Journal of Human Hypertension (2000) 14, 739–747
 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00
www.nature.com/jhh
REVIEW ARTICLE
Hypertension in developing nations in
sub-Saharan Africa
YK Seedat
Faculty of Medicine, University of Natal, Durban, South Africa
There is a rapid development of the ‘second wave epidemic’ of cardiovascular disease that is now flowing
through developing countries and the former socialist
republics. It is now evident from WHO data that coronary heart disease and cerebrovascular disease are
increasing so rapidly that they will rank No. 1 and No. 5
respectively as causes of global burden by the year
2020. In spite of the current low prevalence of hypertensive subjects in some countries, the total number of
hypertensive subjects in the developing world is high,
and a cost-analysis of possible antihypertensive drug
treatment indicates that developing countries cannot
afford the same treatment as developed countries. Control of hypertension in the USA is only 20% (blood
pressure ⬍140/90 mm Hg). In Africa only 5–10% have a
blood pressure control of hypertension of ⬍140/90
mm Hg. There are varying responses to antihypertensive therapy in black hypertensive patients. Black
patients respond well to thiazide diuretics, calcium
channel blockers vasodilators like ␣-blockers, hydralazine, reserpine and poorly to ␤-blockers, angiotensinconverting enzyme inhibitors and AII receptor antagonists unless they are combined with a diuretic. A comprehensive cardiovascular disease (CVD) programme in
Africa is necessary. There are social, economic, cultural
factors which impair control of hypertension in
developing countries. Hypertension control is ideally
suited to the initial component on an integrated CVD
control programme which has to be implemented. Primary prevention, through a population-based lifestyle
linked programme, as well as cost-effective methods of
detection and management are synergistically linked.
The existing health care infrastructure needs to be
orientated to meet the emerging challenge of CVD, while
empowering the community through health education.
Journal of Human Hypertension (2000) 14, 739–747
Keywords: Sub-Saharan Africa; cardiovascular disease; developing countries
Introduction
A World Health Organisation analysis showed that
the prevalence of hypertension in developing countries varied from 1% in some African countries to
more than 30% in Brazil.1 Hypertension is common
in the black population of Africa.2 Throughout subSaharan Africa there is a difference in the prevalence of hypertension between the urban and rural
black populations. Blood pressure (BP) assumes
much more importance with increasing age. Mortality statistics from six developing countries for 35
to 74-year-olds showed a downward trend in mortality from hypertension and cardiovascular diseases (CVD) in most countries. In spite of the current
low prevalence of hypertension in some countries,
the total number of hypertensive subjects in the
developing world is high, and a cost-analysis of
possible antihypertensive drug treatment indicates
that developing countries cannot afford the same
treatment as developed countries.1
Our age-corrected prevalence studies showed that
in the adult population of Durban, hypertension
(WHO criteria) was highest in urban Zulus (25%),
intermediate in whites (17.2%) and lowest in ethniCorrespondence: Professor YK Seedat, Faculty of Medicine, University of Natal, Private Bag 7, Congella 4013, Durban, South
Africa. E-mail: seedaty1얀gwise.med.und.ac.za
Received 11 October 1999; revised and accepted 25 April 2000
cally Indian people (14.2%).3 In contrast, the prevalence of hypertension in rural studies is lower: 4.1%
in Ghana,4 5.9% in Nigeria,5 7% in Lesotho6 and
7.37% in the rural Zulu.3 BP in the Bushmen in the
Kalahari Desert was shown not to rise with age.7
This will change with the process of acculturation.
In a large USA study the prevalence of hypertension
was evaluated between 1988 and 1991. The National
Health and Nutritional Survey (NHANES) showed
that urban black men have a higher prevalence of
hypertension compared to urban black females,
white males and white females.8 Thus even in the
USA black people have a far higher prevalence of
hypertension compared to the Caucasian population. The prevalence of hypertension in black
people in the West Indies and in the USA is higher
than those in any part of sub-Saharan Africa. This
may be because African Americans have been accultured for 300 years, whereas urban Zulus have been
accultured only since the turn of the 20th century. It
is possible that the BP differences in the time since
acculturation may explain the BP differences
between African Americans, West Indians, Nigerians and urban Zulus.3 Accurate national estimates
of the prevalence of hypertension in developing
countries are lacking. Inadequate funds, inexperience and lack of infrastructure are also important
barriers to hypertension research. The Egyptian
National Hypertension Project serves as a model for
similar studies elsewhere. It addresses a number of
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
740
Table 1 Regional differences in burden of CVD (1990)
Region
Developed regions
Developing regions
Established market economies
Former socialist economies
India
China
Other Asian countries and islands
Sub-Saharan Africa
Middle Eastern Crescent
Latin America
Population
(millions)
CVD mortality
(thousands)
Coronary
mortality
(thousands)
Cerebrovascular
mortality
(thousands)
