GUIDELINE

South African Dyslipidaemia Guideline Consensus Statement

A joint statement from the South African Heart Association (SA Heart) and the Lipid and
Atherosclerosis Society of Southern Africa (LASSA)

The European Society of Cardiology together with the European

Atherosclerosis Society published updated dyslipidaemia guidelines
in 2011. SA Heart and the Lipid and Atherosclerosis Society of
Southern Africa officially adopt these guidelines. This statement
adapts aspects of the guidelines to the South African situation. Using
the updated Framingham risk charts, interventional strategies are
based according to the cardiovascular risk score and low-density
lipoprotein cholesterol (LDL-C) levels. The Framingham risk score
refers to the 10-year risk of any cardiovascular event, and includes

1. Introduction

In 2003, the South African Heart Association (SA Heart) and the
Lipid and Atherosclerosis Society of Southern Africa (LASSA)
officially adopted the European Guidelines for the Prevention of
Cardiovascular Disease1 to replace the South African Lipid Guidelines
published in 2000.2 The European document has recently been
updated with the publication of the European Society of Cardiology
(ESC)/European Society of Atherosclerosis (EAS) Guideline for the
Management of Dyslipidaemias in 2011.3 This Consensus Statement
promotes current best management of dyslipidaemia and should be
adopted by all health care professionals in South Africa.
South Africa is a multi-ethnic society, with a large range of cultures
and lifestyles at different stages of epidemiological transition. In all
sub-populations, cardiovascular disease is a major cause of morbidity
and mortality. Every day, approximately 80 people die of myocardial
infarction or heart failure, while another 60 die due to stroke.4
The INTERHEART Africa study indicated that more premature
acute myocardial infarctions occur in sub-Saharan Africa than in
any other of the 52 countries participating in the INTERHEART
study.5,6 This statistic reflects a lack of prevention, early detection
and effective management of cardiovascular risk factors in the
countries of this region.5 In particular, in the black population, with
increasing urbanisation and adoption of an unhealthy lifestyle, the
prevalence of CVD and the incidence of premature death are likely to
continue to increase.4 Consequently, the timely institution of lifestyle
modification, early diagnosis and effective management of CVD risk
factors are essential to curb the epidemic of CVD that has been seen
in other countries.5

Task Force: Chairman Dr E Q Klug, MB BCh, MMed, FCP (SA), Members

F J Raal, FCP (SA), FRCP, FRCPC, MMed, PhD, A D Marais, MB ChB, FCP (SA),
M-R Taskinen, MD (Finland), A J Dalby, MB ChB, FCP (SA), FACC, C Schamroth,
MB BCh, MMed, FCP (SA), FACC, N Rapeport, MB BCh, FCP (SA), FACP (Hon),
D Jankelow, MB BCh, FCP (SA), D J Blom, MB ChB, MMed, FCP (SA), PhD,
R Catsicas, RD (SA), D A Webb, BSc (Hons), MB BCh

Corresponding author: Eric Klug (eklug@global.co.za)

178

March 2012, Vol. 102, No. 3 SAMJ

four categories of risk. Treatment targets are those of the European

guidelines. The LDL-C goal is 1.8 mmol/l for the very high-risk
group (>30%), 2.5 mmol/l for the high-risk group (15 - 30%),
and 3 mmol/l for those below 15% risk. Intensive management
of dyslipidaemia in South Africa will significantly reduce the
cardiovascular disease health burden.
S Afr Med J 2012;102:177-188.

2. When to use the cardiovascular risk

score
2.1 Very high-risk individuals do not require risk
scoring

Individuals who are considered to be at very high risk of cardiovascular

events are listed in Table 1. Patients in this group DO NOT
require cardiovascular risk scoring, because the risk score will be an
underestimate in these settings.

2.2 Individuals who do not fall into the very high-risk

category

Risk scoring using well-documented key risk factors is appropriate

to estimate the total cardiovascular risk in asymptomatic adults.
Furthermore, risk scoring is especially important in individuals with
the following:

hypertension and/or on antihypertensive medication

smoking: cigarette smoking is defined as any cigarette smoking
Abbreviations
ACS

acute coronary syndromes

ALT

alanine aminotransferase

ARVs

antiretroviral drugs

BP

blood pressure

CHD

coronary heart disease

CK

creatine kinase

CVD

cardiovascular disease

GFR

glomerular filtration rate

HDL-C

high-density lipoprotein cholesterol

LDL-C

low-density lipoprotein cholesterol

hsCRP

high-sensitivity C-reactive protein

Lp(a)

lipoprotein (a)

MI

myocardial infarction

TC

total cholesterol

TG

triglyceride

TLC

therapeutic lifestyle change

ULN

upper limit of normal

GUIDELINE

Table 1. Subjects considered to be at very high risk of cardiovascular events

Established atherosclerotic disease, i.e.
coronary artery disease
cerebrovascular disease
peripheral arterial disease
Type 2 diabetes
Type 1 diabetes with micro-albuminuria or proteinuria
Genetic dyslipidaemia, e.g. familial hypercholesterolaemia
Chronic kidney disease (GFR <60 ml/min/1.73 m2)

in the past month or a history of 20 cigarettes per day for 10

years (10 pack years)
BMI 30 kg/m2 or waist circumference >94 cm for men, >80
cm for women
family history of premature CVD (male before 55 years of age,
female before 60 years)
auto-immune chronic inflammatory disease, e.g. rheumatoid
arthritis, systemic lupus erythematosus, psoriasis.

