaisa Sire`n, MD, PhD; Henrik Ekblad, MD, PhD;
Tero Tikanoja, MD, PhD; Heikki Julkunen, MD, PhD; and Terho Paavilainen, MD, PhD

C
ABSTRACT. Objectives. Few data are available in the ongenital complete heart block (CHB) without
literature regarding the long-term outcome of newborns intracardiac structural abnormality is a poten-
with congenital complete heart block (CHB). The aims of tially lethal disease affecting fetuses and new-
this retrospective study were to assess neonatal morbid- borns.1–3 In previous studies, it has been estimated
ity and mortality, incidences of dilated cardiomyopathy that 1 of every 15 000 to 20 000 live births results in
(DCM), and associated heart defects, and to establish an infant with CHB.4 In a recent study, Siren et al5
prenatal and postnatal factors that might predict adverse found that the incidence during the last decades in
outcome in children with CHB. Finland has increased from 1:25 000 to 1:11 000. It
Design and Setting. The cohort includes 91 infants may be attributable to the better diagnostic methods
with CHB diagnosed in 5 tertiary centers in Finland and more effective antenatal and neonatal care of the
between 1950 and 1998.
children with CHB. It is also possible that the actual
Patients. Maternal connective tissue disease was ev-
incidence has increased because of the increasing
ident in 89% of the patients. At birth, the median gesta-
tional age was 37.1 weeks, and the median weight was
number of successful pregnancies in women with
2969 g. Of the 91 infants, 60 (66%) were girls and 7 (8%) connective tissue disease.
were twins. CHB is associated with a maternal autoimmune
Results. Incidences of perinatal morbidity and mor- disorder with autoantibodies against SS-A/Ro
tality were 58% and 7%, respectively. The total mortality and/or SS-B/La antigens,6 which may subsequently
of CHB was 16%; 11 of 15 (73%) died during the first 12 elicit an immune-mediated tissue injury.1,7 Histolog-
months. Cumulative probability of survival at 10 years ically, there is fibrous replacement of the conducting
old was 82%. Pacing as a newborn was indicated in 48 of tissue,7 which is best interpreted as resulting from
90 cases (53%), and 36 received pacemakers at older ages. apoptosis.8 Transplacentally mediated maternal anti-
Cardiac defects not causally related to CHB were found bodies may cause immunomyocarditis and severe
in 38 of 90 patients (42%), of whom 22 were operated on. prenatal or postnatal dilated cardiomyopathy
DCM was found in 21 (23%), of whom 13 died. During (DCM).9,10
the follow-up, among 75 survivors with a median age of Few data are available regarding the long-term
9 years, 54 (72%) are free from symptoms. Poor outcome outcome of newborns with CHB. Asymptomatic ne-
defined as clinically or pathologically evident congestive onates do not have absolute indications for pacing,
DCM was associated with intrauterine hydrops, low fetal but low heart rate combined with long QT interval
and neonatal heart rate, low birth weight, male sex, and has a remarkably poor outcome.10 In previous re-
neonatal problems attributable to prematurity or neona- ports, the mortality rates of CHB varied from 8% to
tal lupus. 19%11,12 and were mostly attributable to cardiac fail-
Conclusions. Despite early pacing, CHB carries high
ure in the neonatal period.12 Accordingly, the objec-
mortality during the first 12 months of life. High inci-
tive of the present study was to assess neonatal mor-
dences of DCM and associated heart defects indicate
close echocardiographic monitoring of all children with
bidity and mortality, causes of death, indications for
CHB. Pediatrics 2000;106:86 –91; heart block, pediatrics, pacemaker treatment, and incidences of DCM and
cardiomyopathy, heart defects, follow-up studies. anatomic heart defects of the patients with CHB. The
secondary objective was to establish prenatal and
postnatal factors that might predict adverse outcome
ABBREVIATIONS. CHB, complete/congenital heart block; DCM, in children with CHB.