DALYs lost
(thousands)
1144.0
4123.4
797.8
346.2
849.5
1133.7
682.5
510.3
503.1
444.3
5328.0
9016.7
3174.7
2153.3
2385.9
2566.2
1351.6
933.9
992.3
786.7
2678.0
2469.0
1561.6
1116.3
783.2
441.8
589.2
109.1
276.6
269.1
1447.9
3181.2
782.0
665.9
619.2
1271.1
350.4
389.1
327.4
224.1
39 116
108 802
22 058
17 060
28 592
28 369
17 267
12 252
12 782
9 538
DALY indicates disability-adjusted life year. Adapted from Murray and Lopez.12
important questions: (1) why conduct a national
hypertension survey in a developing country?; (2)
what kind of data are needed?; (3) where to start and
how to raise funds?; (4) who will carry out the survey?; (5) how to design your sample and why to survey?; (6) how to organise and perform field operations?; (7) how to collect accurate data and do
quality control measures?; and (8) how to handle
the data?9
Developing countries contribute a greater share to
the global burden of cardiovascular disease than the
developed countries.10,11 Yet it has received less
comment and little public health response, even
within these countries. In 1990 it has been estimated
that 5.3 million deaths were attributable to CVD
whereas the corresponding figure for developing
countries ranged between 8 to 9 million (ie, relative
access of 70%). Regional estimates of CVD mortality
indicate that the difference would be even higher if
the term ‘developed countries’ is restricted to established market economies only and excludes the former socialist economies (Table 1).10
In 1990 the developing countries contributed 68%
of the total global deaths due to non-communicable
disease and 63% of the world mortality due to
CVD.12 Table 2 shows the regional contribution to
mortality. A greater cause for concern is the early
age of CVD in developing countries compared with
the developed countries. For example, in 1990, the
Table 2 Regional contribution to mortality (1990)
Region
Established market economies
Former socialist economies
India
China
Other Asian countries and islands
Sub-Saharan Africa
Middle Eastern Crescent
Latin America
World
All causes
(%)
CVD
(%)
14
8
19
18
11
10
9
6
100
22
15
17
18
9
7
7
5
100
Values are given as percent of world total. Adapted from Murray
and Lopez.12
Journal of Human Hypertension
proportion of CVD deaths occurring below the age
of 70 years was 26.5% in the developed countries
compared with 46.7% in developing countries.12
Another cause for alarm is the projected rise in both
proportional and absolute CVD mortality rates in the
developing countries over the next 25 years.13,14
This is related to the greater life expectancy due to
decline in deaths occurring in infancy, childhood,
and adolescence and was related to more effective
public health responses to perinatal, infectious and
nutritional deficiency, social factors like improved
female literacy and improved indicators such as per
capita income.15 Adverse lifestyle changes
accompanying industrialisation and urbanisation
will contribute to the increasing rates of CVD mortality. Salt consumption in Africa has increased.16
The globalisation of food production and marketing
is also contributing to energy-dense foods, poor in
dietary fibre and several micronutrients.17 The ‘foetal origins hypothesis’ which may lead to glucose
intolerance, hypertension and dyslipidaemia in later
life and CVD as a consequence, if proved, may be
an important risk for CVD because of the vast numbers of poorly nourished infants in developing countries.18–21 Tobacco consumption patterns are rising
in developing countries in contrast to the overall
decline in developed countries. Recent projections
from the World Health Organisation suggest that by
the year 2020, tobacco will become the largest single
cause of death, accounting for 13.3% of global
deaths.22
This paper deals essentially with the black
peoples in sub-Saharan Africa. The northern part of
Africa has largely non-black populations and this
population is not discussed in this paper. There are
substantial Asian and white minorities in East and
South Africa. The population of South Africa is
about 40 million and is growing at the rate of 2.5%
per year. The population is 76.2% black, 13.3%
white, 8.6% ‘mixed’ and 2.6% Asian.23 Coronary
heart disease (CHD) is by far the most important
cause of death among white and Asians of South
Africa in the category of diseases of the circulatory
system—and actually the most important of all
causes of death. Their total rates of 165.3 and 101.2
per 100 000 respectively, surpass by far that of the
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
‘mixed’ group (55.1/100 000) and the black group
(5.3 per 100 000). Cerebrovascular disease is first
among the ‘mixed’ group and blacks and second
among whites and Asians in the broad category of
causes of death. The disease has the highest death
rate among the ‘mixed’ group (80.6) followed by the
whites, Asians and then blacks with decreasing rates
of 73.6, 62.5 and 36.5 per 100 000.24
Determinant factors of hypertension in
black subjects
The biochemical differences in black and white subjects is shown in Table 3. Genetic factors, personal
characteristics, autonomic nervous system function,
cardiac function, and various environmental factors
have been examined in hypertensive black subjects
and contrasted with hypertensive whites. Black
hypertensive subjects have higher plasma sodium
and lower plasma potassium concentrations than
normotensives.25
The hormonal differences between black and
white hypertensive subjects is shown in Table 4.
