versão On-line ISSN 2078-5135
versão impressa ISSN 0256-9574
SAMJ, S. Afr. med. j. vol.102 no.3 Cape Town Mar. 2012
South African dyslipidaemia guideline consensus statement
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 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.
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
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 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 history of premature CVD. When Lp(a) is used as a risk marker, the cut-off value is >50 mg/dl.
5.6 Secondary dyslipidaemias
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
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.
7. Treatment targets
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.
LDL-C goals for patients at different levels of Framingham risk are listed in Table 4.
8. Management of dyslipidaemia
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
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 individual's 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.
8.2 Dietary supplements
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
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 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:
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 CK regularly. If the CK is <5 times the ULN and there are no muscle symptoms:
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).
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 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.
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).
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. [ Links ]
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. [ Links ]
3. Reiner Ž, 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. [ Links ]
4. Steyn K. Heart disease in South Africa. Media data document. Heart and Stroke Foundation South Africa, July 2007. [ Links ]
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. [ Links ]
6. Yusuf S, Hawken S, Ôunpuu S. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004;364(9438):937-952. [ Links ]
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. [ Links ]
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. [ Links ]
9. D'Agostino 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. [ Links ]
10. Batki AD, Nayyar P, Thomason HL. Buyer's 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). [ Links ]
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. [ Links ]
12. VioliI F, Pignatelli P, Basili S. et al. Nutrition, supplements and vitamins in platelet functions and bleeding. Circulation 2010;121:1033-1044. [ Links ]
13. Mursu J, Robien K, Harnack LJ, et al. Dietary supplements and mortality rate in older women. The IOWA Women's Health Study. Arch Intern Med 2011;171(18):1625-1633. [ Links ]
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. [ Links ]
15. Schaars CF, Stalenhoef AFH. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr Opin Lipidol 2008;19:553-557. [ Links ]
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. [ Links ]
17. Eckel RH. Approach to the patient who is intolerant of statin therapy. J Clin Endocrinol Metab 2010;95(5):2015-2022. [ Links ]
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. [ Links ]
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. [ Links ]
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. [ Links ]
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. [ Links ]
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. [ Links ]
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. [ Links ]
Corresponding author: Eric Klug (firstname.lastname@example.org)
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
A joint statement from the South African Heart Association (SA Heart) and the Lipid and Atherosclerosis Society of Southern Africa (LASSA)