CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 1, January/February 2011
AFRICA
23
caused by smoking, as they are generally known to have higher
HDL-C levels than Caucasians.
26
Moreover, the infrequent use of cigarettes and more use
of snuff in Africans with lower SES than in Caucasians has
revealed no change in HDL-C values between smokers and
non-smokers.
30-32
This is a finding that is likely to apply in our
African participants, with consequently less HDL-C destruction
by oxidant gases from smoke. However, a higher HDL-C level in
African smokers than in their non-smoker counterparts is a find-
ing that needs further research for more clarity.
Smoking was also correlated with other cardiometabolic
variables and, in comparison to previous findings,
1,4,13
smoking
correlated poorly with the measured variables, especially after
adjustment for confounders. PWV, HDL-C and hs-CRP were the
only variables with stronger correlations observed in Africans.
The generally weak correlations in the study may be due to
the relatively young age of the smokers, with stronger correla-
tions only expected at older ages. Weak correlations may also
be affected by misclassification of chronic smoking by partici-
pants, as it was determined by self-reporting only,
33
especially
in Africans, who may suspend smoking on financial grounds.
24
The weak correlations in Caucasians may be explained by the
less nicotine-packed brands they use and their generally lower
arterial stiffness and TPR compared to Africans.
6,26
The higher
cotinine levels of Caucasians may be explained by the generally
low clearance rate of cotinine in Caucasians.
3
The higher TG levels of the smokers in this study is a finding
consistent with the literature.
1,4,29,34,35
Increased TG levels are due
to nicotine-mediated lipolysis and also increased corticosteroid
and growth hormone levels, inducing insulin resistance,
1,4
espe-
cially in smokers who are also snuff users.
1
Hs-CRP, a well-known inflammatory marker,
36
correlated
positively with smoking duration in both groups, and with
acute smoking in Caucasians (Table 5). Endothelial dysfunc-
tion caused by smoking promotes inflammation that leads to
increased hs-CRP levels in smokers.
35,37
Age, gender, ethnic-
ity, obesity, chronic infections and low SES are responsible for
variations in hs-CRP levels.
38
As a result, the concentration of
hs-CRP between smokers and non-smokers may be masked. This
is reflected to some extent in this study, where hs-CRP levels
showed weak correlations with acute smoking throughout and
also in the women participants.
TABLE 5. CORRELATIONS BETWEEN SMOKINGAND MEASURES OF CARDIOVASCULAR
FUNCTIONAND LIPIDS IN CAUCASIAN PARTICIPANTS
Men (
n
=
161)
Women (
n
=
211)
Whole group (
n
=
372)
Smoking duration
Cotinine
Smoking duration
Cotinine
Smoking duration
Cotinine
Variables
r
-value
p
-value
r
-value
p
-value
r
-value
p
-value
r
-value
p
-value
r
-value
p
-value
r
-value
p
-value
SBP (mmHg)
0.05 0.556 –0.07 0.397 –0.03 0.694 –0.05 0.454 0.07 0.161 –0.01 0.889
DBP (mmHg)
0.04 0.597 –0.05 0.558 0.13 0.061 0.06 0.362 0.09 0.078 0.03 0.565
HR (beats/min)
0.18 0.021 0.18 0.023 0.20 0.004 0.17 0.019 0.15 0.005 0.15 0.004
CO (l/min)
0.03 0.751 0.09 0.226 0.10 0.137 0.11 0.118 0.09 0.095 0.13 0.013
TPR (mmHg.s/ml)
0.00 0.989 –0.10 0.199 –0.06 0.426 –0.09 0.156 –0.05 0.329 –0.12 0.019
Cwk (ml/mmHg)
–0.13 0.098 0.07 0.410 0.02 0.762 0.06 0.364 0.01 0.786 0.13 0.016
C-R PWV (m/s)
0.09 0.279 –0.12 0.154 0.05 0.444 0.04 0.588 0.01 0.870 –0.01 0.902
C-P PWV (m/s)
–0.01 0.902 –0.02 0.770 0.00 0.956 –0.02 0.779 0.03 0.558 0.01 0.921
HDL-C (mmol/l)
–0.16 0.046 –0.20 0.014 –0.03 0.702 –0.00 0.945 –0.17
≤
0.001 –0.15 0.004
LDL-C (mmol/l)
0.07 0.379 0.06 0.493 0.03 0.716 –0.04 0.617 0.06 0.286 0.02 0.737
TG (mmmol/l)
0.15 0.052 0.10 0.194 0.08 0.237 –0.00 0.974 0.16 0.003 0.08 0.116
hs-CRP (mg/l)
0.14 0.073 0.14 0.087 0.09 0.191 0.07 0.303 0.09 0.102 0.08 0.113
Cotinine (ng/ml)
0.71
≤
0.001
–
–
0.84
≤
0.001
–
–
0.74
≤
0.001
–
–
After adjustment for age, BMI and WC
SBP (mmHg)
0.02 0.854 –0.04 0.660 –0.00 0.970 0.01 0.924 –0.00 0.957 –0.01 0.813
DBP (mmHg)
0.14 0.863 –0.02 0.844 0.18 0.013 0.14 0.050 0.07 0.198 0.06 0.240
HR (beats/min)
0.20 0.016 0.17 0.033 0.20 0.006 0.17 0.023 0.18
≤
0.001 0.17 0.002
CO (l/min)
0.09 0.296 0.06 0.482 0.13 0.066 0.16 0.021 0.09 0.102 0.11 0.044
TPR (mmHg.s/ml)
–0.07 0.406 –0.05 0.569 –0.05 0.477 –0.11 0.138 –0.05 0.327 –0.07 0.161
Cwk (ml/mmHg)
–0.07 0.364 –0.08 0.300 –0.02 0.807 0.22 0.755 –0.07 0.216 –0.02 0.649
C-R PWV (m/s)
–0.18 0.349 –0.23 0.226 –0.45 0.096 0.22 0.438 –0.27 0.056 0.02 0.901
C-P PWV (m/s)
–0.00 0.980 –0.11 0.557 –0.03 0.925 0.39 0.156 –0.11 0.457 0.10 0.490
HDL-C (mmol/l)
–0.20 0.012 –0.18 0.027 –0.03 0.652 –0.02 0.395 –0.12 0.026 –0.10 0.052
LDL-C (mmol/l)
0.06 0.470 0.07 0.393 0.04 0.539 0.00 0.985 0.04 0.413 0.04 0.459
TG (mmmol/l)
0.16 0.050 0.12 0.131 0.11 0.111 0.05 0.503 0.13 0.012 0.09 0.088
hs-CRP (mg/l)
0.17 0.037 0.14 0.096 0.11 0.106 0.12 0.090 0.13 0.015 0.13 0.017
Cotinine (ng/ml)
0.73
≤
0.001
–
–
0.84
≤
0.001
–
–
0.74
≤
0.001
–
–
PWV was additionally adjusted for MAP. SBP: systolic blood pressure; DBP: diastolic blood pressure; HR: heart rate; CO: cardiac output; TPR:
total peripheral resistance; Cwk: Windkessel compliance; C-R PWV: carotid-radialis pulse wave velocity; C-P PWV: carotid-dorsalis pedis pulse
wave velocity; HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol; TG: triglycerides; hs-CRP: high-sensi-
tivity C-reactive protein; MAP: mean arterial pressure.