dilated cardiomyopathy; ECG, electrocardiogram; VSD, ventricu-
lar septal defect; PDA, patent ductus arteriosus; ASD, atrial septal
defect. METHODS
We undertook a retrospective follow-up study of 91 children
who have CHB without major structural abnormality diagnosed
in utero or immediately after birth in 5 tertiary referral centers in
From the Hospital for Children and Adolescents, Helsinki University Hos- Finland between 1950 and 1998. Of them, 64 fetuses and children
pital, Helsinki, Finland. have been diagnosed and followed at the Hospital for Children
Received for publication Aug 9, 1999; accepted Feb 8, 2000. and Adolescents in Helsinki, and 27 have been followed by pedi-
Reprint requests to (M.E.) Hospital for Children and Adolescents, Helsinki atric cardiologists in other university hospitals. This study was
University Hospital, Stenba¨ckinkatu 11, 00290, Helsinki, Finland. E-mail: approved by an institutional review board. In 1998, 22 patients are
marianne.eronen@dlc.fi ⬎15 years old and are followed by an adult cardiologist at 5
PEDIATRICS (ISSN 0031 4005). Copyright © 2000 by the American Acad- university hospitals. The median follow-up age is 9.0 years (range:
emy of Pediatrics. .5– 47.5 years).

86 PEDIATRICS Vol. 106 No. 1 July 2000
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The most of 90 patients. Hydrops was evident in 24 adult patients. Digitalis was pregnancy. Of these children. The fetus with weight of 2614 g radiograph and poor left ventricular function on echocardiogra- phy. Postmortem examination revealed were lesions not considered causally related to heart block. left ventricular function during follow-up. The recurrence rate in the same family was cardiograms (ECGs) were registered. Neonatal infection 15 17 The time of detection of CHB was defined as the Neonatal lupus erythematosus 16 18 first prenatal record of bradyarrhythmia. fetuses with hydrops than in those without hydrops ture and histology were collected when available. treatment was Pulmonary hypertension 4 4 started after the identification of CHB. gestational length of the pregnancy. 8 (15%) had rheumatoid arthritis. defined as septicemia or infectious pneumo- evident congestive DCM. the age and number of cardiac procedures. and chest radiographic and Holter monitor (ambulatory 7% (Table 1). P ⫽ . 8 cases immediately after birth. Poor outcome was defined as clinically or pathologically fection. Echocardiographic data and electro. Of the 53 deliveries by cesar- arrhythmia in the prenatal medical record of the mother. (range: 29 – 41 weeks). 2017 . 1 death resulted from multiorgan failure as- stenosis. and in 3 sets. The records of the mothers were reviewed to assess gestational cylic acid for underlying clinical disease activity. The time of detec. In 12 cases. and wire placement (Table 2). parents. P ⫽ . in 7 families. If available. Dexamethasone sodium (6 mg per Neonates 5 dose) was started by intramuscular injection every 12 hours for a total of 4 doses. such as enlarged heart without structural abnormality. However. Neonatal Morbidity (n ⫽ 90) and 2 (4%) had undifferentiated autoimmune syn. mode of delivery. In these patients. patent ductus arteriosus neonates who died early had severe congestive heart (PDA). emergency section was performed in 15 SSA/Ro or SSB/La was registered. weeks of detection of CHB. Neonatal in- (range). The total incidence of connective tissue dis- ease was 89%. In utero. Seven mothers were No morbidity 38 42 taking prednisone (10 – 40 mg/day) and 2 acetosali- ARTICLES 87 Downloaded from by guest on February 25. and the age both twins had CHB. including pacemaker implantation and heart Total perinatal morbidity was 58% and mortality surgery. Two mothers received ␤-sympathomimetics (salbu- nancy. There were 5 sets of twins. In every case. and mild-to-moderate mitral valve regurgitation. Fetus 1 monary outcome. pulmonary valve failure. 