There are also overt differences in potassium transport, which suggest that black people have a more
limited capacity to exchange intracellular potassium
and that a higher percentage of this exchange is
dependent upon oubain-sensitive mechanisms.26 In
the South African black population, red cell magnesium and serum levels of potassium, magnesium
and calcium were found to be significantly lower in
black hypertensive subjects.27 Lymphocyte intracellular sodium concentrations were significantly
higher in hypertensive, compared with normotens-
Table 3 Hypertension in blacks and whites biochemical differences
Feature
In blacks
Total cholesterol
Triglycerides
High-density lipoproteins
Low-density lipoproteins
Very low density lipoproteins
Response to Na+ load
Urine Na+/K+ ratio
Plasma Na+/K+ ratio
Transport
Quinidine Na+ pump activity
Lower
Lower
Higher
Lower
Lower
Delayed
Higher
Higher
High intracellular Na+
Reduced
Table 4 Hypertension in blacks and whites hormonal differences
Feature
Plasma renin activity
Plasma noradrenaline
Dopamine ␤-hydroxylase
Aldosterone
Kallikrein
Circulating inhibition of Na/K ATPase
In blacks
Lower
Equal
Lower
Higher
Lower
Higher
ive Zulus.28 Black subjects excrete sodium loads
more slowly and have a markedly lower rate of urinary kallikrein excretion.29 Renin is lower in black
people and does not increase in response to sodium
and volume depletion.30
Suppression of the renin-angiotensin system has
been demonstrated.31–33 We have found a higher
plasma renin activity (PRA) in rural compared to
urban Zulus. This suggests that the cause of a low
PRA in black subjects may not be genetic. However,
there was no correlation between PRA and urinary
sodium, suggesting that dietary sodium was not a
factor. There was no correlation between renin and
aldosterone in hypertensive urban Zulus, suggesting
a defect in the renin-aldosterone in the patients.34
The lack of stimulation of PRA by natriuresis with
furosemide confirmed a hypo-responsive renin-angiotensin system in hypertensive urban Zulus.27 A
hereditary cause for this has been postulated.35 A
difference in salivary Na-K ratios between white and
black patients with low-renin essential hypertension
has been noted,36 but daily sodium intake in South
African blacks (based on the urinary sodium) was
similar to that seen in typical Western diets.34,37 A
potassium deficient diet as shown by us may play a
role in the aetiology of hypertension in South
African blacks.34 Serum angiotensin-converting
enzyme (ACE) levels have been studied in black and
white normotensive subjects. Renin activity was significantly and inversely associated with systolic and
diastolic BP in both black and white subjects. ACE
levels, however, were inversely associated with BP
in the black subjects but positively associated with
BP in the white subjects (P = 0.02) for interaction on
diastolic BP, even after adjustment for age, gender,
body mass index, alcohol consumption and heart
rate. These results suggest that levels of ACE are
similar in blacks and whites but their association
with BP may possibly reflect underlying ethnic differences in regulation of BP.38 Socio-economic position has been found to be a major contributor to
differences in death rates between black and white
men. Differentials in mortality from some specific
causes do not simply reflect differentials in income,
however, and more detailed investigations are
needed of how differences are influenced by
environmental exposures, lifetime socio-economic
conditions, lifestyle, racism and other socio-cultural
and biological factors.39
The first study to demonstrate familial aggregation
of hypertension in black people was that of Miall
et al40 in Jamaica. Obesity is an important cause of
hypertension, especially in the urban black women
of sub-Saharan Africa. It is more common in urban
than in rural Zulu women.41 In Los Angeles (LA)
Campese et al42 found that the bulk of whites exhibit
salt-resistant state and the majority of the blacks
have a salt-sensitive state.42 The Multiple Risk Factor Intervention Trial (MRFIT) study demonstrated
that black people had a higher serum creatinine
level for the same level of BP than white subjects.43
From the therapeutic perspective it is important to
consider drugs that reduce renal vascular resistance
and glomerular pressure such as calcium channel
blockers.
741
Journal of Human Hypertension
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
742
Black patients whose haemodynamic and fluid
status are similar to those of their white counterparts
tend to have lower heart rates and greater responsiveness to intravascular volume.44 Changes in peripheral resistance associated with hypertensive
heart disease may start in young black men before
elevated BP occurs.45 Adult black subjects with mild
hypertension have as much as a two-fold greater
prevalence of left ventricular hypertrophy on echocardiography when compared with matched white
subjects.46 A study of black and Indian medical students in Durban, South Africa, showed that black
students had higher systolic and diastolic BP
throughout the day, night and critical time periods
compared with the Indian students. BP load was
higher in black (40.8%) than in Indian participants
(29.6%) (P ⬍ 0.05) and there was less dipping at
night. Left ventricular mass was significantly higher
in black than in Indian participants. Risk factors
leading to coronary heart disease (CHD) were more
common in Indian than in white participants.47
Thus, qualitative differences exist between black,
white and Indian people in respect of the cardiac
adaptive process to systemic hypertension. Hypertension is commonly associated with cerebral and
aortic atheroma, but CHD is rare in sub-Saharan
Africa. Congestive heart failure is common.48,49 In
contrast in the USA, CHD is common in the African
Americans.50 Serum cholesterol concentration is
lower and serum high-density lipoprotein is higher
in black compared with the Indian and white people
of Durban.51 Malignant hypertension is common in
the black population of sub-Saharan Africa and is
an important cause of end-stage renal failure.3
Treatment of hypertension in black
subjects
Thiazide diuretics are effective antihypertensive
agents in black hypertensive patients and studies
suggest that they cause a greater decrease in BP in
blacks than in whites.52,53 The better hypotensive
response in black hypertensive patients is probably
due to the fact that, in comparison with whites,
more black patients have an expanded intracellular
volume and low PRA. In developing countries, in
which the majority of black people live, the cost of
therapy is important. Because of their low cost, thiazide diuretics are important baseline drugs in the
treatment of hypertension. The low incidence of
ischaemic heart disease in the black population of
Africa2,48 may mitigate the seriousness of the consequence of the metabolic effects of thiazide diuretics,
eg, hyperlipidaemia, and hypokalaemia. The
response to antihypertensive agents in black and
white communities is shown in Table 5.
Table 5 Antihypertensive agents in white and black communities
Agent
Thiazide
Rauwolfia
␤-blockers
␤-blockers + thiazides
␣-and ␤-blockers
Methyldopa
Vasodilators
ACE inhibitors
ACE inhibitors + thiazides
Calcium channel blockers
Angiotensin II antagonists
White
Black
+
+
+
+
+
+
+
+
+
+
+
++
+
±
+
+
+
+
±
+
+
±
hydrochlorothiazide in black patients.54 In
developing countries where the cost of therapy is
important, it may be preferable to use a combination
of reserpine and hydrochlorothiazide as baseline
drugs in hypertension.
