1977;59;250-256 Pediatrics Dorothy J. Radford and Teruo Izukawa ...

Atrial Fibrillation in Children Dorothy J. Radford and Teruo Izukawa Pediatrics 1977;59;250-256

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://www.pediatrics.org

PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 1977 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

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Atrial

Fibrillation

Dorothy

ABSTRACT. reports

Atrial

associated

fibrillation it with

J. Radford,

in Children

M.B.,

M.R.C.P.(UK),

and Teruo

Cardiology

is rare

Previous

subaortic stenosis’#{176} is well known, but the arrhythmia is more prone to develop in adults with such lesions. In recent years the incidence of rheumatic heart disease has decreased considerably. However, new problems with arrhythmias have arisen since the introduction of modern surgical techniques for correcting congenital cardiac 1 1-13 In addition, the “sick-sinus syndrome” is now recognized in both adults’4’5 and children.’6’7 In this condition, which is characterized by bradyarrhythmia and tachyarrhythmias, resolution of symptoms and therapeutic problems has occurred, with the onset of permanent atrial fibrillation, in adults.’82’ Whether this applies in

heart disease

and

a poor

prognosis. This review is of the unique experience of 35 cases of atrial fibrillation in children in the past 22 years; 23 patients were boys. The age of onset ranged from 1 day to 19 years (average, 8 years). Associated cardiac conditions were severe rheumatic mitral regurgitation (3 cases), cardiomyopathy (5), atrial tumors (2), infective endocarditis (1), paroxysmal atrial tachycardia of infants (4), idiopathic paroxysmal atrial fibrillation (1), Marfan’s syndrome with mitral regurgitation (1), endocardial fibroelastosis (1), and stnictural congenital heart malformations (17). Surgical correction of congenital heart lesions was directly related to the development of atrial fibrillation in 14. Varying arrhythmias of the sick-sinus syndrome were observed in five children. The atrial fibrillation was paroxysmal or transient in 21 patients and persistent in 14. Treatment depended on the underlying condition. Digoxin was used in all cases and cardioversion attempted in ten; no patient was given anticoagulants. Three children had cerebral emboli, with residual defects. Eighteen patients are known to be alive, 13 are dead, and 4 are lost to followup. Atrial fibrillation in childhood is an indication for complete investigation of the patient and for the institution of treatment appropriate to the underlying disease. Pediat59:250-256, 1977, ATRIAL FIBRILLATION, ARRHYTHMIA,

children

The

SICK-SINUS

changing

arrhythmia

prompted condition

us to review and to assess

Toronto,

Ontario,

face of

of

atrial

the

rare

fibrillation

our experience with this the etiology and outlook.

PATIENTS AND METHODS

SYNDROME.

All cases of atrial from the computerized cardiology department.

Atrial fibrillation is a rare arrhythmia in childhood.’3 The majority of reported cases have been in patients with severe rheumatic heart disease, in whom atrial fibrillation indicated a poor prognosis.4_6 Association with atnal septal defect,78 Ebstein’s anomaly,9 and idiopathic hypertrophic

250

Sick Children,

is unknown.

apparently

childhood

tics, HEART,

for

F.R.C.P.(C)

of Paediatrics,

in children.

Hospital

M.D.,

From the Department Canada

severe rheumatic

Division,

lzukawa,

(Received 21,

March

22; revision

arrhythmia record The

were selected system of the ECGs were re-

accepted

for publication

June

1976.)

Dr. Radford is the recipient Fellowship. ADDRESS FOR REPRINTS: atrics, Cardiology Division, University Avenue, Toronto,

of an Ontario (D.J.R.) Hospital Ontario,

PEDIATRICS Downloaded Vol. 59 No.from 2 February 1977 at Queensland Health on May 12, 2009 www.pediatrics.org

Heart

Foundation

Department of Paedifor Sick Children, 555 Canada M5C 1X8.

LEAD t

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.

