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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014
AFRICA
221
to the observation in our study. Patients with renal impairment
often develop cardio-renal syndrome, which is caused by low
cardiac output. These patients often developmultiple alterations at
the vascular level, leading to endothelial dysfunction, coagulation
abnormalities, insulin resistance, hyperhomocystinaemia and
activation of the sympathetic nervous system, as well as the renin–
angiotensin and aldosterone system. They are prone to unstable
HF and susceptible to high catecholamine levels. Furthermore
HF patients with renal dysfunction are also less likely to receive
proven medications for HF.
Hyponatraemia and hypokalaemia were associated with a
better prognosis in our study. This is contrary to most reports
from the Western world, although in a Polish study, Biegus
et
al
.
8
reported that hypokalaemia was associated with a better
outcome. This may be related to better response to diuretics
in the survivors, leading to the electrolyte derangement. It may
also be speculated that sodium may play a lesser role in the
pathophysiology of HF in our setting.
We also observed that left atrial size, left atrial area, left
ventricular size, higher E/A ratio and presence of mitral and
tricuspid regurgitation were associated with poorer outcomes.
This has been well recognised by earlier studies.
7,9
Left atrial or
ventricular size reflects left atrial or ventricular pressure and
volume overload, and the severity and duration of increases
in LV filling in response to cardiac functionl abnormality
associated with HF.
36
A plausible reason for the younger age at presentation for
HF in our study and many parts of Africa may be related to the
aetiology of the condition, which is conditions that present in
young and middle age (for example rheumatic heart disease and
cardiomyopathies). In addition, hypertension and related target-
organ damage present at a younger age in Africans and people
of African descent.
The dominance of
de novo
presentation of HF in our cohort
may be related to poorer long-term outcome of HF in our
setting, that is, few people are living with chronic HF. Another
reason may be because of poor or inadequate health education.
Most often patients do not keep to one health facility when they
have chronic illnesses such as HF. They often move from one
facility to another (including alternative healthcare facilities)
seeking a cure.
The relatively low mortality rate in our cohort may be related
to the fact that the study was conducted in a cardiology unit
and may not reflect what happens in a general medical ward or
in private practice in the country. The clinical characteristics of
our patients may also be explanatory. Our subjects were younger
compared to the typical patients with HF in the Western world,
who are generally elderly.
The average length of hospital stay was longer in our setting
(nine days) compared to 6.1 days in the USA
28
and nine days in
Europe.
7
However it was shorter than the 21 days reported from
Japan.
37
It is possible that longer stay in hospital affords patients
the opportunity to recover well and get used to medications
for HF. HF outcome is generally better in Japanese patients
compared to other high-income countries.
7,8,10
Furthermore it is also possible that the aetiology of HF
in our cohort could have affected the outcome. Hypertension
is predominantly the major risk factor for HF in our cohort.
Ischaemic heart disease is relatively uncommon. It is well known
that mortality rates from coronary artery disease (CAD) are
generally worse than in those with non-ischaemic heart disease.
Mitchell
et al
.
38
reported a total mortality rate of 30% at three
years in the placebo group of ischaemic HF patients compared
to a rate of 15% in the non-ischaemic HF group.
The poorer outcome of women in our study may be because
the women were less educated and more likely to be unemployed
and dependent than the men, and may not be able to pay for HF
medications. Clinic follow up may also be poorer in the women.
The finding of low frequency of use of some disease-
modifying drugs in our cohort is an opportunity for future
Table 4. Clinical and demographic predictors of outcome on
univariate analysis (six-month survival).
Variable
All (
n
=
285)
Alive (258) Dead (23) OR 95% CI
p
-value
Age (years)
57.3
±
15.4 57.4
±
14.0 57.2
±
19.1 0.99 0.96–1.01 0.324
Female gender
(%)
52.6
54.5
50
1.14 0.48–2.70 0.764
No education
(%)
33.3
32.8
30.0 0.77 0.26–2.28 0.635
Not married
(single) (%)
67.8
69.6
52.9 1.51 0.56–4.07 0.417
Body mass
index
24.0
±
5.4 23.7
±
4.9 23.4
±
3.6 0.97 0.87–1.08 0.580
Non-smoker (%)
81.8
82.3
85.0 1.51 0.43–5.34 0.521
Alcohol use (%)
6.0
5.6
5.0
0.79 0.32–1.95 0.609
Presence of
diabetes (%)
13.0
13.1
10.0 0.65 0.14–2.92 0.574
Respiratory
rate (bpm)
28.3
±
6.2 28.0
±
6.6 29.2
±
5.3 1.02 0.96–1.08 0.639
Heart rate
(bpm)
95.5
±
17.1 95.0
±
17.4 100.5
±
15.9 1.00 0.97–1.03 0.846
SBP (mmHg) 136.1
±
29.4 137.3
±
27.7 122.5
±
20.0 0.98 0.96–6.99 0.017
DBP (mmHg) 87.1
±
29.4 88.6
±
18.7 80.0
±
13.4 0.98 0.95–1.00 0.085
Pulse pressure
> 30 mmHg (%)
3.3
2.1
5.0
0.42 0.16–1.10 0.078
NYHA (III,
IV) (%)
91.5
90.4
95.0 4.03 1.53–10.65 0.005
Serum sodium
(mmol/l)
136.9
±
4.6 136.0
±
6.4 137.2
±
7.4 1.03 0.96–1.11 0.428
Serum potas-
sium (mmol/l)
3.7
±
0.5 3.6
±
0.7 4.0
±
1.0 1.64 0.72–3.75 0.243
Blood glucose
(mg/dl)
112.3
±
56.0 117.0
±
58.5 111.8
±
58.5 1.00 0.99–1.01 0.501
Packed cell
volume (%)
41.0
±
7.6 37.6
±
7.0 32.2
±
8.4 0.92 0.86–0.97 0.004
Total white
blood cell count
6.8
±
3.1 6.9
±
3.4 9.2
±
5.1 1.13 1.02–1.25 0.024
Serum creati-
nine (mg/dl)
0.8
±
0.3 1.2
±
1.0 2.1
±
2.5 1.38 1.04–1.83 0.024
QRS duration
(ms)
107.1
±
9.4 110.3
±
29.5 110.9
±
32.2 1.01 0.99–1.03 0.171
Corrected QT
(ms)
439.4
±
40.9 449.3
±
34.4 457.3
±
34.6 1.01 0.99–1.04 0.173
Atrial fibrilla-
tion (%)
13.3
14.6
20.0 1.14 0.36–3.55 0.827
E/A ratio
2.2
±
1.0 2.1
±
1.3 2.7
±
1.6 1.40 0.99–1.97 0.060
Left atrial area
(cm
2
)
26.2
±
6.7 26.8
±
7.5 34.2
±
12.1 1.11 1.01–1.21 0.025
Left atrial
diameter (cm)
4.8
±
0.9 4.6
±
0.9 5.0
±
1.1 1.56 0.94–2.60 0.084
LVID (cm)
5.47
±
1.55 5.6
±
1.5 5.7
±
1.2 1.11 0.74–1.67 0.614
HF with systol-
ic dysfunction
66.4
67.5
70.6 0.66 0.27–1.59 0.356
MR (yes) (%)
19.6
20.2% 25.0 1.34 0.50–3.60 0.562
TR (yes) (%)
15.1
13.1% 35.0 2.64 1.00–6.95 0.050
SBP = systolic blood pressure, DBP = diastolic blood pressure, LVID
=
left ventric-
ular internal diameter, MR
=
mitral regurgitation, TR
=
tricuspid regurgitation.