3. When to start screening

In South Africa, because the prevalence of familial

hypercholesterolaemia is as high as 1 in 100 in some communities,
each individual should be tested, preferably with a full lipogram or
at least TC/LDL-C, at least once in young adulthood (from 20 years
of age). Particular attention should be paid to individuals with other
risk factors for CVD.

4. How to screen: using the

Framingham Risk Score

The European guidelines use the Systematic Coronary Risk Estimation

(SCORE) system to estimate cardiovascular risk. Because this scoring
system is based on an exclusively European population, it may not
accurately reflect coronary risk in South Africa. While it is recognised
that it would be impossible to accurately estimate risk in all South
African subpopulations with a single data set, the Adult Treatment
Panel (ATP) III Framingham risk tables,7 which provide an estimate
of the 10-year risk of CHD, have been validated in white and black
populations in the USA and are transportable to other culturally
diverse populations. Consequently, we considered this approach to
be more appropriate for South Africa. Nevertheless, these risk tables
are likely to underestimate risk in South African black and Indian
patients. The Framingham CHD tables may also underestimate
total CVD risk in middle-aged and older women, whose risk of
stroke and heart failure is typically higher than that of CHD. Even
when multiple elevated risk factors are present, it is difficult for a
woman younger than 75 years to exceed a 10% predicted risk for
CHD, precluding her from qualification for more aggressive CVD
prevention.8 Consequently, more recent Framingham equations
predict 10-year total CVD risk (including CHD, stroke, transient
ischaemic attack and heart failure).8,9
The updated Framingham CVD risk tables for men and women
and an algorithm for management and cholesterol goals have been
incorporated into these recommendations (Appendix 1).

5. Measuring lipids

5.1 Low-density lipoprotein cholesterol

LDL-C is preferred when deciding on treatment and assessing its

effect. LDL-C is used in preference to other tests as it is modifiable

by treatment and the beneficial effects of lowering LDL-C are known.

LDL-C may be measured directly or calculated from the Friedewald
equation (in mmol/l) (LDL-C = TC HDL-C TG/2.2), provided the
triglycerides do not exceed 4.5 mmol/l.

5.2 Total cholesterol

Once the relationship between on-treatment TC and LDL-C is

known, it may be appropriate to monitor TC only. TC may be used
as an alternative for screening, risk assessment and monitoring of
treatment efficacy if there are cost constraints or if there is difficulty
in obtaining either direct or indirect LDL-C values.
Equivalent target values for TC are:

TC = 4.5 mmol/l is approximately equivalent to LDL-C = 2.5
mmol/l

TC = 4.0 mmol/l is approximately equivalent to LDL-C = 1.8
mmol/l.
If TC values remain uncontrolled and LDL-C measurement is
unavailable, the patient should be referred to a specialist physician.

5.3 Cost-effective testing

A full lipogram (TC, HDL-C, LDL-C and triglycerides) is

recommended for initial diagnosis of dyslipidaemia. In patients
with pure hypercholesterolaemia, LDL-C alone is adequate for
follow-up, but a full lipogram is recommended where increased
LDL-C is not the only abnormality in the lipid profile. After
initiating TLC alone, follow-up testing should be performed every
6 months. After initiating pharmacotherapy, changing the dose or
changing the specific drug prescribed, testing should be repeated
at 8 (4) weeks and thereafter, once the patient is at goal, every 6
months.

5.4 Point-of-care finger prick testing

Various point-of-care tests are available. They provide various

results, ranging from TC alone to a full lipogram. Where finger prick
testing is performed, the facility should ensure that adequate quality
controls are in place, that the test strips and devices are stored under
appropriate conditions of temperature, humidity and light, and that
precautions are taken to perform the test properly, with an adequate
blood sample volume and without contamination.10 The finger
should not be squeezed or milked, as this will give inaccurate results.
Finger prick testing is appropriate for screening and follow-up to
determine where advice on lifestyle intervention is required (e.g. TC
>5 mmol/l), but is not appropriate to commit a patient to a lifetime
of therapy. Where a screening finger prick TC measurement is high
(>5 mmol/l), the patient should be encouraged to discuss their
finger prick screening result with their doctor, who should have a
full laboratory-performed fasting lipogram done and then perform
a full cardiovascular risk assessment. Because inappropriately low
results are a concern, TC <2.5 mmol/l on a finger prick test should
be confirmed. Finger prick testing that measures TC alone will not
detect raised triglycerides.

