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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 1, January/February 2021

24

AFRICA

were isolated VSDs detected in 32 (31.4%) neonates, followed

by isolated ASDs in 22 (21.6%). The ductus arteriosus was still

patent in 1 643 (42.6%) of the neonates at enrolment. The highest

frequency of ductal patency was in neonates recruited on the

first day of life (1 220/1 643, 74.3%), and decreased markedly by

the second and third days of life to 12.3% (202/1 643) and 6.5%

(107/1 643), respectively. By the sixth day of life, only 11 neonates

still had ductal patency. However, only seven neonates had a

ductal diameter that exceeded 1.5 mm, therefore satisfying the

criteria for classification as CHD; a prevalence of four per 1 000.

Five (71.4%) of the seven neonates had isolated PDAs while the

remaining two (28.6%) co-existed with other CHD; one ASD

and one VSD (Table 4).

Isolated ASDs were present in 22 of the 24 (91.7%) neonates

with ASD; one ASD co-existed with a PDA and the other with

moderate pulmonary stenosis. Most (95.5%) of the isolated

ASDs were ostium secundum defects; one (4.5%) was an ostium

primum ASD. Thirty-two of the 34 (94.1%) neonates with VSD

had isolated lesions; the other two co-existed, one with a PDA

and the other with a mild pulmonary stenosis. The majority of

the isolated VSDs were peri-membranous defects, which were

detected in 17/32 (53.1%). Muscular VSDs were present in 14/32

(43.8%), while a sub-aortic VSD was detected in one (3.1%) of

the neonates with isolated VSD (Fig. 2).

Sixty four of the 111 neonates with CHD had mild defects

(16.6 per 1 000 population) while 27 had moderate CHD (7.0 per

1 000 population). Severe CHD was detected in 20 neonates with

a prevalence of 5.2 per 1 000. Moderate and severe CHD were

more common in males; 16/64 (25.8%) male versus female 11/49

(22.4%) and 14/64 (22.6%) male versus female 6/49 (12.3%),

respectively, but these were not significantly different (

p

= 0.75

and

p

= 0.08, respectively). More female neonates (32/49 or

65.3%) had mild CHD compared with males: 32/64 or 51.6%,

but the difference was also not significantly different;

p

= 0.11

(Fig. 3).

Mild CHD was present in 42 of the 2 340 neonates delivered

in the study hospitals (17.9 per 1 000 live births) while moderate

and severe lesions were present in 14 (6.0 per 1 000 live births)

and eight (3.4 per 1 000 live births) patients, respectively.

Admitted neonates with CHD had more severe lesions

compared with those who were not admitted (

p

= 0.001). There

was no significant association between the severity of CHD and

gender, place of delivery, maternal age, gestational age at delivery

or birth weight (Table 3).

Mothers of neonates with CHD were older (30.6 ± 5.6 vs 28.4

± 6.8 years,

p

< 0.001) and had higher parity (3.5 ± 2.0 vs 2.8 ±

1.9,

p

< 0.001). Neonates with CHD had lower birth weight (2.8

± 0.6 vs 3.1 ± 0.6 kg,

p

< 0.001), were four times more likely to

receive in-patient care [OR 4.4 (95% CI 2.8–6.8),

p

< 0.001] or

had dysmorphic features (

p

< 0.001). There was no difference

in mean gestational age between neonates born with CHD and

0

10

Male Female

Mild

Male Female

Moderate

Male Female

Severe

20

30

Fig. 3.

The distribution of CHD based on severity

Table 4. Prevalence and spectrum of CHD

Total

(3 857)

Male

(2 016)

Female

(1 841)

Spectrum of CHD

n

per 1 000

n

per 1 000

n

per 1 000

Acyanotic CHD

102 (26.4) 55 (27.3) 47 (25.5)

Atrial septal defect

24 (6.5)

10 (5.0)

14 (7.6)

Ventricular septal defect

34 (9.2)

16 (7.9)

18 (9.8)

Combined atrial and ventricular septal defect 13 (3.4)

10 (5.0)

3 (1.5)

Atrioventricular septal defect

5 (1.3)

3 (1.5)

2 (1.1)

Isolated pulmonary stenosis

9 (2.3)

7 (3.5)

2 (1.1)

Isolated patent ductus arteriosus

5 (1.3)

2 (1.0)

3 (1.5)

Coarctation of the aorta

4 (1.1)

2 (1.0)

2 (1.1)

Bicuspid aorta valve

4 (1.1)

3 (1.5)

1 (0.5)

Aortopulmonary window

1 (0.3)

1 (0.5)

0 (0.0)

Double-outlet right ventricle

1 (0.3)

0 (0.0)

1 (0.5)

Partial anomalous pulmonary venous return 1 (0.3)

1 (0.5)

0 (0.0)

Cortriatriatum dexterum

1 (0.3)

0 (0.0)

1 (0.5)

Cyanotic CHD (severe)

9 (2.3)

7 (3.5)

2 (1.1)

Tetralogy of Fallot

1 (0.3)

0 (0.0)

1 (0.5)

Truncus arteriosus

1 (0.3)

1 (0.5)

0 (0.0)

Ebstein’s anomaly

1 (0.3)

1 (0.5)

0 (0.0)

Critical CHD

Hypoplastic left heart syndrome

4 (1.1)

3 (1.5)

1 (0.5)

Total anomalous pulmonary venous return 1 (0.3)

1 (0.5)

0 (0.0)

Transposition of great arteries

1 (0.3)

1 (0.5)

0 (0.0)

Otium primum

Ostium secundum

Perimembranous

Sub-aortic

Muscular

Fig. 2.

A. Types of ASD detected. B. Types of VSD detected.

A

B