CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 2, March 2013
38
AFRICA
countries except in South Africa and Namibia, where smoking
prevalence among women was 5.5 and 5.9%, respectively.
34
Various estimates of smoking prevalence in African men
between 1976 and 2005 revealed rates below 10% in many
African countries. But in Tanzania, Mozambique, South Africa,
Mauritius and Seychelles, smoking prevalence rates ranged
between 15 and 30%. Smoking prevalence rates in adults
increased substantially across SSA by 2009, especially in
Mauritius where a third of adults smoked, closely followed by
South Africa, Tanzania, Burkina Faso and Senegal with smoking
rates of 27.5, 27.1, 22.0 and 19.8%, respectively. Even in Nigeria
and Ghana, where smoking rates were relatively low before
2003, estimated at 6.1% in Nigerian men, 0.1% in Nigerian
women, 4.6% in Ghanaian men and 0.2% among Ghanaian
women, overall smoking prevalence more than doubled in men
to 13 and 10.2% in Nigeria and Ghana, respectively in 2009 but
remained quite low in women.
Although deaths from tobacco-related causes probably
accounted for only 5 to 7% in African men and 1 to 2% in
African women in the year 2000,
34
by 2030, tobacco is expected
to be the greatest contributor of deaths in SSA. Most victims will
die 20 to 25 years prematurely of various cancers, respiratory
diseases, IHD and other circulatory disorders.
Regrettably, most governments in African countries have
avoided action to control smoking for fear of harmful economic
consequences on their fragile economies. Without effective
tobacco-control measures, SSA risks becoming the biggest
global ashtray as many transnational tobacco companies shift
their targets to middle- and low-income countries.
Dyslipidaemia
There is overwhelming epidemiological evidence implicating
cholesterol as a cause of atherosclerosis. Most black Africans
reportedly have low levels of total cholesterol associated with
high high-density lipoprotein (HDL) cholesterol levels.
35
Higher
cholesterol levels however, have been found in diabetic patients
from Zimbabwe and Tanzania. The total serum cholesterol was
also significantly higher in women than men. Reports from
West Africa indicate a worrying trend of dyslipidaemia among
patients with either type 1 or type 2 diabetes mellitus.
36
Data
from the Transition of Health during Urbanisation of South
Africa (THUSA) study indicate that black South Africans may
be protected from IHD because of favourable lipid profiles
characterised by low total cholesterol and high HDL cholesterol
levels.
37
In Nigeria, IHD contributes very little to mortality rates in
middle-aged men and women, partly because of particularly low
mean cholesterol levels.
38
Different black African communities
may be at different stages of their epidemiological transition,
as shown in an epidemiological study of coronary heart disease
risk factors in the Orange Free State in South Africa.
39
Table 4
illustrates this point quite vividly. Selected countries representing
the different regions of SSA show wide differences in mean total
cholesterol levels with a tendency to higher cholesterol levels in
females in some countries.
The cardiovascular impact of HIV/AIDS
SSA bears a disproportionate share of the global HIV burden. The
interaction between HIV infection, acquired immunodeficiency
syndrome (AIDS), its treatment with highly active antiretroviral
drugs (HAART), and cardiovascular disorders is complex and
incompletely understood.
The transformation of HIV/AIDS into a chronic disorder
with the advent of antiretroviral drugs is associated with
the emergence of certain characteristic cardiovascular risk
factors, and raises apprehension about the potential increase in
prevalence of cardiovascular diseases, including IHD, in SSA.
In Botswana, for instance, where antiretroviral therapy coverage
exceeds 90%, AIDS-related deaths declined by approximately
50% between 2002 and 2009.
40
The repertoire of immunological responses associated with
acute and chronic HIV infection is quite complex and will be only
highlighted here. Perturbations of cytokine expression, cellular
dysfunctions, redistribution of lymphocyte sub-populations,
increased cellular turnover and apoptosis are some of the
features of general activation of the host’s immune system that
characterise chronic HIV infection.
41
Chronic HIV infection, and
not its pharmacological treatment, induces changes in markers of
endothelial function.
42
Untreated HIV infection is also associated
with impaired elasticity of both large and small arteries.
43
Some authors have suggested that HIV infection accelerates
atherosclerosis via a pro-inflammatory effect on the endothelial
cells through the effects of various cytokines, especially
interleukin-6 and D-dimers.
44,45
Other mechanisms of arteriopathy
include the direct toxic effects of HIV-associated g1p20 and tat
proteins on vascular or cardiac cells. There is also evidence of
a hypercoagulable state, which inversely correlates with CD
4
count.
46
Although traditional risk factors for cardiovascular diseases
might overshadow the role of non-traditional risk factors, there
is increasing evidence that young, asymptomatic, HIV-infected
men with long-standing HIV disease demonstrate an increased
prevalence and degree of coronary atherosclerosis compared
with non-HIV-infected patients.
47
Furthermore, HIV-infected
patients tend to develop perturbations in lipid metabolism,
characterised by decreased HDL cholesterol and low-density
lipoprotein (LDL) cholesterol levels, followed by an increase in
TABLE 4. ESTIMATED MEAN TOTAL CHOLESTEROL IN
SELECTEDAFRICAN COUNTRIES BY REGION IN FEMALESAND
MALESAGED 15YEARSAND OLDER, 2011
Region/country
Females mean total
cholesterol (mmol/l)
Males mean total
cholesterol (mmol/l)
Eastern Africa
Uganda
UR Tanzania
4.4
5.2
4.7
4.4
Central Africa
DR Congo
Rwanda
4.3
4.3
4.3
4.3
Western Africa
Nigeria
Ghana
3.7
5.9
3.6
4.4
Southern Africa
Botswana
South Africa
4.7
4.4
4.7
4.4
Islands
Mauritius
Seychelles
5.2
5.9
5.2
5.8
DR Congo = Democratic Republic of Congo, UR Tanzania = United Republic
of Tanzania.
Source:
https://apps.who.int/infobase/Comparisons.aspxAccessed on 31
December 2011.