Beta-blockers
There are numerous studies that have shown that ␤blockers are no more effective than placebo in black
people. Comparative studies between white and
black subjects have shown that white and Indian
hypertensive patients respond better to ␤-blockers
than black hypertensive patients. Beta-blockers
when combined with a thiazide diuretic produce an
appreciable hypotensive response in black hypertensive patients.55 Renin classification does not
appear to be instrumental in the initial selection of
diuretics or ␤-blockers in the therapy of black hypertensives, but diuresis is more effective.56 Warren and
O’Connor57 proposed that racial (black/white) differences in clinical severity, haemodynamic profile
and response to therapy of essential hypertension
may be mediated largely by the vasodilatory and
natriuretic renal kallikrein-kinin system. They felt
that deficiency in the kallikrein-kinin renal vasodilatory system may explain many of the unique features of essential hypertension in at least some black
people, especially older subjects with low PRA.
Antihypertensive agents like propranolol, which
decrease urinary kallikrein excretion may not be
effective in all black subjects. Conversely, if a drug
like a thiazide diuretic increases urinary kallikrein
in black people, it may have specific advantages in
this group of patients.57
Labetalol and carvedilol
Reserpine or rauwolfia extracts
Reserpine or rauwolfia extracts offer the advantage
of low cost, once-daily administration. Side effects
like nasal congestion or depression are minimal provided the dosage of reserpine does not exceed
0.1 mg once daily. Reserpine combined with hydrochlorothiazide is as effective as sotalol with
Journal of Human Hypertension
These antihypertensive agents block ␣1, ␤1 and ␣2
adrenergic receptors. They may be more effective
than non-selective ␤-blockers in black patients.58
We have shown that carvedilol, a new non-cardioselective, vasodilating ␤-adrenoceptor blocker,
without intrinsic sympathetic activity is an effective
agent for treating hypertension in black patients.59
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
Calcium antagonists
Diabetic black hypertensive patients
Data have shown that black patients, who are prone
to a low PRA, respond to calcium channel blockers
(CCB). Fadoyami et al,60 Moser et al,61 Leary and
Asmal,62 and M’buyamba-Kabangu et al,63 have
shown a good response to CCB in black hypertensive
patients. Cruickshank et al64 found, in their study
on the treatment of hypertension in black compared
with white non-insulin-dependent diabetics, that ␤blockers are not effective in treating hypertension in
black diabetics. Verapamil was effective although
less so than in white patients. The authors conclude
that, as yet, no ideal monotherapy exists for hypertension in black diabetic patients.64
Materson et al65 found in a randomised doubleblind study of 1292 men with diastolic BP of 95–
109 mm Hg that diltiazem ranked first for younger
whites and atenolol for older whites. The patients
were randomised after a placebo washout period to
receive placebo or one of the six drugs: hydrochlorothiazide (12.5–50 mg per day), atenolol (25–100 mg
per day), captopril (25–100 mg per day), clonidine
(0.2–0.6 mg per day), a sustained-release preparation of diltiazem (120–360 mg per day) or prazosin (4 –20 mg per day). CCB may also have a natriuretic effect and thus lower the BP. A further additive
hypotensive effect is achieved when CCBs are combined with a diuretic in black patients.
ACE inhibitors combined with a small dosage of a
thiazide diuretic, for example hydrochlorothiazide
12.5 mg daily, is the treatment of choice. Suitable
alternative antihypertensive agents are CCB or ␣adrenergic blocking agents like prazosin or doxazosin.
ACE inhibitors
Studies with ACE inhibitors have shown that in
black patients the response is poor. However the
response is the same as whites when ACE inhibitors
are combined with a low-dose diuretic. ACE inhibitors are effective in black hypertensive patients but
in higher doses compared to white and Indian
people.66
Angiotensin II receptor blockers
There is only limited data on the response to angiotensin II (AT1) receptor antagonists in hypertensive
blacks. Analysis of the responses in the sub-group
of black patients (n = 10–17/study) confirmed that
losartan did lower BP in black patients. The magnitude of the fall in black patients appears to be less
than in the non-black patients.67–69 Data on the
newer AT1 receptor antagonists like candesartan,
irbesartan, or valsartan and their efficacy in black
hypertensive patients are few in a number of
patients.
Elderly black hypertensive patients
The data of Materson et al65 on elderly patients
showed that the best antihypertensive response
occurred with diltiazem, followed by hydrochlorothiazide, clonidine and prazosin. Atenolol was only
slightly better than placebo and captopril was worse
than placebo.
743
Black hypertensive patients with renal disease
The incidence of end-stage renal disease (ESRD) is
increasing at the rate of 8–10% per year and poses a
major national health problem in the USA.70 In 1998
nearly 300 000 persons in the USA either underwent
dialysis or received a renal transplant for ESRD.71
Hypertension was found to be the underlying cause
in 29% of these patients, second only to diabetes. In
black subjects, hypertension was found to be the
most common cause of ESRD. This is in contrast to
the trend from two major complications of hypertension, myocardial infarction and stroke, both of
which decreased in incidence by about 25% in the
same decade.72,73
The ultimate goal is to prevent renal failure or
slow its progression. ACE inhibitors may be more
effective than beta-blockers in slowing renal progression.74 The dihydropyridine CCB’s like nifedipine are not as effective as the non-dihydropyridine
like verapamil or diltiazem in decreasing proteinuria.75
Black hypertensive patients respond well to thiazide diuretics, CCB, vasodilators like prazosin, doxazosin, or labetalol (combination of a non-selective
␤-adrenergic blocker and an ␣-␤-blocker). It is suggested that in black hypertensive patients a thiazide
diuretic should be added if a ␤-blocker or an ACE
inhibitor is used. This is summarised in Table 4.