60 (66%) were girls and 41 were matic disease. The information of maternal serum samples containing antibodies to ean section. Deaths 6 7 glucocorticoid was started to improve neonatal pul. All small ventricular septal defect (VSD). makers as newborns (Fig 1). We regarded P ⬍ . secundum atrial septal defect (ASD).05 as significant. No child with chromosomal abnormality was included. Of the 91 offspring. DCM was defined as clinically evident gestation (CHB diagnosed by fetal echocardiogram 7 severe congestive heart failure associated with cardiomegaly in weeks before death). Continuous variables were ana. Dichotomous variables were contrasted using ␹2 lupus were evident in 18% of the patients (Table 1). Clinical up- sociated with cardiac perforation after endocardial to-date information was collected from the hospitals. The obtained by sending a questionnaire to the mothers. incidences of neonatal morbidity and mortality. rate. was placed on organ system involvement characteristic of a rheu. Emphasis median birth weight was 2969 g (range: 905. and symptoms of neonatal were compared. No cases PDA 14 16 were detected before 17 weeks of gestational age. The median gestational age at birth was 37. 5 when gestational age was ⬍37 weeks. n % drome. low-up (from 67 to 42 beats/minute. There was 1 stillbirth at 38 weeks of 24-hour ECG) information. 6 (25%) died within 3 months recent echocardiographic or radiographic data and ECGs were of age. 8 lyzed by Student’s t test. Respiratory distress 7 8 Necrotizing enterocolitis 6 7 Antenatal medication was administered in a total Intraventricular hemorrhage 5 6 of 20 pregnancies.0001). 71 of the mothers’ next pregnan- were reviewed to demonstrate associated structural abnormalities. Records of the affected neonates were reviewed to assess heart boys. The 2 groups (good or poor prognosis) nia.4370 g). perinatal echocardiographic reports were started in 2 mothers because of fetal cardiac decom- reviewed to note the presence or absence of effusions or hydrops pensation and hydrops. Dermatitis 4 dian gestational age at diagnoses was 29. after the delivery diagnosis has been Hydrops 24 27 Cardiac failure without hydrops 19 21 made in 17 mothers. Detection was most frequently Hemolytic anemia 2 Pneumonitis 5 (59%) clustered between 25 and 34 weeks. Ordered cate- goric variables and skewed discrete variables were contrasted Forty-eight of the 90 children (53%) required pace- using the Mann-Whitney U test. only 1 twin had at pacemaker implantation. CHB. The records of older patients 10%. cies resulted in a second child with CHB. heart rate was significantly lower in reviewed. Only tion of CHB. Thirty-six children have RESULTS been paced later during the study. was evident in 17%. Abnormal liver function 2 17 cases (20%) were first identified after 35 weeks of Isolated pericardial effusion 2 gestation. Information of necropsy analysis of the cardiac struc. analysis (1-tailed) or by Student’s t test (2-tailed).3 weeks Thrombocytopenia 2 (range: 17– 40 weeks).0001). The me. Additional information was cases. and the obstetric history of all pregnancies before and after the affected tamol) to increase fetal heart rate. All the subjects gave informed consent. (17%) died within the first year of life attributable to cardiac failure (Table 2). Data are presented as mean ⫾ standard deviation or as median (50/minute vs 61/minute. Associated structural abnormalities included in this study had no hydrops. The study population consists of 91 offspring of 89 heart rate decreased significantly during the fol- pregnancies of 82 mothers. symptoms of connective tissue disease 6 patients of the whole study population have not were evident in 55 mothers (67%). in 2 of these sets. of these. At the time of identifica. TABLE 1.1 weeks tion of CHB is taken as the earliest documentation of a brady. and the atrial and ventricular rate of the fetus. medications taken during the preg. 9 (16%) had systemic lupus erythematosus. of whom 36 (65%) had Sjo¨gren’s syndrome.

Two patients (2%) have pulmo- Congestive heart failure 30 63 6 17 nary valve stenosis with a gradient ⬍40 mm Hg. and death for 90 children with CHB. 2017 . ASD secundum was evi. PDA. 1 after ASD operation. respiratory distress. heart function normal 3840 41 Male ⫺ 47 y Sudden death.TABLE 2. been paced during the follow-up years. Of the 8 surviving patients. endocardial fibroelastosis 3650 36 Female ⫺ Neonatal (3 d) DCM. Indications DCM died. Cardiomegaly 6 13 12 33 DCM was found in 21 of 91 offspring (23%). The other patient a Newborn Newborn Period with floppy regurgitating mitral valve is doing well n % n % with a pacemaker. During the follow-up. sepsis pneumococcica 2505 34 Female ⫹ Infant (5 mo) DCM 3510 40 Female ⫹ Infant (9 mo) DCM. Sixteen of 21 cases (76%) were Long QT 1 2 0 0 diagnosed before 1 year of age (Fig 1). hepatic lesion. intraventricular hemorrhage 2500 33 Male ⫹ Neonatal (5 d) DCM. Two patients (2%) had mitral valve defects. ASD operated on 3760 41 Male ⫹ 16 y Suicide. Of the 90 live-born infants. endocardial