VI

FIG.

1. EGG

diagnostic

of atrial

fibrillation:

the

totally

viewed, been

and

cases

in which

documented

fibrillation

Atrial features

were

of

distorting the ular conduction which

the during

ately

postoperatively.

Some

with

(Fig.

patients

varying in completely

had

cardiac

atrial

1). We

fibrillation

only

by

chaotic

baseline, resulting

deflections

had

the

ECG

atrioventricirregular

excluded

cases

past

or

had

additional

are

between

flutter

with

atrial

fibrillation

block was the latter cases were of 35 cases during the varying

years.

in CLINICAL

immedi-

FEATURES

Twenty-three boys.

had

responses

(Fig. 2), and This left a total

22

transiently

catheterization

ventricular

differentiation atrial

attempted excluded.

deflections

occurred

and

Careful and

diagnosed

and

Q RS complexes22

fibrillation

studied.

was

irregular

atrial

atrial

irregular.

arrhythmias.

The

cardiac

of the

clinical diagnoses

35 children

data

are

had

been

shown

studied in Table

confirmed

were I. The

by cardiac

VI

1_1,I1_T_JT_I_L_I_T:11I’I 1’1 1

1 TI 1I’.l Iii 1 I’’i

i

(::;fj:.

:1”i:‘1’1-IT1IiITIIIIIfIIIIIIiT:L ItJ’.f#{149}’J_ LI 1.1LII ii 11.1 ‘

FIG. 2. Atrial lead

flutter V,.

The

with

varying

ventricular

atrioventricular responses

are

block. regularly

#{149}

Regular related

flutter to

the

waves atrial

are

well

seen

in

deflections.


ARTICLES

251

TABLE CLINICAL

Patient No. Sex

Associated

Cardiac

DATA

Conditions

ON

35

Age at Onset

CHILDREN

WITH

ATRIAL

FIBRILLATION

Atrial

Fibrilla

tion

(AF)

.

Type regurgitation

I

and

Duration

Outcome

1

F

Rheumatic

mitral

10 yr

Persistent

Died;

necropsy

2

NI

Rheumatic surgery

heart

disease;

valve

14 yr

Persistent despite mitral valve replacement and triscimpid repair

Alive,

aged

3

1

Rheumatic

heart

disease;

valve

10 yr

Paroxysmal replacement

until

Alive; bral

in SR; spastic embolus

19 yr

Paroxysmal

for 3 mo before

death

Died;

necropsy

Persistent

death

Died;

necropsy

surgery from hemochromasyndrome

for 9 mo before

mitral

death

valve

4

F

Cardiomyopathy tosis; sick-sinus

5

M

Cardiomopathy

13 yr

6

F

Cardiomyopathy

10#{189} yr Persistent

7

F

Cardiomopath

7 yr

Paroxysmal

8

NI

Cardiomyopath

13 yr

Paroxysmal

Alive,

9

Ni

Rhabdomyoma of right berous sclerosis

Persistent

Lost

10

NI

Hepatoblastoma, and cardiac

11

NI

Infective endocarditis; syndrome

12

NI

Congenital

atrial

flutter

1 day

1:3

NI

Paroxysmal

atrial

tachycardia

3 ‘no

14

M

Paroxysmal

atrial

tachycardia

15

F

Paroxysmal

atrial

tachycardia

16

F

Idiopathic paroxysmal fibrillation

17

F

Marfan’s

atrium;

tu-

with pulmonary metastases nephrotic

syndrome;

atrial mitral

2#{189}yr

for

15 mo before

for 3 nio before for

4 yr before


for

4 da’vs before


for 20 days

death death

aged to

necropsy

Transient

Alive;

in SR

Transient

Alive;

in SR

3 mo

Transient

Alive;

in SR

3 mo

Transient

Alive;

in SR

13 yr

Paroxysmal

Alive

10 yr

Persistent

death

cere-

20

follow-up

Died;

for 3 mo before

from

Died

necropsy

death

in AF

Died

Died;

before

death

20;