5.5 Additional testing

The use of novel biomarkers of CVD (e.g. hsCRP) and imaging

technologies (e.g. coronary calcium scoring, carotid intima-media
thickness) is not recommended routinely and should be reserved to
refine risk assessment in patients considered to be at moderate risk
where there is uncertainty about whether to initiate drug therapy.8 It
should be noted that hsCRP is a nonspecific inflammatory marker
that may be elevated from many causes (e.g. acute infections or
non-infectious inflammatory disorders). Measuring Lp(a) is only
appropriate in HIGH CVD risk subjects and/or when there is a family

March 2012, Vol. 102, No. 3 SAMJ

179

GUIDELINE
history of premature CVD. When Lp(a) is used as a risk marker, the
cut-off value is >50 mg/dl.

LDL-C goals for patients at different levels of Framingham risk are

listed in Table 4.

5.6 Secondary dyslipidaemias

8. Management of dyslipidaemia

Dyslipidaemia may occur in response to another condition or

treatment. Table 2 lists those encountered most commonly. The
appropriate diagnostic tests should be performed when secondary
dyslipidaemia is suspected and the underlying abnormality treated.

6. Strategy for intervention

Because the total cardiovascular risk is the product of a number

of risk factors, the treatment of dyslipidaemia must always be seen
within the broader framework of cardiovascular disease prevention.

8.1 Lifestyle modification

The risk levels determined for the SCORE system refer to the 10-year
risk of a fatal CVD event, whereas the Framingham scoring system
refers to the 10-year risk of any CVD event. Risk thresholds for the
Framingham score are therefore approximately 3 times those for
SCORE.
Table 3 sets out the recommended appropriate intervention
strategies according to the percentage risk calculated from the
Framingham risk score and the LDL-C value obtained.

It should be emphasised that the cornerstone of any programme to

reduce cardiovascular risk is TLC (healthy diet, regular exercise). In
order for the changes to be sustainable, dietary and exercise advice
must be practical and tailored specifically to the individuals personal
and cultural preferences.11 Diets may need to be modified for people
with unusual or specific disorders (e.g. hypertriglyceridaemia) and
referral to a dietician and fitness professional is encouraged. An
example of lifestyle and dietary advice that is relevant to the South
African population is listed in Appendix 2.

7. Treatment targets

8.2 Dietary supplements

Although we recommend the use of the Framingham risk charts

to estimate cardiovascular risk, the management of patients, once
risk has been determined, and the goals of therapy, are those of the
European guidelines.
Table 2. Secondary causes of dyslipidaemia
Diabetes mellitus
Hypothyroidism
Liver disease
Renal disease, e.g. nephrotic syndrome
Alcohol excess
Medications:
progestins
steroids

Epidemiological and interventional studies support the role of

healthy dietary choices as a whole to help reduce the risk of
cardiovascular events. However, insufficient evidence exists
to recommend the use of dietary supplements in patients with
dyslipidaemia. While some dietary supplements have been shown
to influence plasma lipids, there are no outcomes data that show
benefits with regard to CVD prevention. Conversely, there is evidence
that some supplements may be harmful to health and may interact
with prescription medicines.12,13 Consumers should be advised to
beware of unsubstantiated advertising claims relating to long-term
health benefits.
Although there are no known risks associated with its use, the
routine use of coenzyme Q10 to reduce statin-related myalgia or
myopathy is not supported by systematic reviews of the medical
literature.14,15

8.3 Statin therapy

antiretroviral agents

Statins have demonstrated effectiveness in both primary and

secondary prevention. The effect is dependent on the extent to
which LDL-C is lowered and not on the type of statin used. At their

retinoids

Table 3. Intervention strategies as a function of Framingham total CVD risk score and LDL-C levels3*
Total CVD risk score

LDL-C levels
<1.8 mmol/l

1.8 - <2.5 mmol/l

2.5 - 4.9 mmol/l

>4.9 mmol/l

<3%
Low risk

No lipid intervention

No lipid intervention

Lifestyle intervention

Lifestyle intervention,
consider drug if
uncontrolled

3 - 15%
Moderate risk

Lifestyle intervention

Lifestyle intervention

Lifestyle intervention,
consider drug if
uncontrolled

Lifestyle intervention,
consider drug if
uncontrolled

15 - 30%
High risk

Lifestyle intervention,
consider drug

Lifestyle intervention,
consider drug

Lifestyle intervention
and immediate drug
intervention

Lifestyle intervention
and immediate drug
intervention

>30%
Very high risk

Lifestyle intervention,
consider drug

Lifestyle intervention
and immediate drug
intervention

Lifestyle intervention
and immediate drug
intervention

Lifestyle intervention
and immediate drug
intervention

Based on Table 3 from Reiner , et al., Eur Heart J 2011;32:1769-1818.3

Based on the Framingham CVD risk tables.9
In patients with MI, statin therapy should be considered regardless of LDL-C levels.

180

March 2012, Vol. 102, No. 3 SAMJ

GUIDELINE

Table 4. LDL-C treatment targets

Total Framingham CVD risk (%)

ESC/EAS risk classification

ESC/EAS LDL-C target

<3

Low risk

<3.0 mmol/l

3 - 15

Moderate risk

<3.0 mmol/l

15 - 30

High risk

<2.5 mmol/l

>30

Very high risk

<1.8 mmol/l

maximum doses, the various statins differ in their capacity to lower

LDL-C.
For every mmol/l reduction in LDL-C there is a:

10% reduction in mortality

20% reduction in all-cause morbidity

23% reduction in major cardiac events

17% reduction in stroke.
The effect of statin therapy is similar in all patient subgroups and
becomes significant after 1 year, increasing progressively thereafter.

