CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 7, August 2012
394
AFRICA
We identified more than six years of formal education as
being independently predictive of high TC and LDL-C, and low
HDL-C levels, which corresponds to other findings from the
Heart of Soweto study.
6
These results may indicate a progression
in income/socio-economic status, enabling greater access to a
Western diet and increased tendency for sedentary behaviour,
27
especially in women.
23
However, we have shown that the ethnic-
based patterns of dyslipidaemia presented in this report persisted
even after controlling for BMI. This important finding alludes to
the influence of other factors that contribute to the presentation
of heart disease and its risk factors.
Other factors, such as very low TG levels,
3
and novel
factors unrelated to dyslipidaemia (such as more effective
homocysteine metabolism),
28
may confer relative protection
against atherosclerotic heart disease in African populations.
Patterns of hypertension and obesity, which persist even in
migratedAfrican populations,
3
may suggest predisposing factors.
However, the case for attributing genetic susceptibility to
heart disease solely
on the basis of ‘race/ethnicity’ is proving
increasingly futile.
29
In this study, we could clearly discount monogenic disorders of
lipoproteins as the cause of lipid differentials across ethnicities,
as they were uncommon. We have seen features of dyslipidaemia
change in these populations over time,
20-22
especially with regard
to HDL-C levels. It is more likely that risk factors that can
influence lipids, particularly obesity and its antecedents (poor
diet and lack of physical activity),
23
are driving the patterns of
dyslipidaemia reported here. Relying on genetic susceptibility
to explain ethnic differences in lipids, without recognising the
role of gene–environment interaction in CVD risk will only
prove counterproductive in addressing current prevention and
management of CVD.
Given that dyslipidaemia does not occur in isolation, future
work should focus on likely contributors to these trends,
irrespective of ethnicity. Insulin resistance or the metabolic
syndrome dyslipidaemia is strongly associated with
atherosclerotic CVD and may play a role in the consistently
low HDL-C levels across ethnic groups, as reported here. In
Indian patients, the prevalence of diabetes was 18%, which may
contribute to the high rates of CAD in this group (half of primary
diagnoses in those of Indian ethnicity), an association that has
been shown previously.
5
Despite a lower prevalence of diabetes
in other ethnicities, overall high obesity rates in this cohort
will likely contribute to an increased prevalence of both insulin
resistance and diabetes in coming generations.
23,30
Additionally, we found an inverse association between the
inflammatory marker CRP and HDL-C levels in those whom
the inflammatory marker was measured. Despite the subset
representing only 30% of those with a reported lipid profile,
the negative association was striking and may indicate enhanced
CVD risk beyond other clinical risk factors.
14
Therefore, the
possible contribution of chronic, low-grade inflammation to
dyslipidaemia warrants additional investigation, as it is associated
with both chronic infection and atherosclerotic CVD.
14
There are a number of limitations that require consideration.
Clinical data (other than routine echocardiography and 12-lead
ECG) were obtained according to clinical presentation and only
those with suspected atherosclerotic disease had lipid levels
measured. Systematic bias, therefore, needs to be carefully
considered before attributing broad patterns in lipid profiles
according to ethnicity and may overestimate the utility of
measuring/treating dyslipidaemia within the wider community.
Adiposity (BMI), a major confounder of both dyslipidaemia
and heart disease, was recorded in 73% of patients in this cohort.
However, its inclusion in the regression analyses did not alter the
significant findings. Central obesity measurements (e.g. waist-
to-hip ratio) may have offered greater delineation of CVD risk,
given its strong association with low HDL-C levels, particularly
in women of African descent,
10
however this was an impractical
variable to obtain consistently, given the nature of the study
setting. CRP was only measured in around one-third of selected
cases and related data require careful interpretation.
Conclusion
Differences in CVD risk factors, especially lipid profiles, were
apparent in the ethnically diverse enclave of Soweto in South
Africa. We have shown that while dyslipidaemia is an important
risk factor in heart disease presentation, overall, disparities
exist in the extent of lipid abnormalities. Significantly, low
HDL-C levels persisted in all ethnicities. These trends have
important public health and clinical implications that require
further consideration. While there are inherent limitations in
the interpretation of racial and ethnic comparisons, irrespective
of the healthcare setting, rational approaches to secondary
prevention of heart disease may require a diversity of strategies
because of these ethnic differences.
We thank all the doctors, nurses and patients who participated in the regis-
try; and Elisabeth Tshele, Bridget Phooko, Maureen Kubheka and Phutuma
Mathusi who contributed to the meticulous collection and management of
clinical data.
The Heart of Soweto registry was supported by the University of the
Witwatersrand and unconditional research grants from Adcock-Ingram, the
Medtronic Foundation USA, Servier, Bayer Health Care and BHP Billiton.
SS, MJC and JGL are supported by the National Health and Medical
Research Council of Australia. JGL is supported by the National Heart
Foundation of Australia and Cardiac Society of Australia and New Zealand.
This work was supported by the Victorian Government’s OIS Program.
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