Health care and economic consequences
However, in spite of the effective drug therapy available for hypertensive patients in general, economic
and social considerations continue to influence the
lower rate of detection, treatment and control of
hypertension in the black population of the USA
with regard to the cost–benefit ratio. We should be
cognisant that thiazide diuretics become the baseline therapy of hypertension.75,76 We should be
aware of the special needs of black patients when
initiating therapy. As yet there is no ideal monotherapy in black hypertensive patients. An ideal antihypertensive drug should have not only natriuretic
effects, but also the capability to reduce vascular
resistance.77 Whereas the stepped-care treatment of
hypertension is widely used, it has become appropriate to consider an individualised patient profile
in the treatment of hypertension.78 Race should constitute an added criterion when an antihypertensive
agent is chosen.54,79–81 For regions in which health
care resources are particularly scarce, investment in
population-based primary prevention strategies may
yield the largest benefit. The most cost-effective
hypertension treatment programmes will involve
the use of lowest cost drugs (eg, diuretics, reserpine,
Journal of Human Hypertension
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
744
␤-blockers, generic formulations of ACE inhibitors,
angiotensin II antagonists, calcium antagonists, and
other generic agents) in the highest risk groups. The
selective treatment of patients with pre-existing cardiovascular or renal disease (irrespective of hypertension severity) or with severe hypertension
(systolic BP ⬎180 mm Hg or diastolic BP ⬎110
mm Hg) will result in the greatest ratio of events prevented to the number of patients treated.82 The
medical and socio-economic consequences of the
projected increase in the burden of CVD will be disastrous for the developing countries. The total care
for risk factors leading to CVD will be beyond the
scope of most developing countries. Expensive
investigations and costly drugs may not be available,
accessible only to an elite minority. Most
developing countries will experience the double
burden of pre-transitional diseases (like infections
and nutritional diseases) and post-transitional diseases like CVD. Acquired immunodeficiency syndrome (AIDS) will have a major impact on the economy of countries in Southern Africa.
CVD control programmes
The essential components of any CVD programme
are: (1) establishment of efficient systems for estimation of CVD-related burden of disease and its
secular trends; (2) estimation of the levels of CVD
risk for example smoking, elevated cholesterol or
blood pressure in representative population samples
to identify risk factors that require immediate attention; (3) evaluation of emerging risk factors for
example diabetes, obesity, fibrinolytic status, homocysteine that may be of relevance to the population
studies; (4) identification of health behaviour determinants that influence the levels of both traditional
and emerging risk factors in the context of each
society; (5) development of a health policy that will
integrate population-based measures of CVD risk
modification and cost-effective case management
strategies for individuals who have clinically manifested CVD or are detected to be at a high risk of
developing it.15
Barriers to prevention policy
National policies control of CVD have not yet
emerged in developing countries because of: (1)
Competing priorities. Infectious and nutritional disorders are still a major health challenge and AIDS
takes up a large portion of health resources; (2)
Technology-based interventions. This is favoured by
policy makers and the media. The proximity of
respected clinical cardiologists to policy makers
who belong to the social class most affected by CVD
often results in iniquitous resource allocation; (3)
Inadequate epidemiological data. There is a paucity
of reliable data on the burden of the disease and the
distribution of risk factors; (4) Poor presentation of
message to policy-makers and the media; (5) Discordant messages. False claims are made that risk factors for CVD are not important; (6) Failure to recognise the importance of prevention and costeffectiveness. Many health professionals are unconJournal of Human Hypertension
cerned about preventive action because of the lack
of epidemiological orientation during training,
pressures of providing health care in crowded clinics and the absence of concern of cost-effectiveness;
(7) Anonymity. Health professionals receive no
direct recognition for their endeavours from their
beneficiaries as they do when providing health care;
(8) Economic and social constraints. Dietary advice,
although scientifically sound may be irrelevant or
impractical for reasons of the availability, affordability and acceptability of foodstuffs; (9) Vested
interests. Tobacco and salt companies influence policy makers and the media; (10) Lack of community
mobilisation. No concerted efforts have been made
to educate the community about the risk factors and
dangers of CVD.83
Imperatives of heart health policy
This should consist of: (a) strengthening the epidemiology base; and (b) development of recommendations on cost-effective control. The higher socioeconomic group and the emerging rural elites must
be targeted for a population-based approach and
involves: (a) lipid screening of adult members of
families in whom there is a history of CVD, hypertension, diabetes or persons suspected of having
familial hyperlipidaemia; (b) BP measurements in
all persons over 30 attending health care facilities
and advocacy of self-referral for measurement; (c)
clear, target-specific recommendations; (d) dissemination of messages; (e) prioritisation and sequencing. Multiple-risk-factor interventions may not be
feasible. Priority should be given to the most costeffective strategy for example tobacco control or
non-pharmacological measures for hypertension or
hyperlipidaemia; (f) highlighting of cost-effectiveness of lifestyle changes; (g) building coalition of
health care professionals and activists. A concerted
effort against tobacco, in collaboration with cancer
control programmes and a linkage with environmental groups to highlight the deforestation associated
with tobacco cultivation and cigarette manufacture
is an example of such a group; (h) making education
more prevention-oriented; (i) community mobilisation; (j) multi-media campaigns.83
Prevention of CVD in Africa
When cardiovascular mortality reached its height in
the developed world, the community became more
alarmed of its importance. Counselling for lifestyle
modification to reduce the risk of cardiovascular disease was more readily accepted. This led to a
decrease in cardiovascular mortality in the
developed world. In contrast in the developing
world the communities are struggling with the burden of pre-transitional and post-transitional disease
and the communities are not very aware of the dangers of cardiovascular disease. Moreover the
developing world is in a transition of more industrialisation and urbanisation. This increases consumer
aspirations which seeks an indulgent lifestyle. It
may be difficult to implement moderation in lifestyle.