8.4 High-dose simvastatin treatment

Although the incidence of myopathy is very low for all the statins, it
is approximately 3 times as high with 80 mg simvastatin compared
with maximum doses of atorvastatin and rosuvastatin. Accordingly,
the American Food and Drug Administration (FDA) has mandated
safety-labelling changes for medicines containing simvastatin, which
include the following recommendations:16

The use of 80 mg simvastatin should be restricted to those who
have been using the dose chronically (longer than 12 months),
without signs or symptoms of myopathy.

Patients who are using simvastatin 80 mg and who need to start
taking another drug that may interact with simvastatin should
be switched to an alternative statin with a lower risk of drug
interactions, such as rosuvastatin or atorvastatin.

Patients who do not reach their LDL-C goal with 40 mg
simvastatin should be switched to an appropriate alternative
more potent statin with a lower potential for myopathy.

To reduce the incidence of myopathy:

do not exceed 10 mg simvastatin with amiodarone, verapamil,
or diltiazem

do not exceed 20 mg simvastatin with amlodipine

simvastatin is contraindicated with azole antifungals,
macrolide antibiotics, HIV protease inhibitors, gemfibrozil,
cyclosporine and danazol.

8.5 Statin toxicity

When used in appropriate patients, statins are remarkably safe

drugs and the benefits of cardiovascular protection far outweigh
the potential for toxicity. However, patients should be encouraged
to make and sustain healthy lifestyle choices and the lowest dose of
statin to achieve LDL-C target should be used.
8.5.1 Statin-related myalgia and rhabdomyolysis
The presence of any musculoskeletal pain should be documented
before starting statin therapy to facilitate the recognition of statininduced myalgia during treatment.
A CK measurement prior to commencing statin treatment is
recommended. Statins should not be started if the CK is >5 times
the ULN. Routine CK monitoring is not necessary during treatment,
unless the patient develops myalgia. Increased vigilance regarding
CK and myopathy is necessary in the elderly, in those on concomitant

interfering treatment or on multiple medications, and in the presence

of liver or renal disease.
If myalgia develops and the CK is >5 times the ULN:

stop treatment

check renal function

monitor CK every 2 weeks

consider causes of transient CK elevation, e.g. exercise

consider alternative causes of myopathy.
If myalgia develops and the CK is <5 times the ULN:

monitor symptoms

monitor CK regularly.
If the CK is <5 times the ULN and there are no muscle symptoms:

continue statin

alert patient to report symptoms

consider monitoring CK.
The incidence of rhabdomyolysis is very low.
In patients who are intolerant to statin therapy, potent statins, such
as atorvastatin or rosuvastatin, may be used on alternate days (e.g.
Monday, Wednesday, Friday) or even less frequently to reduce sideeffects.17 Alternatively, a combination therapy of a low-dose statin
with a lipid-lowering drug of another class (e.g. ezetimibe) can be
considered.
8.5.2 Statin-induced rises in alanine aminotransferase
Baseline ALT measurement should be performed before initiating
treatment with a statin. If the ALT is normal, it does not need to
be repeated. Raised ALT does not exclude statin therapy, where
treatment should be individualised. Alternative reasons for raised
ALT (e.g. haemochromatosis, fatty liver) should be investigated
where necessary.
If the ALT is raised <3 times the ULN while on treatment, continue
the statin and recheck ALT in 4 - 6 weeks. If the ALT is raised >3
times the ULN on treatment, stop the statin and repeat ALT in 4 - 6
weeks. Cautious reintroduction of the statin can be considered once
the ALT has returned to normal.
8.5.3 New-onset diabetes
Recent meta-analyses have demonstrated a very small increase in
the risk of new-onset diabetes associated with statin use, notably
in patients treated with intensive-dose statin therapy and in older
patients.18,19 However, this small potential adverse risk is outweighed
by the absolute reduction in CV events and should not discourage
initiation of statin therapy.3,19,20

8.6 Scheme for introducing statin treatment

First evaluate the risk.

Involve the patient in CV risk management decisions.
Identify the appropriate LDL-C target.
Calculate % reduction in LDL-C required to reach target.
Choose the statin (and dose) able to achieve the desired
reduction (Table 5).

