Cardiovascular Journal of Africa: Vol 27 No 1 (January/February 2016)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 1, January/February 2016 28 AFRICA
These findings may be as a result of ventricular dysfunction as
well as autonomic dysfunction and the increased basal metabolic
rate seen in HIV/AIDS patients.24
There were significant differences in the systolic and diastolic
blood pressure of the HIV and AIDS groups in our study
compared with the controls. Those with HIV or AIDS had
higher blood pressure values than the controls. There are
conflicting reports in the literature. Some workers found no
differences in blood pressure,26-28 while others noted an increased
frequency of systemic hypertension among patients with HIV/
AIDS.13,24 The compensatory mechanism of a normal or low
blood pressure, seen in chronic malnutrition, which is prevalent
in children with HIV/AIDS, may play a role.29 Haemoglobin
level in the HIV/AIDS groups was significantly lower than in
the controls. This was expected, due to chronic infection and
malnutrition as a result of chronic diarrhoea.
The HIV group had significantly higher mean left ventricular
end-diastolic dimensions than the controls. Fractional shortening
and ejection fraction, on the other hand were significantly lower
in the HIV and AIDS groups than in the controls, being lowest
in the AIDS group. This was similar to the findings of Hecht
et al.30 and Nzuobontane et al.2 They noted that end-diastolic
dimensions were significantly higher in HIV-positive patients,
while fractional shortening was significantly lower in AIDS
subjects. This suggests that ventricular dilatation occurs earlier
in the course of the disease than impaired contractility.
In identifying a possible link between certain variables and
the presence of left ventricular systolic dysfunction, this study
noted that BMI, blood pressure, except DBP (in the AIDS
group), haemoglobin concentration, WBC, ESR and stage of
the disease were not associated with the presence of systolic
dysfunction (Table 3). Advanced stage of the disease, which
is a known risk factor for cardiac involvement,1,31 was not
significantly associated with the presence of LVSD in this study,
even though the prevalence of LVSD was higher in the AIDS
group. The reason for this was not obvious, however, it may
be connected with the population studied, as racial or genetic
differences had been noted.18 It is hoped that future studies will
further investigate this finding.
Lower CD4 + count and younger age were significantly
associated with the development of LVSD in the logistic
regression model. This agrees with the report of Herskowitz et
al., who studied adults, and found a median CD4+ count of 30
cells/μl in HIV-infected patients with left ventricular dysfunction
compared to a median count of 187 cells/ml in those without
ventricular dysfunction.32 Lower CD4+ cell count is a marker
of terminal disease associated with HIV cardiomyopathy, and
younger children20 had been noted to have a rapid course of
disease progression with end-organ effects.
Increased pulse rate was found in our study to be associated
with LVSD, however, this was not noted by other investigators.15,33
This may not be unconnected with the population studied and the
high prevalence of ventricular dysfunction observed in this study.
Multiple regression analysis showed that CD4+ cell count
and age of the patients predicted the development of left
ventricular systolic dysfunction, with CD4+ cell count being
the best predictor (r = 0.396, CI = 0.002) (Table 4). This implies
that significant decrease in CD4+ cell count was the highest risk
factor for the development of LVSD in our subjects. This finding
is at variance with Lipshultz et al.16 and Lobato et al.,34 who
noted the presence of HIV encephalopathy as a predictor of LV
dysfunction in HIV infection. This difference may have been due
to the inclusion criteria, as only perinatal acquired HIV infection
was included.
A limitation of the study is that the presence or absence of
pre-existing cardiac abnormality prior to enrolment into the
study was based on patients’ medical records or medical history.
This did not completely exclude cardiac abnormality, as clinical
evaluation alone is inadequate, as shown in the HIV-negative
controls who had cardiac abnormalities.
Conclusion
This study demonstrated a high prevalence of LVSD in children
with HIV and AIDS, who apparently had no clinical evidence of
heart failure. CD4+ cell count and age of the children were the
best predictors of LVSD. The younger the age and the lower the
CD4+ cell count, the higher the number of children with LVSD.
Since LVSD was asymptomatic in these children, it is
recommended that HIV and AIDS children should undergo
baseline and periodic evaluation using echocardiography. Cardiac
care providers should be incorporated in the management of
children with HIV/AIDS in our environment to implement
appropriate preventative and therapeutic measures. This will
maximise survival and improve the quality of life of these
children.
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