Died;

necropsy

Died;

necropsy

regurgitation 18

NI

19

Ni Transposition

Endocardial tard drome

fibroelastosis

of great vessels; Mitsoperation; sick-sinus syn-

20

Ni

Transposition of great tard operation

vessels;

21

F

Transposition of great tard operation; sick drome

vessels; Mt,ssinus syn-

Mtms-

4 yr

Paroxysmal

for 2 days

4 yr

Paroxysmal

since

4#{189} yr Transient; 5 yr

to

four

252

less

years

before

death;

in

four,

death

than three weeks after its onset. Eighteen patients are still alive, 13 are known to have died, and the present status of the other 4 (last seen between 1953 and 1968) is unknown. Cerebral embolism occurred in three children, all of whom have residual defects from the event. occurred

death operation

by cardioversion

Paroxysmal

catheterization and angiocardiography in most cases and at necropsy also in nine. The atrial fibrillation was sustained in 14, paroxysmal in 14, and only transient in 7. The age at onset of atrial fibrillation ranged between 1 day and 19 years (average, 8 years). In the patients who died, the arrhythmia started one day

relieved

before

Mustard

Associated

Alive

Alive;

in SR

Alive; bral

hemiparesis embolus

from

cere-

Conditions

Three children had rheumatic heart disease with severe mitral regurgitation and giant left atria; one died before surgical intervention. The other two have prosthetic mitral valves: one has permanent atrial fibrillation, and the other has sinus rhythm but residual spasticity from a cerebral embolus. Five children had cardiomyopathy; four have died. The etiology is definite in only one patient, a girl with thalassemia major who had hemochromatosis involving the heart and other organs. The others had large, dilated, poorly functioning ventricles and mitral insufficiency.

ATRIAL FIBRILLATION Downloaded from www.pediatrics.org at Queensland Health on May 12, 2009

I ‘(CorrrINuED)

TABLE Pat ient No. Sex

Associated

Cardiac

Conditions

Age at Onset

Atrial Type

22

M

Transposition Mustard

of great operation

23

F

Secundum repaired

atrial

vessels;

septal

3 yr

defect:

12#{189} yr Transient, surgery digoxmn

24

F

Common atrium: surgically partitioned; sick-sinus syndrome

25

NI

Total anomalous pulmonary venous drainage: repaired; sick-sinus syndrome

26

M

Tetralogy tricuspid

of Fallot: corrected; valve replaced

27

M

Tetralogy

of Fallot:

28

M

Pulmonary

atresia:

pulmonary

valves

16 yr

Paroxysmal

2 yr

Paroxysmal

18 yr

repaired tricuspid

Persistent

and

for

Persistent

4 yr

Transient;

ation

(AF)

Duration

1 day

starting operation;

Outcome

before

death

3 mo after resolved

responded

Died

aged

3 years

Alive;

in SR

Alive;

varying

rhythms

Alive;

varying

rhythms

with

Persistent

15 yr

replaced

and

Fibrill

to

cardioversion

Lost

to follow-up

Alive;

in AF

Alive;

in SR;

defects

since

minor

from

1968

residual

cerebral

embolus 29

NI

Pulmonary shunt

atresia:

30

M

Ebstein’s

anomaly

31

M

Ebstein’s defect

anomaly; closed

32

M

Atrial septal coarctation:

33

F

Congenital coarctation:

34

F

Eisenmenger’s

35

NI

Single

Blalock-Taussig

13 yr

atrial

10 yr

6 yr septal

defect; mitral stenosis; corrective surgery mitral regurgitation; corrective surgery complex

ventricle

Persistent

Persistent

7 yr

Paroxysmal

11 yr

Paroxysmal replaced

four

cases

of atrial

12 days

until

mitral

Persistent

for

Transient;

cardioversion

in

before

death

necrops to follow-up

Died Alive

4 yr

tachycardia

Died; Lost

for

13 yr

necropsy.