March 2012, Vol. 102, No. 3 SAMJ

181

GUIDELINE

Table 5. Practical guide to initiating statins depending on baseline LDL-C and target LDL-C values*
Goal: <1.8 mmol/l

Goal: <2.5 mmol/l

% reduction
required

>6.2

>70

Rosuvastatin 40 mg
Atorvastatin 80 mg

>60

Rosuvastatin 40 mg
Atorvastatin 80 mg

>55

Rosuvastatin 40 mg
Atorvastatin 80 mg

5.2 - 6.2

65 - 70

Rosuvastatin 40 mg
Atorvastatin 80 mg

50 - 60

Rosuvastatin 20 mg
Atorvastatin 40 mg

40 - 55

Rosuvastatin 10 mg
Atorvastatin 20 mg

40 - 50

Rosuvastatin 10 mg
Atorvastatin 20 mg
Simvastatin 40 mg

30 - 45

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 20 mg
Lovastatin 40 mg
Fluvastatin 80 mg

25 - 30

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 10 mg
Lovastatin 20 mg
Pravastatin 40 mg
Fluvastatin 80 mg

25 - 35

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 10 mg
Lovastatin 20 mg
Pravastatin 40 mg
Fluvastatin 80 mg

10 - 25

Any statin at lowest

dose

35 - 45

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 20 mg
Lovastatin 40 mg
Fluvastatin 80 mg

10 - 25

Any statin at lowest

dose

<10

Any statin at lowest

dose

22 - 35

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 10 mg
Lovastatin 10 mg
Pravastatin 20 mg
Fluvastatin 40 mg

<10

Any statin at lowest

dose

<22

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 10 mg
Lovastatin 10 mg
Pravastatin 20 mg
Fluvastatin 40 mg

4.4 - 5.2

3.9 - 4.4

3.4 - 3.9

2.9 - 3.4

2.3 - 2.9

1.8 - 2.3

60 - 65

55 - 60

45-55

Statin dose

Rosuvastatin 40 mg
Atorvastatin 80 mg

Rosuvastatin 40 mg
Atorvastatin 80 mg

Rosuvastatin 10 mg
Atorvastatin 40 mg

% reduction
required

Goal: <3.0 mmol/l

Starting LDL-C
(mmol)

35 - 40

Statin dose

Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 20 mg
Lovastatin 40 mg
Fluvastatin 80 mg

% reduction
required

Statin dose

*Based on weighted average of pooled analysis at starting dose. Dose should be titrated according to response.
Maximum LDL-C reduction achievable with high-dose statin monotherapy is 50 - 60%. To achieve a reduction in LDL-C of >60%, another cholesterol-lowering agent in addition to statin therapy
may be required.
Adapted from Reiner , et al., Eur Heart J 2011;32:1769-18183 and Weng T-C, et al., J Clin Pharm Ther 2010;35:139-151.21

It is mandatory to up-titrate the dose to achieve the LDL-C

target.
If target is not reached at maximal dose, consider a more potent
statin or add a lipid-lowering drug from another class.
The final statin choice will be influenced by concomitant
conditions, concomitant drug therapy and tolerability.

8.7 Other cholesterol-lowering agents

The cholesterol absorption inhibitor ezetimibe in combination

with simvastatin was shown to reduce major atherosclerotic events
in patients with advanced chronic kidney disease.22 Although

182

March 2012, Vol. 102, No. 3 SAMJ

no other outcome studies have been completed, ezetimibe is

recommended:

as second-line treatment in combination with a statin when the
LDL-C target is not reached at the highest tolerated statin dose

when there is intolerance to statins

when there is a contraindication to a statin.
Bile acid sequestrants and nicotinic acid have cholesterollowering properties. They may occasionally be useful alone or
in combination with statin therapy. However, their side-effects
limit wider application.

GUIDELINE
8.8 Treatment directed at other components of the lipid
profile

Whereas low levels of HDL-C and high levels of TG are undoubtedly

associated with a higher cardiovascular disease risk, no currently
available treatment directed at reversing these changes has been
shown to significantly benefit cardiovascular outcome.
A high triglyceride level, particularly if >10 mmol/l, can result in
acute pancreatitis and should be treated without delay.

9. Special circumstances
9.1 Metabolic syndrome

The European Guidelines recognise the importance of identifying

patients with the metabolic syndrome, who are at increased risk of
cardiovascular disease. The presence of the syndrome approximately
doubles the risk of cardiovascular disease. Lifestyle changes,
particularly reducing body weight and increasing physical activity,
are the cornerstone of management of the metabolic syndrome.23

9.2 Acute coronary syndromes

A lipid profile should be obtained at the time of admission in patients

presenting with ACS. They should be treated with high-dose statin
therapy during their acute care and the statin dose should be adjusted
at the time of discharge according to the admission lipid profile.

9.3 HIV infection

Dyslipidaemia frequently accompanies HIV and may be aggravated

by ARVs. While there is limited information, particularly in South
Africa, it is important to measure lipids in patients with HIV and
estimate their CVD risk, and a full lipogram should be performed
before initiating ARV treatment. The Framingham tables will
generally underestimate CVD risk in this population. In patients
with high lipid levels already on ARV treatment, switching to an
alternative ARV and cautious use of a statin or fibrate as necessary
should be considered. Simvastatin is contraindicated in patients using
protease inhibitors.

9.4 Unusual conditions

Unexplained cutaneous or tendinous deposits (xanthomata),

very premature vascular disease, some endocrine, metabolic and
neurological disorders constitute reasons for referral. Unusually low
TC (<2.5 mmol/l), LDL-C (<1.5 mmol/l), HDL-C (<0.7 mmol/l) or
unusually high TG (>10mmol/l), TC (>15 mmol/l), LDL-C (>12
mmol/l), HDL-C (>2.5 mmol/l) also deserve special consideration.

