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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 1, January/February 2019
AFRICA
19
failure to titrate statin dosages, failure to use combination
therapy, poor adherence and limited effectiveness of current
LMTs, particularly for achieving the lower LDL-C goals
recommended for patients at very high cardiovascular risk.
There was poor agreement between physician-estimated
cardiovascular risk and risk assessed using SCORE; in general,
physicians underestimated risk. As a patient’s LDL-C goal
depends on assessment of their cardiovascular risk, this
underestimation may result in a lack of intensification of LMT,
leaving many patients undertreated. There may be a need for
better dissemination of local lipid-management guidelines to
improve physicians’ understanding of risk assessment and to
promote adherence to guideline recommendations.
Funder barriers and affordability may also limit the use of
appropriate doses and intensity of statin therapy, as well as
the use of combination therapy with ezetimibe. IMPROVE-IT
demonstrated that the addition of ezetimibe to statin therapy
resulted in an incremental lowering of LDL-C and improved
cardiovascular outcomes in patients with acute coronary
syndrome (ACS).
17
The proportion of patients on a statin plus
ezetimibe in the current study was low, and greater use of this
combination may improve LDL-C goal attainment.
Cost and lack of access are major reasons for the low use
of ezetimibe. It is envisaged that generic ezetimibe will enter
the market in South Africa soon. Its lower cost, together
with the findings of IMPROVE-IT,
16
may increase access and
uptake of ezetimibe, at least for patients at very high risk of
atherosclerotic CVD. In addition, the introduction of novel
LMT combinations, not yet available in South Africa, may
further improve dyslipidaemia management and reduce the risk
of cardiovascular events.
Recent studies have demonstrated the efficacy of the PCSK9
inhibitors in high-risk patients treatedwith statins.
8,9
InFOURIER,
evolocumab reduced LDL-C levels by 59% and cardiovascular
events by 15% compared with placebo in patients treated with
statins who had atherosclerotic CVD and LDL-C
≥
70 mg/dl
(1.8 mmol/l).
9
ODYSSEY OUTCOMES examined the effect of
alirocumab in patients with a recent ACS and elevated cholesterol
level despite intensive or maximum-tolerated statin therapy.
8
Rates
of major adverse cardiovascular events and all-cause mortality
were reduced by 15% with alirocumab versus placebo.
The findings of the present study revealed socio-economic
differences between ethnic groups, which may reflect a legacy of
the previous political system that limited opportunities for black
South Africans. For example, 57.9% of black African patients
had completed secondary or university education compared
with 86.7% of Asian and 99.4% of Caucasian/European patients.
In addition, rates of private health insurance cover were lower
in black African patients (50.0%) than in Asian (77.6%) and
Caucasian/Europeans (93.1%).
Rates of obesity (63.5%) and hypertension (62.5%) were high
in black African patients. It should be noted that obesity was
defined as BMI
≥
30 kg/m
2
for all patients; however, a lower
cut-off point may be more appropriate in Asian patients.
18
Consequently, the true rate of obesity in Asian patients may be
higher than that observed in this group (32.7%).
Diabetes mellitus, a major risk factor for CVD, was also
highly prevalent in both black African (78.1%) and Asian
(87.8%) patients compared with Caucasians/Europeans (42.4%).
These differences between ethnic groups contrast with those from
the South African National Health and Nutrition Examination
Survey (SANHANES-1), which examined the prevalence of
Table 2. Laboratory values and lipid-modifying therapies at enrolment in the study population overall and by cardiovascular risk level
Risk level
Total
(
n
=
396)
Low
(
n
=
1)
Moderate
(
n
=
7)
High
(
n
=
123)
Very high
(
n
=
223)
Not assessable
a
(
n
=
42)
Lipid values
LDL-C, mmol/l, mean (SD)
2.6 (1.0)
2.0
3.6 (0.7)
2.5 (1.0)
2.5 (1.0)
3.1 (0.9)
Total cholesterol, mmol/l, mean (SD)
n
=
382
n
=
1
n
=
7
n
=
121
n
=
212
n
=
41
4.5 (1.1)
4.0
5.5 (1.0)
4.5 (1.1)
4.3 (1.1)
5.2 (1.0)
HDL-C, mmol/l, mean (SD)
n
=
375
n
=
1
n
=
7
n
=
120
n
=
206
n
=
41
1.2 (0.5)
1.2
1.3 (0.3)
1.3 (0.8)
1.2 (0.4)
1.3 (0.3)
Triglycerides, mmol/l, median (IQR)
n
=
373
n
=
1
n
=
7
n
=
120
n
=
204
n
=
41
1.5 (1.1–2.2)
0.7 (0.7–0.7)
1.5 (1.5–2.2)
1.5 (1.2–2.1)
1.6 (1.1–2.2)
1.6 (1.2–2.3)
Mixed dyslipidaemia,
b
n
/n
(%)
98/331 (29.6)
NA
3 (42.9)
24/120 (20.0)
71/204 (34.8)
NA
Other laboratory values
Fasting glucose, mmol/l, mean (SD)
n
=
110
n
=
0
n
=
3
n
=
25
n
=
75
n
=
7
7.7 (3.4)
NA
5.2 (0.9)
8.1 (3.4)
7.9 (3.6)
5.5 (0.5)
Serum creatinine, μmol/l, mean (SD)
n
=
252
n
=
1
n
=
4
n
=
77
n
=
153
n
=
17
85.7 (30.2)
78.0
89.2 (12.9)
74.3 (16.8)
91.8 (34.7)
81.4 (21.6)
LMT
Any statin,
n
(%)
391 (98.7)
1 (100.0)
7 (100.0)
120 (97.6)
221 (99.1)
42 (100.0)
High-intensity statin (in statin-treated patients),
c
n/n
(%)
98/391 (25.1)
0 (0.0)
1/7 (14.3)
14/120 (11.7)
76/221 (34.4)
7/42 (16.7)
On highest dose (in statin-treated patients),
d
n/n
(%)
69/389 (17.7)
0/1 (0.0)
1/7 (14.3)
15/120 (12.5)
50/220 (22.7)
3/41 (7.3)
Statin monotherapy,
n
(%)
359 (90.7)
1 (100.0)
7 (100.0)
111 (90.2)
201 (90.1)
39 (92.9)
Statin + fibrate
±
other LMT,
n
(%)
13 (3.3)
0 (0.0)
0 (0.0)
5 (4.1)
8 (3.5)
0 (0.0)
Statin + cholesterol-absorption inhibitor
±
other LMT,
n
(%)
10 (2.6)
0 (0.0)
0 (0.0)
0 (0.0)
9 (4.0)
1 (2.4)
HDL-C: high-density lipoprotein cholesterol; IQR: interquartile range; LDL-C: low-density lipoprotein cholesterol; LMT: lipid-modifying therapy; NA: not available;
SD: standard deviation.
a
Patients without a serious pathology classifying them as very high or high cardiovascular risk, and in whom the SCORE could not be calculated owing to missing data.
b
Total serum triglycerides
≥
1.7 mmol/l (150 mg/dl) and LDL-C
>
target.
c
Atorvastatin 40 or 80 mg or rosuvastatin 20 or 40 mg.
d
Marketed in South Africa.