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Rapid Responses: Rapid Responses published:
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Should absolute risk rule patient's treatment?
- Richard Neary, Sud Ramachandran (15 March 2000)
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Handheld computer program available
- Daniel Sontheimer (17 March 2000)
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Guidelines galore!
- Dougal Jeffries (21 March 2000)
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Prevention of CVS causes of Disease
- A S Mohamed (12 April 2000)
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Overestimating of risc calculation by the European protocol
- Dirk Van Duppen (5 April 2001)
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Richard Neary, Consultant and Senior Registrar in Chemical Pathology North Staffs Hospital Trust, Sud Ramachandran
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Our recent report "Should treatment recommendations for lipid lowering drugs be based on absolute coronary risk or risk reduction?"1 provoked an interesting editorial view from Professor Jackson2 which warrants further discussion. While we all agree that the chance of preventing a coronary event equals the (absolute risk x relative risk reduction), the point at issue is whether the latter is equal in patients of all ages. The meta-analysis of the statin trials by LaRosa3 cited as evidence for this by Professor Jackson, (together with three hypertension trials), does not render Law’s meta-analysis of lipid-lowering trials4 invalid as LaRosa included both primary and secondary prevention trials assuming the difference between them relates only to the absolute risk of a further event. Our report concerned primary prevention and the two relevant statin trials in this meta-analysis suggest that age may influence risk reduction although formal statistical analyses were not reported. One of these trials (WOSCOPS5) showed a relative risk reduction of 40% (CL 16 - 56) below 55 years of age, compared to 27% (8 - 43) above, the other study (AFCAPS/TexCAPS6) showed a 46.5% risk reduction below the median age (58 years) compared to 30.4% above, both consistent with the age effect predicted by Law’s meta-analysis. Our objective was to highlight the potential for leaving young patients with multiple risk factors untreated by assuming that relative risk reduction is not influenced by age. If treatment is based solely on absolute risk, a male, non-smoking, diabetic, systolic blood pressure 180mmHg, total and HDL cholesterol of 6.0 and 0.9mmol/l would not reach the risk threshold for treatment until 53 years of age. Whereas, adjusted for age, a risk reduction threshold of 4.5% is reached at 42years when absolute risk is 8.9%. During this 11 years his average annual CHD risk is approximately 2.4% giving a cumulative event risk of 27.5%, or more than a 1 in 4 chance of an event through delaying treatment. If this was adjusted for life-years gained as suggested in both our lipid and Professor Jackson’s hypertension treatment study7, the benefit of instituting treatment at an early age would become even more apparent. The aim of treatment recommendations should be to maximise use of available trial data to increase their relevance utilising available computer-based technology where appropriate. The latter enables complex guidelines to be handled with ease in a clinical setting and readily updated as new evidence becomes available. 1. Ramachandran S, French JM, Vanderpump MPJ, Croft P, Neary RH. Should treatment recommendations for lipid lowering drugs be based on absolute coronary risk or risk reduction? BMJ 2000; 320: 677-678 2. Jackson R. Guidelines on preventing cardiovascular disease in clinical practice. BMJ 2000; 320: 659-661. 3. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease. meta-analysis of randomized controlled trials. JAMA 1999; 282: 2340-2346 4. Law MR, Wald NJ, Thompson SG. By how much and how quickly does reduction in serum cholesterol lower risk of ischaemic heart disease? BMJ 1994; 308: 367-372 5. West of Scotland Coronary Prevention Group. West of Scotland coronary prevention study: identification of high-risk groups and comparison with other cardiovascular intervention trials. Lancet 1996; 348: 1339-42 6. Downs JR, Clearfield M, Weis S, Whitney E, Shapiro DR, Beere PA, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. Results of AFCAPS/TexCAPS. JAMA 1998;279:1615-22 7. Baker S, Priest P, Jackson R. Using thresholds based on risk of cardiovascular disease to target treatment for hypertension: modelling events averted and number treated BMJ 2000; 320: 680-685 |
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Daniel Sontheimer, Asst. Prof. of Family Medicine Spartanburg Family Medicine Residency
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I wanted to pass on information, that a handheld computer program is available to calculate absolute risk. It is freely available, at www.statcoder.com, from Austin Physician Productivity. It is based on Framingham data, and provides the 10 year CHD risk, for men and women. |
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Dougal Jeffries, G.P. Salisbury