10. Conclusions: implementation of

the 2011 guidelines

In order to implement the guidelines, we propose a simple chart that

has been updated to accommodate the new Framingham CVD risk
tables (Appendix 1). The chart is a guide to management only and
should not replace an individualised assessment and treatment plan
based on the clinical judgement of the doctor. We encourage the
reader to read the 2011 European guidelines in full, which may be
accessed on the ESC website www.escardio.org/guidelines. We hope
that dissemination of these guidelines will go some way towards
helping to reduce the burden of CVD in South Africa.

11. Mechanism of guideline

preparation

In October 2011 a broad-based group of participants from the medical

and allied health community, medical funders, pharmaceutical
companies, the Department of Health, the Board of Health Funders
and the Heart and Stroke Foundation met together with Professor

Marja-Riitta Taskinen in Sandton, Johannesburg, to examine and

discuss the joint ESC/EAS dyslipidaemia guidelines. Professor
Taskinen is a co-author and Task Force Member of these guidelines
and attended on behalf of the European Atherosclerosis Society.
The following day a writing committee met to construct the South
African Consensus Document.
Additional delegates attending the Dyslipidaemia Guidelines
Meeting Discussion Group were Dr A Amod (SEMDSA), Ms G
Bartlett (Universal Health), Ms U Behrtel, Dr S Bhana (Netactive),
Ms M Campbell (Discovery), Mr D Craythorne (Cipla), Mr A
Dansay (PharmaDynamics), Ms L Doms (Medscheme), Ms A du
Plessis (Vital Health), Ms U du Preez (Astra Zeneca), Dr R Espaillat
(Abbott Laboratories), Dr Craige Golding (Solal Laboratories), Ms
K Jamaloodien (National Department of Health), Dr D Katzman
(MSD), Dr S Kahn, Mr M Lambert (Aspen), Dr M Makotoko, Mr M
Mashego (Adcock Ingram), Ms Y Misra (MediKredit), Dr M Mpe,
Dr V Mungai-Singh (Heart and Stroke Foundation), Ms L Naidoo
(Sanlam Healthcare), Ms N Nel, Dr R Patel (Board of Healthcare
Funders), Ms D Pithey (MSD), Mr J Rall (Ranbaxy), Dr J Snyman
(Agility Global Health Solutions), Dr M Sussman (SA Heart), Dr
M Swanepoel (Medihelp), Professor J P van Niekerk (South African
Medical Journal), Ms L Xiphu (QUALSA/Metropolitan).
References
1. De Backer G, Ambrosioni E, Borch-Johnson K, et al. European guidelines on cardiovascular disease
prevention in clinical practice. Eur Heart J 2003;24:1601-1610.
2. South African Medical Association and Lipid and Atherosclerosis Society of Southern Africa Working
Group. Diagnosis, management and prevention of the common dyslipidaemias in South Africa
Clinical Guideline, 2000. S Afr Med J 2000;90:164-178.
3. Reiner , Catapano AL, De Backer G, et al, for the Task Force for the management of dyslipidaemias of
the European Society for Cardiology (ESC) and the European Atherosclerosis Society (EAS). ESC/EAS
guidelines for the management of dyslipidaemias. Eur Heart J 2011;32:1769-1818.
4. Steyn K. Heart disease in South Africa. Media data document. Heart and Stroke Foundation South
Africa, July 2007.
5. Steyn K, Sliwa K, Hawken S, et al. Risk factors associated with myocardial infarction in Africa. The
INTERHEART Africa Study. Circulation 2005;112:3554-3561.
6. Yusuf S, Hawken S, unpuu S. Effect of potentially modifiable risk factors associated with myocardial
infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004;364(9438):937952.
7. National Institutes of Health, National Heart, Lung & Blood Institute. Third Report of the National
Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High
blood Cholesterol in Adults (Adult Treatment Panel III). Executive Summary. NIH Publication No.
01-3670, May 2001. Bethesda, Md, 2001.
8. Mosca L, Benjamin EJ, Berra K, et al. Effectiveness-based guidelines for the prevention of
cardiovascular disease in women 2011 update: A guideline from the American Heart Association.
Circulation 2011;123:1243-1262.
9. DAgostino RB, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care:
the Framingham Heart Study. Circulation 2008;117:743-753.
10. Batki AD, Nayyar P, Thomason HL. Buyers guide: Point-of-care testing for cholesterol measurement.
NHS Purchasing and Supply Agency. Center for Evidence-based Purchasing. CEP 09020; September
2009. http://www.healthcheck.nhs.uk/Library/pointofcare_testing_for_cholesterol_measurement.pdf
(accessed 26 October 2011).
11. Sacks F, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat,
protein, and carbohydrates. N Engl J Med 2009;360(9):859-873.
12. VioliI F, Pignatelli P, Basili S. et al. Nutrition, supplements and vitamins in platelet functions and
bleeding. Circulation 2010;121:1033-1044.
13. Mursu J, Robien K, Harnack LJ, et al. Dietary supplements and mortality rate in older women. The
IOWA Womens Health Study. Arch Intern Med 2011;171(18):1625-1633.
14. Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy. A systematic
review. J Am Coll Cardiol 2007;49(23):2231-2237.
15. Schaars CF, Stalenhoef AFH. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr
Opin Lipidol 2008;19:553-557.
16. Egan A, Coleman E. Weighing the benefits of high-dose simvastatin against the risk of myopathy. N
Engl J Med 2011;365(4):285-287.
17. Eckel RH. Approach to the patient who is intolerant of statin therapy. J Clin Endocrinol Metab
2010;95(5):2015-2022.
18. Preiss D, Seshasai SRK, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with
moderate-dose statin therapy. JAMA 2011;305(24):2556-2564.
19. Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis
of randomised statin trials. Lancet 2010;375(9716):735-742.
20. Rajpathak SN, Kumbhani DJ, Crandall J, et al. Statin therapy and risk of developing type 2 diabetes: A
meta-analysis. Diab Care 2009;32:1924-1929.
21. Weng T-C, Kao Yang Y-H, Lin S-J, et al. A systematic review and meta-analysis on the therapeutic
equivalence of statins. J Clin Pharm Ther 2010;35:139-151.
22. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus
ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): a randomised
placebo controlled trial. Lancet 2011;377:2181-2181.
23. Alberti KGMM, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome. A joint interim
statement of the International Diabetes Federation Task Force on Epidemiology and Prevention;
National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation;
International Atherosclerosis Society; and International Association for the Study of Obesity.
Circulation 2009;120:1640-1645.