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
Strategies to prevent the acquisition or enhancement of CVD risk factors in developing countries
(primordial prevention) must be combined to
reverse and reduce risk factors elevations in the
urban communities (primary prevention). The
approach would be non-pharmacological, population based and lifestyle linked. This would obviate
the biological and economic costs of a pharmacologic approach.
There is a need to develop cost-effective methods
for the diagnosis and low-cost life saving measures
for all the risk factors of cardiovascular diseases.
Although tertiary care is growing, the pattern should
be the optimisation of resources and avoidance of
heavy investment in high-cost, low-yield technologies.
17
18
19
20
21
22
References
1 Nissinen A, Bothig S, Granroth H, Lopez AD. Hypertension in developing countries. World Health Stat Q
1988; 41: 141–154.
2 Akinkugbe OO. World epidemiology of hypertension
in blacks. In: Hall WD, Saunders E, Shulman N (eds).
Hypertension in Blacks: Epidemiology, Pathophysiology and Treatment. Year Book Medical Publishers:
Chicago, 1985, pp 13–16.
3 Seedat YK. Race, environment and blood pressure: the
South African experience. J Hypertens 1983; 1: 7–12.
4 Pobee JOM et al. Blood pressure distribution in a rural
Ghanaian population. Trans Roy Soc Trop Med & Hyg
1977; 71: 66–72.
5 Oviasu VO. Arterial blood pressures and hypertension
in a rural Nigerian community. Afr J Med and Med Sci
1978; 7: 137–143.
6 Mokhobo KP. Arterial hypertension in rural societies.
East Afr Med J 1976; 52: 440– 424.
7 Kaminer B, Lutz WPW. Blood pressure in Bushmen of
the Kalahari Desert. Circulation 1960; 22: 289–295.
8 Burt VL et al. Trends in the prevalence, awareness,
treatment and control of hypertension in the adult US
population: data from the health examinations surveys, 1960 to 1991. Hypertension 1995; 26: 60–69.
9 Ibrahim MM. Hypertension surveys in the developing
world. Lessons from the Egyptian National Project
(NHP). J Hum Hypertens 1998; 11: 709–726.
10 Lopez AD. Assessing the burden of mortality from cardiovascular disease. World Health Stat Q 1993; 46:
91–96.
11 Whelton PK, Brancati FL, Appel LJ, Klag MJ. The challenge of hypertension and atherosclerotic cardiovascular disease in economically developing countries. High
Blood Press 1995; 4: 36– 45.
12 Murray CJL, Lopez AD. Global Comparative Assessments in the Health Sector. World Health Organisation: Geneva, Switzerland, 1994.
13 Pearson TA, Jamison DT, Tergo-Gauderies J. Cardiovascular disease. In: Jamison DT, Mosley WH (eds).
Disease Control Priorities in Developing Countries.
Oxford University Press: New York, NY, 1993.
14 Omran AR. The epidemiologic transition: a key of the
epidemiology of population change. Milibank Memorial Fund Q 1971; 49: 509–538.
15 Reddy KS, Yusuf S. Emerging epidemic of cardiovascular disease in developing countries. Circulation
1998; 97: 596–601.
16 INTERSALT Cooperative Research Group. Intersalt: an
international study of electrolyte excretion and blood
23
24
25
26
27
28
29
30
31
32
33
34
35
36
pressure. Results for 24 hour urinary sodium and potassium excretion. Br Med J 1988; 297: 319–328.
Lang T. The public health impact of globalisation of
food trade. In: Shetty PS, McPherson K (eds). Diet,
Nutrition and Chronic Disease: Lessons from contrasting worlds. Wiley: Chichester, UK, 1997; pp
173–187.
Barker DJP. Foetal origins of coronary heart disease.
BMJ 1995; 311: 171–174.
Barker DJP et al. Growth in utero and serum cholesterol concentration in adult life. BMJ 1993; 307:
1524 –1527.
Martyn CN et al. Growth in utero, adult blood pressure
and arterial compliance. Br Heart J 1995; 73: 116–121.
Law CM, Shiell AW. Is blood pressure inversely
related to birth weight? The strength of evidence from
a systematic review of the literature. J Hypertens 1996;
14: 935–941.
World Health Organisation. Tobacco or Health. First
Global Status Report. World Health Organisation:
Geneva, Switzerland, 1996.
World Bank. Better Health in Africa. The World Bank:
Washington, 1994.
Central Statistical Service. 1990a: 1.4, 3.26–3.34.
South African Statistics 1990. Government Printer:
Pretoria, 1990.