were

death

Paroxysmal

Two children had tumors involving the heart. Thoracotomy revealed an unresectable rhabdomyoma of the right atrium in one of these patients, who also had tuberous sclerosis. The other child had had a hepatoblastoma resected four years earlier; atrial fibrillation developed four days before he died, and necropsy revealed lung metastases extending along the pulmonary veins into the left atrium. One patient had endocarditis resultant upon long-standing nephrotic syndrome and staphylococcal abscess of recent onset in the axilla. Atrial fibrillation developed 20 days before death and a vegetation on the mitral valve was found at There

for 5 mo before

1 mo before

valve

Alive;

in SR

death

Died;

necropsy

successful

Lost

to follow-up

infancy. One neonate had been delivered by caesarian section because of fetal heart irregularity; he had atrial flutter and atrial fibrillation on the first day of life, for which he was given digoxin therapy. Tachyarrhythmias developed at the age of 3 months in the other three infants; one had supraventricular tachycardia as well as atrial fibrillation, and the other two had atrial flutter, changing to atrial fibrillation during digoxin therapy. None of the four patients had congenital heart disease, myocarditis, or Wolff -Parkinson-White

syndrome;

in

all,

the

arrhythmias

resolved during digoxin therapy. One girl was classified as having idiopathic paroxysmal atrial fibrillation. Her heart was dinically normal and there was no ECG evidence of a


ARTICLES

253

TABLE CARDIAC

ABNORMALITIES

IN

II 35

CHILDREN

WITH

Amii

FIBRILLATION

Condition

No. Miscellaneous disease

Heart

with later with sinus patient

tachyarrhythmias in whom sinus rhythm was restored by drug therapy, in one patient rheumatic heart disease in whom normal rhythm occurred after surgery, and in one with cardiomyopathy who died of this

disease

Disease

some

time

later.

Tetrology

of Fallot

2

Sixteen patients underwent surgery of their basic lesions: 2 had rheumatic valve disease and 14 had congenital heart disease. Both patients with rheumatic disease had mitral replacements, with tricuspid annuloplasty in one and excision of a huge left atrial appendage in the other. The latter patient is now in sinus rhythm. The operations for transposition of the great arteries, common atrium, and total anomalous pulmonary venous drainage involved insertion of an atrial baffle or patch, and closure of the atrial septal defect was by suturing. Two patients with tetralogy of Fallot and one with pulmonary atresia had severe tricuspid regurgitation postoperatively and were treated by further surgery to the tricuspid valve. The other patient with

Pulmonary

atresia

2

pulmonary

2

artery

2

necropsy

1

atrium.

Rheumatic

heart

3

Cardiomyopathy

5

Tumor

2

Infective

endocarditis

Paroxysmal

1

atrial

Idiopathic

tachycardia

paroxysmal

Marfan’s

of infancy

atrial

fibrillation

syndrome

Endocardial

4 1 1

-

fibroelastosis

1

Total

18 Congenital

Transposition Atrial

of great

septal

Common Total

Heart

Malformations

vessels

4

defect

1

atrium

1

anomalous

pulmonary

Ebstein’s

anomaly

Congenital

mitral

Eisenmenger’s Single

valve

veins

1

abnormality

complex

ventricle

1

Total

17

preexcitation syndrome. Investigation, which included tests for thyroid function, pheochromocytoma, and systemic disease, revealed no abnormality. One patient had Marfan’s syndrome, with severe mitral regurgitation and enlargement of the left atrium; she died in congestive cardiac failure in 1956. Endocardial fibroelastosis was diagnosed

clinically

in

one

boy

and

necropsy

showed gross dilatation of both atria. The other 17 patients had structural congenital heart malformations, which are summarized in Table II. One patient who had Ebstein’s anomaly and those who had Eisenmenger’s complex or single ventricle did not undergo surgery. In the other 14, atrial fibrillation developed at various intervals after operation. Therapy

Digoxin was given to all 35 patients, with quinidine in four and propranolol anticoagulants

were

Cardioversion failed in four.