March 2012, Vol. 102, No. 3 SAMJ

183

GUIDELINE

Appendix 1. Cardiovascular risk stratification

Framingham 10-year risk assessment chart for patients without diabetes
Risk of CVD: coronary heart disease, stroke, peripheral artery disease, or heart failure
Estimate of 10-year risk of CVD for men
Age (yrs)

184

Points

Estimate of 10-year risk of CVD for women

Age (yrs)

Points

30 - 34

30 - 34

35 - 39

35 - 39

40 - 44

40 - 44

45 - 49

45 - 49

50 - 54

50 - 54

55 - 59

10

55 - 59

60 - 64

11

60 - 64

65 - 69

12

65 - 69

10

70 - 74

14

70 - 74

11

75 years or older

15

75 years or older

12

Total cholesterol (mmol/l)

Points

Total cholesterol (mmol/l)

Points

<4.10

<4.10

4.10 - 5.19

4.10 - 5.19

5.2 - 6.19

5.2 - 6.19

6.20 - 7.20

6.20 - 7.20

>7.20

>7.20

HDL-cholesterol (mmol/l)

Points

HDL-cholesterol (mmol/l)

Points

1.50

-2

1.50

-2

1.30 - 1.49

-1

1.30 - 1.49

-1

1.20 - 1.29

1.20 - 1.29

0.90 - 1.19

0.90 - 1.19

<0.90

<0.90

Systolic BP untreated (mmHg)

Points

Systolic BP untreated (mmHg)

Points

<120

-2

<120

-3

120 - 129

120 - 129

130 - 139

130 - 139

140 - 159

140 - 149

160

150 - 159

160

Systolic BP on
antihypertensive treatment
(mmHg)

Points

Systolic BP on
antihypertensive treatment
(mmHg)

Points

<120

<120

-1

120 - 129

120 - 129

130 - 139

130 - 139

140 - 159

140 - 149

160

150 - 159

160

7
Points

Smoker

Points

Smoker

No

No

Yes

Yes

March 2012, Vol. 102, No. 3 SAMJ

GUIDELINE

Points total for men

Points total for women

Points total

10-year risk (%)

Points total

10-year risk (%)

-3 or less

<1

-2 or less

<1%

-2

1.1

-1

1.0

-1

1.4

1.1

1.6

1.5

1.9

1.8

2.3

2.1

2.8

2.5

3.3

2.9

3.9

3.4

4.7

3.9

5.6

4.6

6.7

5.4

7.9

10

6.3

10

9.4

11

7.4

11

11.2

12

8.6

12

13.2

13

10.0

13

15.6

14

11.6

14

18.4

15

13.5

15

21.6

16

15.6

16

25.3

17

18.1

17

29.4

18

20.9

18 or more

>30

19

24.0

20

27.5

20 or more

>30

Point totals indicate the 10-year risk of cardiovascular disease (coronary, cerebrovascular and peripheral arterial disease, and heart failure).
Low risk Moderate risk High risk Very high risk

Adapted from DAgostino RB, et al., General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation
2008;117:743-7539 and Mosca L, et al., Effectiveness-based guidelines for the prevention of cardiovascular disease in women 2011 update: A
guideline from the American Heart Association. Circulation 2011;123:1243-1262.8