Weissberg PL, Woods KL, West MJ, Beevers DG. Genetic and ethnic influences on the distribution of
sodium and potassium in normotensive and hypertensive subjects. J Clin Hypertens 1987; 3: 20–25.
Hennessy JF, Ober KP. Racial differences in intact
erythrocyte ion transport. Ann Clin Lab Sci 1982; 12:
35– 41.
Touyz RM. Magnesium, calcium, sodium and potassium status in normotensive and hypertensive Johannesburg residents. S Afr Med J 1987; 72: 377–381.
Hoosen S, Seedat YK, Bhigjee AI. A study of urinary
and intracellular sodium and potassium, renin, aldosterone and hypertension in blacks and Indians in
Natal. Cardiovasc Drugs Ther 1990; 4: 363–365.
Zinner SH et al. Familial aggregation of urinary kallikrein concentration in childhood: relation to blood
pressure, race and urinary electrolytes. Am J Epidemiol 1976; 104: 124 –132.
Savage DD, Watkins LO, Grim CE, Kumanyika SK.
Hypertension in black populations. In: Laragh JH,
Brenner BM (eds). Hypertension: Pathophysiology,
Diagnosis and Management. 1st edn. Raven Press, Ltd:
New York, 1990, pp 1837–1852.
Berenson GS et al. Creatinine clearance, electrolytes,
and plasma renin activity related to blood pressure of
white and black children – the Bogalusa Study. J Clin
Med 1979; 93: 535–548.
Hohn AR et al. Childhood familial and racial differences in physiologic and biochemical factors related
to hypertension. Hypertension 1983; 5: 56–70.
Miller JZ, Grim CE. Heritability of blood pressure. In:
Kotchen TA, Kotchen JM, Wright J (eds). High Blood
Pressure in the Young. PS G: Boston, 1983, pp 79–90.
Hoosen S, Seedat YK, Bhigjhee AI, Neerahoo RM. A
study of urinary sodium and potassium excretion rates
among urban and rural Zulus and Indians. J Hypertens
1985; 68: 351–358.
Luft FC, Weinberger MH, Grim CE. Sodium sensitivity
and resistance in normotensive humans. Am J Med
1982; 72: 726–734.
Adlin EV, Marks AD, Channick BJ. The salivary
sodium/potassium ratio in hypertension: relation to
race and plasma renin activity. Clin Exp Hypertens
1982; 4: 1869–1880.
745
Journal of Human Hypertension
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
746
37 Milne J et al. Spot urinary concentrations and 24 hour
urinary excretion. Lancet 1980; 2: 1135.
38 He J et al. The renin-angiotensin system and blood
pressure: differences between blacks and whites. Am
J Hypertens 1999; 12: 555–562.
39 Davey-Smith G et al. Mortality differences between
black and white men in the USA: contribution of
income and other risk factors among men screened for
the MRFIT. MRFIT Research Group. Multiple Risk
Factor Intervention Trial. Lancet 1998; 351: 934 –939.
40 Miall WE, Kass EH, Ling J, Stuart KL. Factors influencing arterial pressure in the general population in
Jamaica. BMJ 1962; 2: 497–506.
41 Seedat YK, Seedat MA, Hackland DBT. Prevalence of
hypertension in the urban and rural Zulu. J Epidemiol
Commun Health 1982; 36: 256–261.
42 Campese VM, Parise M, Karubian F, Bigazzi R. Abnormal renal hemodynamics in black salt-sensitive
patients with hypertension. Hypertension 1991; 18:
805–812.
43 Walker WG et al. Renal function change in hypertensive members of the Multiple Risk Factor Intervention
Trial. Racial and treatment effects. JAMA 1992; 268:
3085–3091.
44 Messerli FH, Schmieder RE. Use of diuretic agents in
obese or black patients with systemic hypertension.
Am J Cardiol 1986; 58: 11A–14A.
45 Burke GL et al. Blood pressure and echocardiographic
measures in children: the Bogalusa Heart Study. Circulation 1987; 75: 106–114.
46 Hammond IW et al. Contrast in cardiac anatomy and
function between black and white patients with hypertension. J Natl Med Assoc 1984; 76: 247–255.
47 Morar N, Seedat YK, Naidoo DP, Desai DK. Ambulatory blood pressure and risk factors for coronary heart
disease in black and Indian medical students. J Cardiovasc Risk 1998; 5: 313–318.
48 Seedat YK, Pillay N, Marcoyannopoulou-Fojas H.
Myocardial infarction in the African hypertensive
patient. Am Heart J 1977; 94: 388–390.
49 Akinkugbe OO. High Blood Pressure in the African. 1st
edn. Churchill Livingstone: Edinburgh, 1972, p 12.
50 William RA. Coronary heart disease in blacks. In: Hall
WD, Saunders E, Shulman N (eds) Hypertension in
Blacks. Year Book Medical Publishers: Chicago, 1985,
pp 71–82.
51 Seedat YK, Mayet FGH, Latiff GH, Joubert G. Study of
risk factors leading to coronary heart disease in urban
Zulus. J Hum Hypertens 1993; 7: 529–532.
52 Veterans Administration Cooperative Study on Antihypertensive Agents: Comparison of propranolol and
hydrochlorothiazide for the initial treatment of hypertension. 1. Results of short-term titration with emphasis on racial differences in response. JAMA 1982; 248:
1996–2003.
53 Moser M, Lunn J. Responses to captopril and hydrochlorothiazide in black patients with hypertension. Clin
Pharmacol Ther 1982; 32: 307–312.
