Cardiovascular Journal of Africa: Vol 32 No 5 (SEPTEMBER/OCTOBER 2021)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 32, No 5, September/October 2021 270 AFRICA studies, 16,17 but at variance with other studies that showed TOF as the commonest cyanotic CHD. 1,4-7,14 It is possible that because the screening in our study was at birth, neonates with TGA were detected before they presented later in the neonatal period with symptoms, whereas most of these other studies were audits of echocardiography laboratory findings in which children with TGA may not have been represented, having died from their condition before accessing diagnostic facilities. In our setting, such babies, because of lack of funds, would have passed on or been missed altogether if delivered outside the hospital setting. The birth prevalence of 14.4/1 000 live births in this study is at variance with the earlier report of low prevalence among Africans compared to Caucasians and Asians. The earlier studies in which low prevalence was reported among Africans could have been due to the method of recruitment. Previous studies utilised the method of clinical evaluation of possible CHDs, with echocardiographic confirmation of such CHDs. 4-7 This method could have excluded asymptomatic cases or ones with delayed presentation later in life. It would seem from this study that the birth prevalence of CHD in Africans compares with that of other races. Babies with CHD in this study were significantly lighter in weight than those without the condition. Similarly, there were more low-birth-weight babies with CHD than those without CHD, although the difference did not reach statistical significance. These findings are consistent with previous work. 18 Although children without CHD were also taller than those with CHD, the difference did not reach statistical significance. Some previous studies have shown this difference to be significant. 18 It has been shown that lower birth weight predicted poorer five-year survival after surgery. 19 The parents of babies with CHD were significantly older than those of children without CHD. This finding is similar to other studies that have described increasing risk of having babies with CHD with increasing maternal and paternal age. 20,21 It is thought to be caused by increased mutations in the germ cell line due to cumulative cell replications. One limitation of this study is the relatively small sample size. The absence of some CHDs such as hypoplastic left heart syndrome, double-outlet right ventricle and Ebstein’s anomaly is also a limitation, which may be due to the low incidence of such CHDs, as seen in previous studies. 2,3,5 It is possible that the screening of a larger population of neonates would yield such CHDs. Another limitation is the small number of CHDs such as TGA, PTA and TOF, which makes the determination of their specific prevalences difficult. Conclusion The birth prevalence of CHDs in this study was high and we found that the prevalence of CHDs in Africans was comparable to that of other races. This information is important for health policy formulators in preparing for interventions for the CHDs in our health facilities. References 1. Blue GM, Kirk EP, Sholler GF, Harvey RP, Winlaw DS. Congenital heart disease: current knowledge about causes and inheritance. Med J Aust 2012; 197 : 155–159. 2. Liu Y, Chen S, Zuhlke L, Black GC, Choy M, Li N, et al. Global birth prevalence of congenital heart defects 1970–2017: updated systematic review and meta-analysis of 260 studies. Int J Epidemiol 2019: 455–463. 3. Ferencz C, Rubin JD, McCarter RJ, et al. Congenital heart disease: prevalence at live birth. Am J Epidemiol 1985; 12 : 31–36. 4. Gupta B, Antia AU. 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