254

ATRIAL

together in five. No

used.

was successful in six children and The failures occurred in two infants

atresia anastomosis;

revealed

had

a systemic-to-pulmonary

he died six years later, severe dilation of the

and right

One patient with Ebstein’s anomaly underwent suture closure of two associated atrial septal defects in 1961. Ten months later, atrial fibrillation developed and his clinical condition deteriorated; an attempt to decompress the atrium by incising the septum was unsuccessful and he died. Both children with congenital mitral valve abnormalities had coarctation of the aorta. One required annuloplasty for mitral regurgitation, after which atrial fibrillation developed; the mitral valve was replaced later, and normal sinus rhythm ensued. The other child had mitral stenosis and an atrial septal defect treated by valvotomy and atrial septal repair; he still has paroxysms of atrial fibrillation, seven years later. Of the 16 patients who underwent surgery, three are dead (one with Ebstein’s anomaly, one with pulmonary atresia, and one with transposition of the great vessels). Five continue to have paroxysmal atrial fibrillation (four with sick-sinus syndrome and one following mitral valvotomy), two have permanent atrial fibrillation (one with rheumatic heart disease and one with tetralogy of Fallot), and the status of one is unknown. Five remain in sinus rhythm, three after surgery for atrioventricular valvular regurgitation and two after

cardioversion.

Downloaded from www.pediatrics.org at Queensland Health on May 12, 2009 FIBRILLATION

Sick-Sinus

Syndrome

The sick-sinus syndrome developed in five patients (cases 4, 19, 21, 24, and 25), characterized by the following bradyarrhythmias and tachyarrhythmias: sinus arrest and junctional bradycardia, atrial ectopic beats, atrial flutter, supraventricular tachycardia, and atrial fibrillation. One patient died (case 4; hemochromatosis cardiomyopathy from thalassemia). The others were operated on for congenital heart lesions (transposition of the great vessels in two, a common atrium in one, and total anomalous pulmonary-venous drainage in one); three have been treated by cardioversion for tachyarrhythmias, without problems. These four patients, who have never had cardiac pacemakers, are being maintained on antiarrhythmia drugs; none has had sustained atrial fibrillation.

DISCUSSION Etiology The association of atrial fibrillation with severe left atrial enlargement is well known,2:3.2 and necropsy studies have demonstrated damage to the sinoatrial node, fibrosis of the internodal tracts, and occlusion of the nodal artery.26 In the majority of our patients we documented atrial distension (particularly by regurgitant valve lesions) or irritation (by surgery or tumor). Endocardial fibroelastosis, also, may be associated with atrial arrhythmias2728; its pathology includes severe atrial fibrosis and dilatation. Thus, mechanical factors play a role in the genesis of atrial fibrillation. In addition, the electrophysiological changes of asynchrony of conduction and refractoriness render the atria vulnerable to fibrillation.2329 This mechanism is most strongly implicated in cardiomyopathy, in which atrial fibrillation develops in a diseased myocardium and usually heralds sudden death, presumably from ventricular fibrillation. It has been shown that patients with the sick-sinus syndrome have atrial disease as well as local sinus-node injury.30 Thus, in this syndrome also, atrial fibrillation is engendered by both mechanical and electrophysiological changes. Paroxysmal

atrial

tachyarrhythmias

are

well

known in infancy3’ and also occur in utero.32 They usually carry a good prognosis, the majority never recurring after the first year of life. Although the prognosis is said to be poor if atrial fibrillation is present,33 this has not been our experience, as all four of our patients are alive and well: two had atrial fibrillation before therapy, and two had

atrial flutter initially which changed to fibrillation when digoxin treatment was started. (There was no evidence of toxicity, but drug induction of this arrhythmia was implicated in these last two patients.) The girl with idiopathic paroxysmal atrial fibrillation (case 16, Table I) presented a rare problem: she did not fit the category of “lone atrial fibrillation,” which occurs predominantly in older men and is not paroxysmal,3 and had no known family history that would justify calling the condition “benign familial.”35 Therapy