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The 11th March issue of the BMJ provided a wealth of information and advice on how we might best bring some logical order into our efforts to reduce cardiovascular risk in the population. As a reasonably conscientious GP I read all the relevant papers (some of them twice) and the accompanying editorial, yet came away feeling that I was floundering around in a muddy present rather than striding out into a brave new evidence based future. I want a simple chart (or computer programme, though they don't seem to help much) which will allow me to assess and reduce risk of cardiovascular disease in patients who may or may not already be on hypotensive treatment. I also wish to give patients some idea of the likely treatment benefit they can expect on treatment. If I have understood things correctly, the following statements are true: i. The Sheffield tables allow for hypertensive patients already on treatment; the Joint British Societies' and the New Zealand tables do not. ii. The joint British Societies' tables and the N.Z. tables are easier to use in practice than the Sheffield tables, but by excluding hypertensives already on treatment they are useless for a large number of patients whose risks I wish to address. iii. Only the N.Z. tables include estimates of expected benefit from treatment, in the form of NNTs and events prevented; but they use 5-year total cardiovascular rather than 10-year coronary heart disease risk estimates. iv. The choice between 30%, 15%, or any other cut-off point for 10- year risk is arbitrary and depends on an as yet unrealised consensus or government diktat. v. None of the tables addresses impact on total mortality or morbidity, and their recommendations are therefore of less interest to the individual patient than to the cardiovascular lobby. So, unless and until someone can clear the waters for me, I think I'll just continue to muddle along. Despite my apparent lack of enthusiasm for the cardiovascular cutting edge, I can be contacted on e- mail! Dougal Jeffries |
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A S Mohamed
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Dear Sir, The brouhaha about prevention of deaths from cardiovascular (CVS) diseases (BMJ 11 March 2000) intrigues me. There is a concern that "heart disease is the commonest cause of death in most developed countries and is increasing in poor countries ". It seems to me we are agreed that death is the inevitable end game of life. Therefore, any one of the different causes of death will be the commonest in different populations at different times. It makes little sense to attack death from CVS disease just because it is the commonest cause of death unless you have plans to abolish death like the British Govt. which announced a strategy to 'save' 40% from heart disease deaths by 2010. Is there a guarantee those 'saved' people will not die from other causes of death? Compared to the alternatives like cancer, infectious diseases (e.g. AIDS) or plain senility, death from CVS diseases does not seem to be such a bad option. An unspoken biblical notion that one is entitled to a life of three scores and a half underlines the prevention strategies. But why does one not accept the more plausible equally biblical notion that everybody has a fixed life span? The increase in life expectancy due to environmental changes in developed countries has little to do with the advances in Medicine. These same changes are also the major cause of the change of pattern of causes of death. It seems to me Medicine is being taken over by the interventionists who want to medicalize life from cradle to coffin: spearheaded by health economists, epidemiologists, and some powerful medical editors. The statisticians have done their part by bolstering the conceitedly named 'evidence based medicine '(EBM) which implies that there is no evidence for any other medicine outside its umbrella. They should call it evidence emphasized medicine (EEM) or if they want to be more exact statistics affiliated medicine (SAM). I submit that doctors are not in the business of looking after well people. This is the responsibility of the people themselves primarily, their families, educators, social workers and even politicians. Very soon, clinicians may be found negligent for not carrying out certain primary or secondary preventive measures when their hands are full looking after ill people. The preventive measures should be done elsewhere in leisure areas, work places, and schools where occupational physicians, aided by epidemiologists, health economists, and social workers should be in action. Sincerely, Dr A S Mohamed
MB ChB (Leeds) DTM&H (Liverpool)
MRCP (UK)
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Dirk Van Duppen Antwerp - Belgium
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We calculated prospectively per patient the absolute risk of developing cardiovascular desease in the next 10 years according to the protocol of the European joint task force (ESC) and according to that of the Dutch College of General practitioners (NHG) on 143 patients known in our general practice in Antwerp with at least one cardiovascular risk factor. The ESC protocol estimated the risk per patient on average 8.5% (95% c.i.: 701-908) higher than the Dutch protocol, although they are both based on the same Framingham data. The main difference between the two protocols is that the European protocol takes the total cholesterol as bases, the risc calculation comes in a higher categorie when the HDL is lower than 40 mmol/l. While the Dutch protocol takes the total cholesterol/HDL ratio as bases, and integrates so the cardiovascular protective value of a high HDL. Our results have been published in "Nederlands Tijdschrift voor Geneeskunde", 24 February, 2001. Van Diest E, Wydooghe L, Stoffelen E, Van Duppen D, Seuntjens L, Van der Stuyft P See Medline |
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