Management and cholesterol goals according to Framingham risk score

Category 1: Individuals considered to be at very high risk who do not need scoring
1. Established atherosclerosis

coronary heart disease

cerebrovascular disease

peripheral vascular disease
2. Type 2 diabetes*
3. Type 1 diabetes with target organ damage
4. Chronic kidney disease (GFR <60 ml/min/1.73 m2)
5. Genetic dyslipidaemias (e.g. familial hypercholesterolaemia)
*In patients with type 2 diabetes younger than age 40 years or with duration of diabetes <10 years and no other CVD risk factors, the LDL-C
target is <2.5 mmol/l.
Goal:
LDL cholesterol <1.8 mmol/l**
**and/or a >50% LDL-C reduction when the LDL-C target cannot be achieved

March 2012, Vol. 102, No. 3 SAMJ

185

GUIDELINE

Category 2: Risk scoring required use the Framingham risk tables

Use correct gender table:

Score:

1. Age

1. ________

2. Total cholesterol

2. ________

3. Non-smoker/smoker

3. ________

4. HDL-C

4. ________

5. Systolic BP

5. ________

Pharmacological treatment is required if LDL cholesterol remains above these levels despite lifestyle modification. At present statins are first-line
drugs for lowering LDL cholesterol.

Secondary causes of dyslipidaemia should be excluded before progressing to risk assessment.

See limitations of Framingham Risk Assessment Score on this page.

Total cholesterol level is used to assign risk score and may be used for follow-up cholesterol measurement in patients on drug therapy, but LDL
cholesterol is the target of treatment.

Limitations of the Framingham Risk Assessment Score charts

1. Patients who are classified in the very high-risk category do not require further risk scoring for management decisions. Risk will also be
underestimated in patients who have a markedly elevated single risk factor (e.g. severe hypertension: systolic BP >180 mmHg and/or diastolic BP
>110 mmHg), or associated target organ damage.
2. Severe hypercholesterolaemia and hypertriglyceridaemia: The Framingham risk assessment chart is only accurate up to total cholesterol values
of 7.25 mmol/l and cannot be used for patients with TC levels above this value. It also does not apply to hypertriglyceridaemia (triglyceride >5
mmol/l).
3. Family history of early atherosclerotic disease is not taken into account. Clinicians should use their judgement in deciding whether to place a
patient with an impressive family history in the high-risk category regardless of their Framingham score.
4. Despite these factors being important risk factors for CVD, impaired glucose tolerance and abdominal obesity are not taken into account in the
risk score.

LDL-C = low-density lipoprotein cholesterol; HDL-C = high-density

lipoprotein cholesterol; TG = triglyceride; CHD = coronary heart
disease; CVD = cardiovascular disease; BP = blood pressure.

186

March 2012, Vol. 102, No. 3 SAMJ

Conversion from mg/dl

Cholesterol:
mmol/l = mg/dl 0.0259
mg/dl = mmol/l 38.6

Triglyceride:
mmol/l = mg/dl 0.0113
mg/dl = mmol/l 88.5

GUIDELINE
Appendix 2. South African Heart Association/LASSA guidelines for lifestyle modification for patients with dyslipidaemia
1.
2.

Stop smoking and avoid exposure to environmental tobacco smoke.

Increase your physical activity. Try to do exercise of moderate intensity, such as brisk walking, for at least 30 minutes on all or most days of
the week.
3. Achieve and maintain ideal body weight.
4. Reduce your intake of saturated fats, trans-fats and cholesterol. Avoid eating fatty meats, processed meats, chicken skin, processed meats,
confectionery such as pies, pastries and cookies, fast foods, deep-fried potato chips (slap chips), butter, ghee, cream, hard cheeses and salty
crackers.
5. Replace saturated fats with unsaturated fats. Avoid the use of hard margarines, butter and ghee for cooking or adding to food. Use
unsaturated fats such as canola oil, olive oil and sunflower oil for cooking. Use oils sparingly and avoid all deep-frying of food. Remove all
visible fat before cooking. Increase your intake of all types of fish, especially oily fish such as sardines and salmon, to a minimum of twice a
week.
6. Increase your intake of fibre, especially soluble fibre. Include foods such as oats, fresh fruit and legumes (dry beans, soya beans, chickpeas,
all types of lentils). Include a minimum of five portions of fresh fruit and vegetables in your daily diet.
7. Replace all refined carbohydrate types of foods with foods high in fibre, such as whole grains. Avoid eating products made from white flour,
such as white bread and rolls, pizzas, vetkoek, samoosas, pies, prego rolls and bakery items such as cakes and biscuits. Incorporate wholegrain foods such as oats, barley, stampkoring (pearl wheat), crushed wheat, samp and beans, brown rice, brown/wild rice, whole-grain
breakfast cereals, health and seed breads.
8. Avoid foods high in free sugars (sucrose, high-fructose corn syrup, fructose) such as sweets, chocolates, all fizzy soft drinks, fruit juices, all
flavoured and sweetened waters, low-fat sweetened milky drinks.
9. If you consume alcohol, do so in moderation no more than 2 drinks for men and 1 drink for women per day.
10. Avoid adding salt to food after cooking. Choose and prepare foods with little or no salt by using more herbs and spices.
11. For dietary lifestyle intervention all patients should ideally be referred to a registered dietician.

Notes

188

March 2012, Vol. 102, No. 3 SAMJ