In been give

our series, the mainstay of treatment has digoxin to control the ventricular rate and inotropic support. In some cases it was necessary to add propranalol or quinidine. Anticoagulants

have

not

been

used:

consideration

might be given to their use, but in children the control of such therapy and the risks of hemorrhage usually outweigh the potential value. The question of cardioversion is important. Cenerally accepted contraindications for this procedure are (1) long-standing atrial fibrillation,

(2)

enlarged

atria,

and

(3)

associated

cardiac

failure.22 These would apply particularly to patients with cardiomyopathy. A modern concept is that atrial fibrillation due to rheumatic heart disease is initially reversible, but later irreversible due to pathological changes in the atria secondary to the arrhythmia itself.23 Thus, early cardioversion is indicated, and such an approach is important in children with rheumatic or congenital heart disease. Also, appropriate surgical int#{233}rvention is necessary in these conditions when atrial distension and high intra-atrial pressures can be reduced. Prognosis

Prognosis obviously depends on the underlying cardiac disease, but it can be worsened by the onset of atrial fibrillation. Our experience with rheumatic heart disease is small, but has shown that a surgical approach can halt clinical deterioration. Cardiomyopathies have a generally poor prognosis, with a rapidly downhill course once atrial fibrillation develops. Contrary to previous statements,33 our experience suggests that atnal fibrillation occurring with other atrial tachyarrhythmias in infancy has the same good prognosis for survival and nonrecurrence as these arrhythmias.

Operation

heart malformations expectency in these itself can precipitate

to

correct

congenital

have greatly improved life conditions. However, surgery arrhythmias and the long-


ARTICLES

255

term natural known.

history

in

these

cases

is not

yet

15.

16.

IMPLICATIONS From this review it is evident that atrial fibrillation is still a rare arrhythmia in children but can occur in association with a wide variety of conditions. We conclude that atrial fibrillation in infancy or childhood is not necessarily a sign of irreversible deterioration. Its recognition is an indication for complete investigation of the patient, and when the underlying condition is treatable, therapy should be aggressive, with drugs, cardioversion, and surgery, as appropriate.

17.

1975.

18. Stock

KH: Supraventricular mias in infants and

and children.

ventricular Cardiovasc

dysrhythClin 4:71,

20. 21.

22.

1972. 2. Hurwitz BA:

23.

3.

24.

Cardiac arrhythmias in infants and children. Curr Probl Pediatr 3:3, 1973. Keith JD, Rowe RD, VIad P: Heart Disease in Infancy and Childhood, ed 2. New York, Macmillan, 1967, p 1049.

4. 5.

6. 7. 8. 9.

10.

11.

Cookson H: Auncular 2:1139, 1929. McEachern D, Baker

fibrillation

in children.

Lancet

25.

Jr: Auricular fibrillation: Its etiology, age incidence and production by digitalis therapy. Am J Med Sci 183:35, 1932. Gibson S: Auricular fibrillation in childhood and adolescence. JAMA 117:96, 1941. Wood P: Diseases of the Heart and Circulation, ed 3. London, Eyre & Spottiswoode, 1968, p 428. Craig RJ, Seizer A: Natural history and prognosis of atrial septal defect. Circulation 37:805, 1968. Watson H: Natural history of Ebstein’s anomaly of tricuspid valve in childhood and adolescence: An international co-operative study of 505 cases. Br Heart J 36:417, 1974. Frank 5, Braunwald E: Idiopathic hypertrophic subaortic stenosis: Clinical analysis of 126 patients with emphasis on the natural history. Circulation 37: 759, 1968. Angelini P. Feldman MI, Lufschanowski R, et al: Gardiac arrhythmias during and after heart surgery: Diagnosis and management. Prog Cardiovase Dis 16:469,

BM

1974.