fibroelastosis 2705 34 Male ⫹ 1. of Exercise intolerance 0 0 6 17 Syncope 0 0 3 8 whom 13 (62%) died.2 y DCM. Three pa- the development of CHB. 1 died structural lesions not known to be associated with and 1 underwent heart transplantation. diagnosis of DCM. Clinical Details of Deaths (n ⫽ 16) Birth Weight (g) Gestational Sex Pacemaker Age at Death Postmortal Diagnosis Age (weeks) (⫹/⫺) Death in utero 38 Male ⫺ Fetal No defect 2690 36 Female ⫹ Neonatal (2 d) DCM. 83% are alive and 17% have died. 12 (13%) patients. endocardial fibroelastosis. of whom 13 were operated cardiac ultrasound. tients had small muscular VSDs (3%) detected by dent in 19 patients (21%).4 y DCM. 5 with CHB accompanied with DCM have been op- erated on because of minor cardiac defects. 4 had DCM. pneumonia 3000 37 Male ⫹ Infant (2 mo) DCM 2170 37 Female ⫹ Infant (5 mo) DCM. Three patients with ASD accompanied with closed spontaneously. Among them. of whom surgical ligation was Thirty-eight (42%) children had miscellaneous needed in 9 cases. PDA was found in for pacing are shown in Table 3. Postmortem examination Indications Pacing as Pacing After revealed dysplastic mitral valve. Low ventricular rate 11 23 7 19 Both patients are paced and are doing well. 1 newborn with severe cardiac failure TABLE 3. these have on. Pacemaker Treatment (n ⫽ 90) attributable to DCM already detected in utero died at 5 days of life (Table 2). both at 3 88 OUTCOME OF CHILDREN WITH COMPLETE HEART BLOCK Downloaded from by guest on February 25.2 y DCM. Timing of pacemaker implantation. cardiac perforation 3100 36 Male ⫹ Neonatal (9 d) DCM. Two Total 48 53 36 40 patients underwent heart transplantation. DCM seemed Ventricular tachycardia 0 0 1 3 to be the primary cause of death during the first 12 Ventricular fibrillation 0 0 1 3 months of life (Table 2). pneumonitis 3020 38 Male ⫺ Infant (2 mo) DCM. ASD 1880 35 Female ⫹ 3. mitral valve regurgitation 2265 32 Female ⫹ Neonatal (6 d) DCM. ASD. Horizontal axis represents various periods from birth and n represents the number of children remaining alive for any part of these designated periods. dilated heart Fig 1. bronchopulmonary dysplasia 2600 36 Male ⫹ 2.

went mitral valve replacement (at 26 and 35 years of Fetal hydrops was associated with poor outcome.4 these children.03 series.years of age. poor outcome defined as (range: . ity of 58% and perinatal mortality of 7% were shown.4 developed severe DCM after infancy. There was no significant difference in the outcome between the Fig 2.2 (29–41) . Clinical and follow-up data of the patients with poor outcome were compared with the data of those with good outcome (Table 4). In our study.425 (. Because of severe hydrops Neonatal heart rate 61 ⫾ 14 51 ⫾ 10 .5– 47. DISCUSSION ability of survival at 10 years old is 82%.007 and bradycardia. The median In this series of 91 children with CHB diagnosed in follow-up age of the 75 survivors is 9 years old utero or after delivery. there was no controlled trial in the manage- Twins 6 (9%) 1 (4%) . poor outcome in this study. patients with cardiac transplantation are included as nonsurvi- drome (QTc ⬎ .421 (. 2 mothers received ␤-sympathomi- Hydrops 11 (16%) 13 (57%) . * Clinically or pathologically evident congestive DCM. early infancy is the time of diagnosis greatest risk of death in CHB.13–16 In this Male sex 19 (28%) 12 (52%) .1 (17–40) 29. they are doing well.50) . The without heart defects. age). During the follow-up. In addition.03 metics17 and 2 received digoxin. He had been paced since birth and had no DCM.45 seconds) was not associated with vors. of whom 27% died in utero and 45% died within the Characteristic Outcome P first 3 months after delivery. Further. male sex was significantly more common in patients with poor outcome than in those with good outcome (52% vs 28%). Two patients with DCM under. Two children underwent heart centiles. Fetal heart rate 60 ⫾ 9 52 ⫾ 9 . None of them extrasystolias were treated with plasma exchange. Of the 75 survivors. or symptoms of neonatal lupus.10 who showed that heart rate ⬍55 beats/minute is associated with greater likelihood of poor outcome. Neonatal morbid- free from symptoms. 