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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 5, September/October 2020
238
AFRICA
the echocardiographic indices are shown in Table 2. Correlation
between different patient factors and cardiac involvement is
shown in Table 3.
Discussion
This study shows the spectrum of echocardiographic
abnormalities in our sample of patients living with HIV and
taking HAART, although none of these patients had clinically
apparent cardiac symptoms. This has been demonstrated in
other similar studies.
3,4,14
In this study, conventional echocardiographic examination
picked up only six straightforward abnormalities (three cases of
LV systolic dysfunction, two of pulmonary arterial hypertension
and one of minimal pericardial effusion), which would have
made the prevalence of cardiac abnormalities in this cohort
only about 4%. However, calculation of the MMI from the LV
M-mode indices (LV end-diastolic diameter, interventricular
septal thickness in diastole, and posterior wall thickness in
diastole), and height and weight of each patient showed that
16 patients actually had abnormal MMI ranging from mild to
severe.
Considering that 17.8% of our patients had moderate-to-
severe malnutrition and knowing the effect of malnutrition on
cardiac muscle (atrophy), it is possible that our calculation of
MMI may actually underestimate the proportion of patients
with abnormal myocardial mass. However, it can also be argued
that the values are still valid reflections as long as they are
indexed for body surface area. There were additional indices,
such as measures of cardiac strain and strain rate, which we did
not measure due to logistic problems. Other investigators have
demonstrated that these indices were also commonly impaired.
27
All the studypatientswereonHAARTandhadgoodadherence
to treatment, except a few patients who interrupted the treatment
for some time in their course due to perceived or confirmed
drug side effects. The reported effect of HAART on incidence
of cardiovascular abnormalities in HIV patients is mixed.
Some studies have reported that HAART is cardioprotective,
28-30
and in some cases, resolution of conditions such as dilated
cardiomyopathy have been reported.
31
But on the other hand,
exposure to HAART is actually one of the mechanisms of
Table 1. Demographic and clinical characteristics of
151 HIV-infected children on HAART
Characteristics
Values
Age (years), mean
±
SD (range)
13.0
±
3.2 (4.0–19.0)
Gender,
n
(%)
Female
83 (55.0)
Male
68 (45.0)
Weight (kg), mean
±
SD (range)
35.5
±
11.3 (12.0–65.0)
Height (cm), mean
±
SD (range)
142.8
±
15.9 (92.0–177.0)
WHO clinical stage at initiation of HAART,
n
(%)
I
13 (8.6)
II
42 (27.8)
III
68 (45.1)
IV
28 (18.5)
Parental status,
n
(%)
Both alive
45 (29.8)
Single orphan
59 (39.1)
Double orphan
47 (31.1)
Maternal education,
n
(%) (alive only,
n
= 62)
Primary or less
29 (46.8)
Secondary
29 (46.8)
Higher
4 (6.4)
Paternal education,
n
(%) (alive only,
n
= 61)
Primary or less
16 (26.2)
Secondary
29 (47.5)
Higher
16 (26.2)
Age at diagnosis (years), mean
±
SD (range)
n
= 119
5.7
±
3.3 (0.12–13)
Age at disclosure (years), (mean
±
SD (range),
n
= 96
11.6
±
2.4 (3–18)
Lowest CD
4
count ever recorded, mean
±
SD (range)
328.8
±
225.8 (3–1210)
Latest CD
4
count, mean
±
SD (range)
706.0
±
389.3 (3–3034)
Age at initiation of HAART (years)
7.34
±
3.54 (0.33–15.75)
HAART duration (months)
59
±
39.1 (1–126)
Cotrimoxazole prophylactic therapy duration
(months),
n
= 148
55.9
±
30.7 (2–120)
WHO, World Health Organisation; HAART, highly active antiretroviral treatment.
Table 2. Conventional echocardiography and TDI indices from
151 HIV-infected children and adolescents on HAART
Echocardiographic indices
Mean
±
SD (range)
(
n
= 151)
Heart rate (beats/min)
86
±
16 (56–125)
LV end-diastolic diameter (cm)
4.0
±
0.5 (3.0–5.5)
Interventricular septal thickness in diastole (cm)
0.73
±
0.15 (0.50–1.20)
LV posterior wall thickness in diastole (cm)
0.73
±
0.16 (0.50–1.30)
Myocardial mass, indexed for body surface area
(gm/m
2
)
73.0
±
25.8 (43–188)
LV ejection fraction (%)
66.2
±
6.0 (50–79)
LV fibre-shortening fraction (%)
36.0
±
4.7 (25–45)
Mitral valve inflow velocity (cm/s)
E
83.3
±
16.4 (36–123)
A
47.7
±
10.8 (27–86)
E/A
1.81
±
0.45 (1.02–2.93)
TDI lateral mitral annulus tissue velocities (cm/s)
E
′
lateral MVA
17.3
±
3.1 (7.9–25.0)
A
′
lateral MVA
7.1
±
1.9 (2.0–12.5)
S
′
lateral MVA
6.8
±
1.5 (3.2–11.7)
IVRT (ms)
63.6
±
12.8 (30–70)
IVCT (ms)
80.6
±
18.6 (40–130)
E/E
′
lateral MVA
5.9
±
1.1 (2.2–8.9)
MPI lateral MVA
0.60
±
0.14 (0.30–0.95)
TDI septal mitral annulus tissue velocities (cm/s)
E
′
septal MVA
13.3
±
4.5 (8.5–63)
A
′
septal MVA
6.7
±
1.8 (2.3–11.3)
S
′
septal MVA
6.1
±
0.9 (4.0–8.9)
IVRT (ms)
68.1
±
13.3 (40.0–70.0)
IVCT (ms)
74.4
±
16.6 (40.0–58.0)
E/E
′
septal MVA
6.40
±
1.30 (0.95–9.87)
MPI-septal MVA
0.58
±
0.12 (0.31–0.95)
Tricuspid valve inflow peak velocities (cm/s)
Et
47.5
±
12.7 (24.0–85.0)
At
27.5
±
9.1 (13.9–56.0)
Et/At
1.8
±
0.6 (1.42–3.15)
TDI lateral tricuspid annulus tissue velocities (cm/s)
E
′
t
15.7
±
3.3 (8.9–29)
A
′
t
9.5
±
2.5 (2.0–20.0)
S
′
t
12.3
±
2.5 (7.4–20.0)
IVRT
54.1
±
35.2 (43–98)
IVCT
66.6
±
21.4 (40–130)
Et/E
′
t
3.1
±
1.0 (1.42–6.15)
RV MPI
0.53
±
0.20 (.09–0.96)
LV, left ventricular, RV, right ventricular; TDI, tissue Doppler imaging; MVA,
mitral valve annulus IVRT, isovolumic relaxation time; IVCT, isovolumic
contraction time; MPI, myocardial performance index.