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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 4, July/August 2016
AFRICA
267
cardiovascular burden that black populations carry,
10,11
our
results suggest that treatment that effectively lowers central
pressure may also significantly lower the risk for stroke and other
cardiovascular events.
Our results were similar for treated and untreated
hypertensives; therefore treatment seems to be largely ineffective
in this population. Indeed, the treatment and control of
hypertension in low-income countries are largely inadequate
despite half of those sampled being aware of their condition.
14,30
South Africa has one of the highest hypertension rates (78%)
for people over 50 years of age, but only 38% are aware of
their hypertensive status and only 7.8% of those treated for
hypertension have controlled hypertension.
14
It therefore remains
to be seen whether effective anti-hypertensive treatment in black
Africans will result in improved carotid distensibility.
Surprisingly, the IMT was similar between the two groups
after adjustments, suggesting a lack of visible structural changes
in the hypertensive blacks. IMT is an important marker of the
atherosclerotic burden of the carotid artery,
31
but it may also
indicate non-atherosclerotic compensatory remodelling of the
arterial wall in response to hypertension.
32
However, neither of
these possibilities seems to be the case in this black population.
On the other hand, IMT was independently associated with
cSBP in the hypertensive group only, therefore suggesting that
the continued high pulsatile load of uncontrolled hypertension
may eventually mediate structural changes in the carotid artery.
This result shows a similar trend to the findings of Wang
et al.
,
33
confirming the relevance of central blood pressure to IMT.
We observed no differences in the inflammatory and
endothelial activation markers, lipid levels and glycaemic status
between the normotensives and hypertensives. Africans are
generally not prone to atherosclerosis and coronary heart
disease,
34
and exhibit a favourable lipid profile,
35,36
possibly
explaining the similar lipid levels between the two groups.
However, our results confirm the commonly found association
between IMT and LDL-C level,
37,38
and an association between
CD and HbA
1c
level in the hypertensive group only.
Although we did not observe structural differences after
adjustment for cSBP, these results suggest glucose metabolism
and lipid abnormalities may play a role in the arterial changes,
although these are not yet detectable with ultrasound.
Inflammation and endothelial activation (as indicated by the
adhesionmolecules) may not play amajor role in the mediation of
central arterial stiffness at this stage of disease progression. These
results are unexpected in the light of previous findings, which
indicate that acute and chronic inflammation are associated with
stiffness of the large arteries,
39
and that endothelial activation
may be an important mediator of hypertensive vascular injury.
40
The findings of this study should be interpreted in the context
of its limitations and strengths. Our study population consisted
of individuals from specific urban and rural areas in the North
West Province of South Africa, and may not be representative
of the whole population. We were not able to use echo-tracking
techniques to determine local arterial stiffness in our field
study; however, the procedures of ultrasound assessment are
standardised
41
and were performed by a single reader in a large
study population. Carotid distensibility was calculated with a
formula that includes cSBP, and we adjusted for cSBP. However,
neither direct measurements such as IMT nor indirect variables
such as carotid distensibility differed after adjustments for
cSBP. Due to the cross-sectional study design, causality cannot
be inferred. Although the results were consistent after several
adjustments, we cannot exclude residual confounding.
Conclusion
Although differences existed in terms of carotid structure and
function between the normotensive and hypertensive Africans, it
seemed to be partially accounted for by the increased distending
pressure of the hypertensive group. Despite their hypertensive
status, structural adaptations, such as IMT thickening, were
not detectable in this African population after adjustment for
potential confounders, and even before cSBP or MAP were
taken into account. The classic cardiometabolic risk factors,
markers of inflammation, endothelial activation and health
behaviour seemed to play only a minor role in the mediation of
carotid distensibility in this population at this stage of disease
Table 7. Forward stepwise multiple regression analyses
with CSWA and max LD as dependent variables
Normotensives
(
n
=
241)
β
(95% CI)
p
-value
Hypertensives
(
n
=
351)
β
(95% CI)
p
-value
CSWA (mm
2
)
Adjusted
R
2
0.23
0.32
Locality (urban)
–0.11 (–0.21– –0.01) 0.022
Gender (male)
0.29 (0.15–0.42)
<
0.001 0.26 (0.15–0.37)
<
0.001
Age, years
0.29 (0.17–0.42)
<
0.001 0.43 (0.30–0.57)
<
0.001
Waist circumfer-
ence, cm
0.18 (0.05–0.31)
0.008 0.02 (–0.12–0.17)
0.77
Central SBP, mm
Hg
0.18 (0.08–0.28)
<
0.001
LDL-C, mmol/l
0.12 (0.01–0.23)
0.026
HbA
1c
(%)
0.08 (–0.02–0.19)
0.13
Creatinine clear-
ance, ml/min
0.11 (–0.05–0.26)
0.18
C-reactive protein,
pg/ml
0.16 (0.02–0.29)
0.025 0.09 (–0.01–0.20)
0.090
γ
-glutamyl transfer-
ase, U/l
0.11 (–0.02–0.24)
0.10 –0.08 (–0.18–0.02)
0.11
Anti-hypertension
medication (yes)
–0.12 (–0.22– –0.02) 0.013
Max LD (mm)
Adjusted
R
2
0.27
0.10
Locality (urban)
–0.08 (–0.21–0.05)
0.21
Gender (male)
0.26 (0.10–0.42)
0.001 0.22 (0.08–0.36)
0.002
Age, years
0.13 (–0.03–0.29)
0.12
Waist circumfer-
ence, cm
0.14 (-0.005–0.28)
0.061
Central SBP,
mmHg
0.20 (0.05–0.35)
0.010 0.14 (0.007–0.27)
0.039
Heart rate, bpm –0.09 (–0.24–0.06)
0.22
LDL-C, mmol/l
–0.16 (–0.30– –0.02) 0.027 –0.14 (–0.2– –0.003) 0.045
Creatinine clear-
ance, ml/min
0.21 (0.05–0.37)
0.011
C-reactive protein,
pg/ml
0.09 (–0.05–0.23)
0.23
ICAM-1, pg/ml
0.16 (0.01–0.30)
0.037 0.08 (–0.05–0.21)
0.25
γ
-glutamyl transfer-
ase, U/l
0.17 (0.03–0.32)
0.023
Data expressed as beta-values and 95% confidence intervals,
p
-values obtained
with forward stepwise multiple regression analyses.
Included in each model: locality, age, gender, WC, HR, cSBP, LDL-C, HbA
1c
,
C-reactive protein, ICAM-1, creatinine clearance,
γ
-glutamyl transferase, tobacco
and anti-hypertensive medication use.
CSWA, cross-sectional wall area; Max LD, maximum lumen diameter; SBP, systol-
ic blood pressure; LDL-C, low-density lipoprotein cholesterol; HbA
1c
, glycated
haemoglobin; ICAM-1,intracellular adhesion molecule-1.