13.

14.

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ATRIAL

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Cardiac 1970, p

DJ, Julian DC: Sick sinus syndrome: Experience of a cardiac pacemaker clinic. Br Med J 3:504, 1974. Conn HE: Sick sinus syndrome treatment. Circulation 48:671, 1973. Vera Z, Mason D, Awan N, et al: Spontaneous development of stable atrial fibrillation in patients with sick sinus syndrome: Autogenous cure and incidence of occurrence, abstracted. Circulation 52:93, 1975. Schamroth L: The Disorders of Cardiac Rhythm. Oxford, Blackwell, 1973, p 58. Noble RJ, Fisch C: Factors in the genesis of atrial fibrillation in rheumatic valvular disease. Cardiovase Clin 5:97, 1973. Probst P, Goklschlager N, Selzer A: Left atrial size and atrial fibrillation in mitral stenosis: Factors influencing their relationships. Circulation 48:1282, 1973. Henry WL, Morganroth J, Pearlman AS, at al: Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 53:273, Radford

1976. 26. Davies

MJ, Pomerance A: Pathology of atrial fibrillation in man. Br Heart J 34:520, 1972. 27. Siderides LE, Antonius NA, Richian A: Unusual auricular flutter in newborn infant: Report of a case and review of the literature. J Pediatr 51:435, 1957. 28. Hung W, Walsh BJ: Congenital auricular fibrillation in a newborn infant with endocardial fibroelastosis: Report of a case with necropsy. J Pediatr 61:65, 1962.

29. 30.

31.

32.

12. El-Said

C, Rosenberg HS, Mullins CE, et a!: Dysrhythmias after Mustard’s operation for transposition of the great arteries. Am J Cardiol 30:526, 1972. Young D: Later results of closure of secundum atrial septal defect in children. Am J Cardiol 31:14, 1973. Ferrer MI: The sick sinus syndrome. Circulation 47:635, 1973.

JPP: Diagnosis and Treatment Arrhythmias, ed 2. London, Butterworth,

214. 19.

REFERENCES 1. Ehlers

Rubenstein JJ, Schulman C, Yurchak PM, et al: Clinical spectrum of the sick sinus syndrome. Circulation 46:5, 1972. Greenwood RD, Rosenthal A, Sloss U, et al: Sick sinus syndrome after surgery for congenital heart disease. Circulation 52:208, 1975. Radford DJ, Izukawa T: Sick sinus syndrome: Symptomatic cases in children. Arch Dis Child 50:879,

33. 34. 35.

Surawicz B, Steffens T: Cardiac vulnerability. Cardiovasc Clin 5: 159, 1973. Kaplan BM, Langendorf R, Lev M, Pick A: Tachycardiabradycardia syndrome (so-called “sick sinus syndrome”). Am J Cardiol 31:497, 1973. Nadas AS, Daeschner CW, Roth A, et al: Paroxysmal tachycardia in infants and children: A study of 41 cases. Pediatrics 9:167, 1952. Radford DJ, Izukawa T, Rowe RD: Congenital paroxysmal atrial tachycardia. Arch Dis Child 51:613, 1976. Moller JH, Davachi F, Anderson RC: Atrial flutter in infancy. J Pediatr 75643, 1969. Evans W, Swann P: Lone auricular fibrillation. Br Heart J 16:189, 1954. Phair WB: Familial atrial fibrillation. Can Med Assoc J 89:1274, 1963.

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Atrial Fibrillation in Children Dorothy J. Radford and Teruo Izukawa Pediatrics 1977;59;250-256 Updated Information & Services

including high-resolution figures, can be found at: http://www.pediatrics.org

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