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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 1, January/February 2016

AFRICA

3

From the Editor’s Desk

It is interesting to one trained in the era that preceded the

availability of new and sophisticated imaging modalities to

see just how well the ‘old’ and often currently poorly regarded

imaging techniques still serve. Ganie and colleagues (page 31)

record how in seven of eight patients with vascular rings, the chest

radiograph was abnormal, and they propose a diagnostic imaging

algorithm for such patients, which includes chest radiographs.

My own observations suggest that the chest radiograph is often

neglected and may not be performed in current practice when

patients are evaluated with symptoms or signs of cardiovascular

disease, and are referred for echocardiography before a chest

radiograph is performed. Echocardiography may fail to detect

extra-cardiac abnormalities and mis-assess the severity of intra-

cardiac abnormalities unless clinically directed. The authors are

to be congratulated on pointing out how simple investigations,

performed at low cost, may be valuable in evaluating patients

with complex cardiovascular abnormalities.

In exploring the genetic contribution to hypertension, Sun and

colleagues (page 21) have identified genes that were risk factors

for nocturnal hypertension in this Chinese Han population, and

their combined effects played an important role in nocturnal

hypertension. However, as the authors acknowledge, even if a

gene were considered associated with hypertension in certain

populations, to expand the conclusion to all human populations

is unwise at this stage. In diseases such as hypertension, obesity

or diabetes, not only genetic factors but many other factors, such

as environment or geographic location, could be important. All

these factors could have different effects on obesity or diabetes

and they could impact on each other. Therefore whether or how

single genes may be associated with nocturnal hypertension is

complicated. Long-term population-based studies are needed to

clarify the relationship.

Arodiwe and co-authors (page 26) point out the paucity of

information on the frequency of cardiac involvement in children

with HIV/AIDS in sub-Saharan Africa, and the importance

of such information given the extent of the epidemic. They

conducted a descriptive cross-sectional echocardiographic study

of HIV-infected children and uninfected controls at a Nigerian

teaching hospital and showed left ventricular systolic dysfunction

in 27% of HIV-infected children and 81% of those with AIDS.

The systolic dysfunction was asymptomatic. This is important

information and hopefully there will be further information

forthcoming from the authors regarding follow up and prognosis

of this particular group of patients, as well as the effects of anti-

retroviral therapy. The impact of usual cardio-active medication

for systolic dysfunction, such as angiotensin converting enzyme

inhibitors and beta-blockers, should also be explored in this

population.

The clinical, laboratory and ECG profiles of 62 children with

sickle cell anaemia (SCA) attending a paediatric haematology

clinic in Nigeria and 40 age- and gender-matched haemoglobin

AA controls were compared (page 16). Adegoke and colleagues

found that ECG abnormalities were common in children with

SCA, and in their discussion, speculate on the mechanisms and

significance of the ECG abnormalities.

Patrick Commerford

Editor-in- Chief

Professor PJ Commerford