24 / 78
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 1, January/February 2019
22
AFRICA
comprised mainly educated patients residing in urban areas with
a high rate of private healthcare insurance, in contrast with the
general population, in which most patients are treated in the
public health sector. In addition, the study only included patients
on stable LMT; therefore, patients with untreated dyslipidaemia
are not represented. We were therefore unable to estimate what
proportion of patients with an indication for LMT was receiving
treatment.
Owing to the observational nature of the study, and in
accordance with the study design, LMTs and doses varied
according to site/physician preference, and patient adherence to
LMTswas not assessed. SCOREwas used to assess cardiovascular
risk; however, its validity in non-European populations has not
been established. Only one patient was classified as at low risk;
therefore, the findings are not representative of this group. In
addition, missing data may have limited some analyses, including
LDL-C values at first diagnosis, and the diagnosis of familial
hypercholesterolaemia based upon genetic/family history data.
Conclusion
Achievement of LDL-C goals is suboptimal in South Africa,
particularly in patients at moderate and very high cardiovascular
risk. Physicians’ assessment of cardiovascular risk was poor,
and the use of high-dose statin or combination therapy was
low, highlighting a gap between guideline recommendations and
clinical practice. Sociodemographic differences between ethnic
groups may also influence the management of dyslipidaemia.
Improving adherence to guidelines, increasing the use of
combination therapy, and the introduction of novel LMTs are
important strategies for improving LDL-C goal achievement.
The authors thank the patients, their families and all investigators involved
in this study. Medical writing assistance and editorial support, under the
direction of the authors, were provided by Fiona Van, PhD, and Ian Norton,
PhD, both of Prime (Knutsford, UK), funded by Sanofi, according to Good
Publication Practice guidelines (link to guidelines:
https://www.ismpp.org/gpp3). Sanofi was involved in the study design, collection, analysis and inter-
pretation of data, as well as data checking of information provided in the
manuscript. However, ultimate responsibility for opinions, conclusions and
data interpretation lies with the authors.
ICLPS SA investigators*
Aslam Amod, Durban; Dirk Blom, Cape Town; Neville Chelin, Umbilo;
Kathleen Coetzee, Paarl; Clive Corbett, Cape Town; Leon Fouche, Thabazimbi;
Nyda Fourie, Bloemfontein; Uttarn Govind, Durban; Shaifali Joshi, Pretoria;
Ilse Kapp, Johannesburg; Hester Johanna Kotze, Centurion; Hemant Makan,
Lenasia; Akbar Anvar Mahomed, Moloto South; Nomangesi Judith Ngcakani,
Port Elizabeth; Trevenesan Padayachee, Durban; Frederick Raal, Johannesburg;
Saadiya Seedat, Port Elizabeth; Hans H Snyman, Brits; Julien Trokis, Cape Town.
References
1.
World Health Organization. The top 10 causes of death, Fact Sheet
2018
.http://www.who.int/mediacentre/factsheets/fs310/en/(2018,
accessed 21 June 2018).
2.
Keates AK, Mocumbi AO, Ntsekhe M, Sliwa K, Stewart S.
Cardiovascular disease in Africa: epidemiological profile and challenges.
Nat Rev Cardiol
2017;
14
: 273–293.
3.
MaredzaM, HofmanKJ, Tollman SM. Ahiddenmenace: Cardiovascular
disease in South Africa and the costs of an inadequate policy response.
SA Heart
2011;
8
: 48–57.
4.
Klug E, South African Heart Association (S A Heart), Lipid and
Table 4. Laboratory values and lipid-modifying therapies at enrolment in the study population overall and by ethnicity
Total (
n
=
396)
Ethnicity
Asian
(
n
=
98)
Black African
(
n
=
96)
Caucasian/European
(
n
=
144)
Other
(
n
=
58)
Lipid values
LDL-C, mmol/l, mean (SD)
2.6 (1.0)
2.3 (0.8)
2.5 (0.9)
2.6 (1.1)
2.9 (1.2)
Total cholesterol, mmol/l, mean (SD)
n
=
382
n
=
96
n
=
95
n
=
134
n
=
57
4.5 (1.1)
4.2 (1.0)
4.6 (1.2)
4.5 (1.0)
4.9 (1.4)
HDL-C, mmol/l, mean (SD)
n
=
375
n
=
90
n
=
92
n
=
137
n
=
56
1.2 (0.5)
1.1 (0.3)
1.3 (0.8)
1.2 (0.4)
1.2 (0.4)
Triglycerides, mmol/l, median (IQR)
n
=
373
n
=
90
n
=
92
n
=
134
n
=
57
1.5 (1.1–2.2)
1.5 (1.1–2.4)
1.6 (1.2–2.2)
1.6 (1.1–2.0)
1.5 (1.0–2.1)
Mixed dyslipidaemia,
a
n/n
(%)
98/331 (29.6)
23/88 (26.1)
18/96 (24.0)
40/114 (35.1)
17/54 (31.5)
Other laboratory values
Fasting glucose, mmol/l, mean (SD)
n
=
110
n
=
16
n
=
20
n
=
41
n
=
33
7.7 (3.4)
7.4 (3.6)
9.5 (4.1)
7.4 (3.2)
7.1 (2.9)
Serum creatinine, μmol/l, mean (SD)
n
=
252
n
=
74
n
=
63
n
=
74
n
=
41
85.7 (30.2)
86.6 (35.6)
79.0 (24.2)
90.3 (28.4)
85.9 (30.5)
LMT
Any statin,
n
(%)
391 (98.7)
98 (100.0)
96 (100.0)
141 (97.9)
56 (96.6)
High-intensity statin (in statin-treated patients),
b
n/n
(%)
98/391 (25.1)
9/98 (9.2)
9/96 (9.4)
69/141 (48.9)
11/56 (19.6)
On highest dose (in statin-treated patients),
c
n/n
(%)
69/389 (17.7)
5/98 (5.1)
12/96 (12.5)
43/139 (30.9)
9/56 (16.1)
Statin monotherapy,
n
(%)
359 (90.7)
95 (96.9)
92 (95.8)
120 (83.3)
52 (89.7)
Statin + fibrate
±
other LMT,
n
(%)
13 (3.3)
1 (1.0)
2 (2.1)
7 (4.9)
3 (5.2)
Statin + cholesterol-absorption inhibitor
±
other LMT,
n
(%)
10 (2.6)
2 (2.0)
0 (0.0)
8 (5.6)
0 (0.0)
HDL-C: high-density lipoprotein cholesterol; IQR: interquartile range; LDL-C: low-density lipoprotein cholesterol; LMT: lipid-modifying therapy;
SD: standard deviation.
a
Total serum triglycerides
≥
1 .7 mmol/l (150 mg/dl) and LDL-C
>
target.
b
Atorvastatin 40 or 80 mg or rosuvastatin 20 or 40 mg.
c
Marketed in South Africa.