2 age.18.3 prolonged exposure to anti-Ro/SSa antibodies might defect be a major reason for the development of DCM in Indication of 34 (50%) 14 (61%) .3 (32–41) 36.004 Neonatal carditis or late-onset DCM from mater- Gestational age 37.9 Associated heart 26 (38%) 12 (52%) .5 years).048 recognized as a serious outcome of CHB. and 2 with normal ventricular function have 25% of fetuses with hydrops died within 3 months of moderate mitral valve regurgitation.6 (20–37) .0001 Noncardiac neonatal 35 (51%) 17 (77%) . Addi- tionally. A Kaplan-Meier survival curve of the patients with CHB.36–. The cumulative prob. Thus. Poor outcome was associated with low fetal and neonatal heart rate. Comparison of Clinical Characteristics of Children With Good Outcome With Those With Poor Outcome reported the total mortality of CHB to be 19%. 3 received sys- Values are mean (standard deviation) or median (range) or per- temic corticosteroids. fetal hydrops. only 3 death attributable to cardiac failure or diagnosed (4%) do not have a pacemaker.78 ing to these studies. transplantion. This finding is comparable with the treated with ␤-blockers.76 normal sinus rate. Those children who survive the first 4 years of life have a good prognosis (Fig 2). evidence of noncardiac neonatal problems. patients with associated minor heart defects to those The cumulative probability of survival at 10 years is 82%.1).0005 birth has been described. Among them the median heart rate was 50 adult patients with long QT syndrome are paced and beats/minute. The total mortality rate of CHB was 16%.19 problem Late development of DCM several months after Symptoms of 6 (9%) 10 (45%) . In addition. The occurrence of DCM was more common in patients with an associated heart defect than in those without a heart defect.20 In our study.9. previous study of Groves et al.35–.9 In a case report.45 sec 10 (15%) 4 (18%) .5 ment of fetuses with CHB. 1 male patient committed suicide at 16 years of age (Table 2). The cause of DCM is unclear but QTc [mt] . 5 children Ventricular 17 (25%) 8 (35%) . P ⫽ . long QT syn. Therapeutic options include treat- pacemaker ment directed at depletion of anti-Ro/SSa antibodies application as a newborn from the child’s circulation. the total Value Good Poor* mortality of CHB was 16% and 11 of 15 children n ⫽ 68 n ⫽ 23 (73%) died during the first 12 months. accord- Gestatinal age at 29. 54 (72%) patients are DCM was evident in 25% of cases.08 nal autoimmune disease is becoming increasingly at birth Birth weight (g) 3056 (1748–4370) 2733 (905–3840) . The study by Buyon et al12 showed that 63% of ARTICLES 89 Downloaded from by guest on February 25. low birth weight. 2017 . McLeod et neonatal lupus al14 described an infant with severe DCM despite a Length of QTc (sec) . but the difference was not statistically significant (57% vs 37%. Buyon et al12 TABLE 4.51) .

25 Although the recurrence rate 3.24 In this study.4:85–101 adult life. tion attributable to low ventricular rate and mended together with pacemaker treatment. This finding might agnosed and followed at the same hospital (the Hos- indicate that the asynchronic function between the pital for Children and Adolescents). this study demonstrates that ASD sign of myocardial damage. low fetal and neonatal heart rate. matory process. accounting for 50% of all defects found. DCM and associated heart defects support the rec- All these patients were paced. in 1965. In the subgroup of the children who did ASD secundum was the most frequently presented present from 1950 to 1980.2% substantially over the study. the first 12 months of life. Al- ventricular rate averaging ⬍60 beats/minute. specificity and immunogenetic background. An. and the risk of the mother having another child chamber pacemaker is indicated to prevent DCM or with CHB was 12%. 90 OUTCOME OF CHILDREN WITH COMPLETE HEART BLOCK Downloaded from by guest on February 25.41: 688 – 690 remains unknown. and high mortality during of cases.live-born children required pacemakers.45 seconds was not associated with poor outcome. the diagnosis of CHB was defect. 1992. Whether an early application of a CONCLUSION dual-chamber pacemaker is indicated in CHB re- mains to be answered.13 In this study.9 Thus.22. the occurrence of associated struc. of the 91 off. In our study. The occur. 1995. Brucato A. 66% were girls. Michaelsson et al26 described the high in. The incidence of The study took place over multiple decades and the 11% of heart defects was shown in the article by technology available to the caregivers has changed Buyon et al. ommendation of close echocardiographic monitoring they were treated with ␤-blockers. 5. Congenital complete heart block: an inter- In the article about long-term outcome of CHB in national study of the natural history. Whether early application of dual- 1. Franceschini F. In this study. 