CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 2, March/April 2014
60
AFRICA
intraventricular block. This baby had severe hyperkalaemia (K
+
:
9.4 mEq/l) caused by congenital adrenal hyperplasia.
Three patients had complete AV block and 2:1 AV block. Six
patients had AV block – three with complete AV block and one
in whom 2:1 AV block later progressed to complete AV block.
Four patients with AV block underwent permanent pacemaker
implantation.
Two patients with tachyarrhythmia had sinus tachycardia. One
of these patients had a persistent heart rate of 180–190 beats/min
and was given short-term treatment with a beta-blocker, which
was discontinued after the newborn period. The other baby did
not have any treatment.
Twenty-three babies had SVT: five had atrial flutter (AF),
one had PJRT, one had multifocal atrial tachycardia (MAT), and
the rest had atrioventricular re-entrant tachycardia (AVRT). No
baby had atrioventricular nodal re-entrant tachycardia (AVNRT).
Sinus rhythm was achieved with cardioversion in four patients
with AF and in one patient with amiodarone infusion. In babies
with SVT without AF, six were treated with adenosine, four were
treated with amiodarone and application of ice to the face, two
were treated with ice initially and then with adenosine, and two
were treated with digoxin. Three babies with SVT had Wolf–
Parkinson–White (WPW) syndrome. Digoxin or propranolol
prophylaxis was given to all patients with SVT and AF.
The average duration of follow up after the newborn period for
all patients was 15 months (minimum three months, maximum six
years). Twenty-three patients with SVT and three with frequent
supraventricular premature beats continued anti-arrhythmia
treatment after discharge (beta-blockers or digoxin). AF did not
recur in any patients. Five patients with SVT had recurrence after
the newborn period. In these patients, rhythm and speed control
was achieved by treatment with sotalol. Patients with PJRT and
multifocal atrial tachycardia required anti-arrhythmia treatment
after the age of one year. Three patients with WPW syndrome
continued to take propranolol prophylaxis.
Four patients died in the newborn period. One baby with
diaphragmatic hernia and one with co-anal atresia died because
of respiratory problems after SVT treatment. The other baby had
supraventricular premature beats diagnosed in the foetal period.
In spite of spontaneously resolved supraventricular premature
beats on the second postnatal day, this patient died because of
metabolic disease. The remaining baby had tetralogy of Fallot
2:1 AV block, which progressed to complete AV block. This
baby died because of sepsis after a pacemaker implantation.
Apart from these four babies, no other patients died during the
follow-up period.
Discussion
The incidence of arrhythmia in the newborn period has been
reported to be about 1%.
4
Most of these arrhythmias are
asymptomatic and rarely life-threatening.
Various studies have identified that 15.3% of arrhythmic
newborns have congenital heart disease. Atrial arrhythmias
in particular are reported more frequently in newborns with
congenital heart disease.
5,6
In a study of 21 arrhythmic newborns,
Satar
et al
.
7
found a congenital heart disease rate of 38%, while
Canpolat
et al
.
8
reported a rate of 23.1%. Of our cases, 30.3%
had congenital heart disease. Although in our study group the
most frequent accompanying pathology was ASD, Satar
et
al
.
7
found that patent ductus arteriosus was the most frequent
pathology.
Ventricular and supraventricular premature beats are
generally self-limiting, benign arrhythmias. Examination of
healthy newborns before discharge determined a 1% frequency
of premature beats. Premature beats may be secondary to
metabolic and biochemical abnormalities and hypoxia; however,
the majority have no clear underlying pathology.
9
The prognosis for premature beats is generally very good,
and most of them disappear after the first months of life. Of
our patients, 39.3% had supraventricular premature beats and
6% had ventricular premature beats. Patients with ventricular
premature beats did not have arrhythmia after the newborn
period. Seven patients with supraventricular premature beats
had persistent arrhythmia beyond one year, but none of them
progressed to SVT. In a study by Poddar
et al
.,
10
premature beats
lasted up to early childhood and spontaneously resolved without
complications in three of nine arrhythmic newborns. Our results
were compatible with the literature.
Congenital complete AV block had an observed rate of 1/15
000–20 000 for live births.
11
Generally, it is secondary to structural
cardiac defects or maternal systemic lupus erythematosus.
12
Complete AV block with severe bradycardia leading to low
cardiac output may result in heart failure. Symptomatic complete
AV block and asymptomatic block with heart rate below
55 beats/min, accompanied by wide QRS escape rhythm or
accompanying cardiomegaly, are indications for emergency
pacemaker implantation.
11
Canpolat
et al
.
8
identified four patients (15.4%) with AV
block, all of whom were diagnosed in the prenatal period.
Only two had mothers with lupus or Sjogren’s disease. In our
study, four of six patients with AV block underwent pacemaker
implantation, and two were diagnosed in the prenatal period.
While SVT is the most frequently observed type of tachycardia
in the newborn period, it can cause postnatal irritability, feeding
difficulties, tachypnoea, tachycardia and heart failure in the
antenatal period. Many newborns can tolerate the first hours of
SVT well, but if SVT continues longer than 6–12 hours, heart
failure caused by stroke volume reduction may develop.
13
Fifteen
per cent of patients have a history of sepsis and medication.
14
Additionally, babies with cardiac anomalies, such as Ebstein
anomaly, transposition of the great arteries, and single ventricle
are known to be at risk for SVT.
11
In our study, SVT was the second most frequent arrhythmia
(22.7%). This result was compatible with the literature. However,
this rate is lower than the SVT rate found in the study by
Satar
et al
.
7
In a similar study,
15
eight patients had major
cardiac pathologies, such as Ebstein anomaly, AV septal defect,
ventricular septal defect and tricuspid atresia. However, none of
our patients had complex cardiac pathologies.
AV nodal re-entrant tachycardia is rarely seen in the newborn
and toddler periods. In this period, AV re-entrant tachycardia is
more frequent. Naheed
et al
.
16
studied 30 foetuses with SVT and
did not detect AV nodal re-entrant tachycardia in the postnatal
period. In a study by Ko
et al
.,
17
only three of 137 (2.1%) had
AV nodal re-entrant tachycardia. No patient in our study had
AV nodal re-entrant tachycardia. In our cases with SVT, AV
re-entrant tachycardia was the most frequent mechanism of
tachycardia.
In WPW syndrome, apart from the normal communicating