54 Seedat YK, Hoosen S, Bhigjee AT. Reserpine plus hydrochlorothiazide and sotalol plus hydrochlorothiazide
in black and Indian hypertensive patients. S Afr Med
J 1984; 65: 915–917.
55 Seedat YK. Varying responses to hypotensive agents in
different racial groups: black versus white differences.
J Hypertens 1989; 7: 515–518.
56 Holland OB, Fairchild C. Renin classification for
diuretic and beta blocker treatment of black hypertensive patients. J Chron Dis 1982; 35: 179–182.
57 Warren SE, O’Connor DT. Does a renal vasodilator system mediate racial differences in essential hypertension? Am J Med 1980; 69: 425– 429.
Journal of Human Hypertension
58 Seedat YK. Labetalol hydrochloride in the treatment
of black and Indian hypertensive patients. Med Proc
1979; 25: 53–57.
59 Seedat YK, Naiker IP. Efficacy of carvedilol in hypertensive black patients: a pilot study. Curr Ther Res
1993; 54: 753–757.
60 Fadayomi MO, Akinroye KK, Ajao RO, Awosika LA.
Monotherapy with nifedipine for essential hypertension in adult blacks. J Cardiovasc Pharmacol 1986; 8:
466– 469.
61 Moser M, Lunn J, Materson BJ. Comparative effects of
diltiazem and hydrochlorothiazide in blacks with systemic hypertension. Am J Cardiol 1985; 56: 101H–
104H.
62 Leary WP, Asmal AC. Treatment of Hypertension with
verapamil. Curr Ther Res 1979; 25: 747–752.
63 M’Buyamba-Kabangu JR et al. Intracellular sodium
and the response to nitrendipine or atenolol in African
blacks. Hypertension 1988; 11: 100–105.
64 Cruickshank JK et al. Treating hypertension in black
compared with white non-insulin dependent diabetics: a double-blind trial of verapamil and metoprolol. BMJ 1988; 297: 1115–1159.
65 Materson BJ et al. Single-drug therapy for hypertension in men. A comparison of six antihypertensive
agents with placebo. N Engl J Med 1993; 328: 914 –921.
66 Parag KB, Seedat YK. Do angiotensin-converting
enzyme inhibitors work in black hypertensives? A
review. J Hum Hypertens 1990; 4: 450– 452.
67 Ikeda LS et al. Comparative antihypertensive effects of
losartan 50 mg and losartan 50 mg titrated to 100 mg
in patients with essential hypertension. Blood Press
1997; 6: 35– 43.
68 Gradman AH et al. A randomized, placebo-controlled,
double-blind, parallel study of various doses of losartan potassium compared with enalapril maleate in
patients with essential hypertension. Hypertension
1995; 25: 1345–1350.
69 Ruilope LM et al. Controlled trial of Losarton given
concomitantly with different doses of hydrochlorothiazide in hypertensive patients. Blood Press 1996; 5:
32– 40.
70 Anonymous. United States Renal Data System 1992
Annual Data Report. Analytical Methods: technical
notes. Am J Kid Dis 1992; 20 (Suppl 2): 100–107.
71 US Renal Data System. USRDS 1994 Annual Data
Report. Bethesda, MD: National Institute of Diabetes
and Digestive and Kidney Disease, 1994. (NIH Publications No. 94-3176).
72 MacMahon SW, Cutler JA, Furberg CD, Payne GH. The
effects of drug treatment for hypertension on morbidity and mortality from cardiovascular disease: a
review of randomized controlled trials. Prog Cardiovasc Dis 1986; 29 (Suppl 1): 99–118.
73 Collins R et al. Blood pressure, stroke, and coronary
heart disease. Part 2, Short-term reductions in blood
pressure: overview of randomized drug trials in their
epidemiological context. Lancet 1990; 335: 827–838.
74 Hannedouche T et al. Randomized controlled trial of
enalapril and beta blockers in non-diabetic chronic
renal failure. BMJ 1994; 309: 833–837.
75 Seedat YK. The stepped-care approach to the treatment of hypertension in black patients. S Afr Med J
1982; 62: 1033–1035.
76 Freis ED. Angiotensin converting enzyme inhibition in
clinical practice. Choice of initial treatment. J Cardiovasc Pharmacol 1985; 7: S112–S116.
77 Weir MR, Saunders E. Pharmacologic management of
systemic hypertension in blacks. Am J Cardiol 1988;
61: 46H–52H.
Hypertension in developing nations in sub-Saharan Africa
YK Seedat
78 Report of the Joint National Committee on Detection,
Evaluation of High Blood Pressure: A Cooperative
Study. JAMA 1977; 237: 255–261.
79 Saunders E. Drug treatment for the hypertensive black
patient. J Fam Pract 1988; 26: 659–664.
80 Seedat YK. Perspective of hypertension in black
patients; black vs white differences. J Cardiovasc Pharmacol 1990; 16: (Suppl 7): S67–S70.
81 Joint National Committee on Prevention, Detection,
Evaluation and Treatment of High Blood Pressure. The
sixth report of the Joint National Committee on Prevention, Detection, Evaluation and treatment of High
Blood Pressure. Arch Intern Med 1997; 157: 2413–
2446.
82 Anonymous. 1999 World Health Organisation-International Society of Hypertension Guidelines for the
management of hypertension. Guidelines Subcommittee. J Hypertens 1999; 17: 151–183.
83 Reddy KS. Cardiovascular disease in India. Wld hlth
Statist Quart 1993; 46: 101–107.
747
Journal of Human Hypertension