2. strated in the study by Buyon et al. ASD was most frequently found to be was not available. The reason fibrosis due to maternal lupus erythematosus. overdistension of the left ventricle and papillary other speculation is that a prolonged QTc time is a muscles. the relative risk for a female early cardiac transplantation should be taken into child compared with a male child to have CHB was consideration. In addition. The primary indications for placement of insufficiency. poor if the cardiac muscle was affected by an inflam- In adult studies. QTc of previously been reported. In this study. At made using ECG because fetal echocardiography operation. pace- of the newborns of Chinese mothers with systemic maker application for a neonate was first performed lupus erythematosus disseminatus. Male sex was more fre. Am J Reprod Immunol. 2017 . Further. tal problems attributable to prematurity or lupus rence of a heart defect was not associated with DCM erythematosus. Limitations of the Study tural heart defects (42%) was more common than has Any retrospective study has inherent limitations. maternal antibody cardiographic monitoring in all subsequent pregnan. close echo. 39% had poor prognosis. Isolated congenital com- of CHB was not very high in this series. De. treatment early in life. but the influences of male hor.12 Secundum type ASD was noted in 2. Arch Dis Child. In this study. Gasparini M. Poor prognosis defined as born children with PDA ligation. The risk of having Pediatric Research. 33% within cidence of unpredictable Stokes-Adams disease with the first 9 days of life. cess. Michaelsson M. pacemaker were congestive heart failure and low only 4% are not paced during the follow-up. early pacing is years). in case of DCM. the prognosis is poor. Congenital heart block and widespread Of the 31 males. ovale from closing.9. a child with CHB after a previous birth of an affected child was 10% (7 of 71). and ␤-blockers have been recom. and neona- small VSD) were similar in both studies.23 a prolonged QTc time associ. 1972. 4. This study was supported by grants from the Foundation for spring with CHB.28: mones or antibody profiles might take part in the 259 –263 development of DCM. Despite early pacing. 1. though the follow-up age in the present study is spite pacing. the low incidence of mitral regurgitation (5%) indicated in most children with CHB. remains to be answered. Hull D. permanent considerable mortality. and a high incidence of acquired mitral newborn. of all infants with CHB. 17% of them died within the first year of shorter than in the previous study26 (9 years vs 38 life because of severe DCM. Joyce D. early pacemaker treat- ated with CHB has been described as a separate ment is indicated to prevent mitral valve regurgita- disease entity. and in the follow-up. In a previous study.22: 533–540 cies is supported. of 75 surviving patients. All these older patients were di- located close to foramen ovale. been reported in previous articles. prognosis was or death. However. such as carditis rather and PDA are more frequently presented than has than a separate syndrome. The high incidences of ⬎. Incidences of other death or severe DCM was associated with fetal hy- associated cardiac defects (pulmonary stenosis and drops. Buyon et al12 described 3 (3%) of 107 live. Engle MA. Cardiovasc Clin. 1966.25 No gender-based differences in clinically significant shunt through the atrial septum the frequency or prognosis of CHB was demon.21 In our study. J Rheumatol. et al. Neonatal lupus syndromes. 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86 The online version of this article. 141 Northwest Point Boulevard. All rights reserved. it has been published continuously since 1948. PEDIATRICS is owned.full. Elk Grove Village. Heikki Julkunen and Terho Paavilainen Pediatrics 2000. 60007. Short. Print ISSN: 0031-4005. published. 2017 . and trademarked by the American Academy of Pediatrics. Online ISSN: 1098-4275. Henrik Ekblad. Illinois. Marja-Kaisa Sirèn. Copyright © 2000 by the American Academy of Pediatrics. Tero Tikanoja. is located on the World Wide Web at: /content/106/1/86. A monthly publication. Downloaded from by guest on February 25.html PEDIATRICS is the official journal of the American Academy of Pediatrics.and Long-Term Outcome of Children With Congenital Complete Heart Block Diagnosed In Utero or as a Newborn Marianne Eronen. along with updated information and services.106.