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Drug therapy for coronary heart disease: the Sheffield table
THE LANCET
I agree with Barber that the Royal Colleges need to be more supportive of their ordinary fellows and members and more aware of their concerns. I hope there will be a flood of letters in response to Barber’s refreshing opening shot and that copies will be sent to the relevant bodies. I suspect, however, that it is far too late and we are now all too weary. Bill Alexander Western General Hospital, Edinburgh EH4 2XU, UK 1
Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
Sir—You announced Sir Kenneth Calman’s resignation as chief medical officer, Department of Health (Oct 11, p 1084)1 one week after Philip Barber’s commentary2 pointing out the problems resulting from the Calman reforms. I wonder if this means that he has now realised the terrible damage he has done to the hospital service. Calman will be remembered for destroying the spirit and structure of the consultant body in UK hospitals. Doubtless, he will be rewarded with a peerage for succeeding where successive governments have failed. Peter Daggett Staffordshire General Hospital, Stafford ST16 3SA 1 2
Anon. Calman to move on. Lancet 1997; 350: 1084. Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
training—when the objectives of their training programmes have been met and they have demonstrated clinical skills to an agreed standard. Although time in the training grades is diminishing overall, the minimum time prescribed by college training programmes has, by and large, not altered in most specialties. Of course, the reforms of specialist training are not being achieved effortlessly. However, the scale of change already achieved has been substantial. Concerns regarding the impact of the reforms, particularly in respect of uncertainties about the characteristics of new certificate holders and the balance between education and service provision have been raised, and these need to be properly and thoroughly evaluated. That is why the Department of Health has commissioned the Joint Centre for Education in Medicine to carry out a full evaluation of the reforms over a 2-year period. The centre’s evaluation, which involves every deanery in England and Wales, will address these concerns and others resulting from the introduction of the reforms. A paper will be published in the new year, charting the reform process and considering its impact in more detail. Kenneth C Calman Department of Health, Richmond House, London SW1A 2NS, UK 1
Kenneth Calman replies SIR—Philip Barber’s commentary1 on the reforms of higher specialist training, and the subsequent correspondence that it has prompted, raise several important issues that challenge everyone involved with introducing the reforms. Although it would not be appropriate to address these in detail here, I would like to offer one or two initial observations. I do not accept, as Barber seems to suggest, that structured training with progressive assessment is worthless. Although British postgraduate medical education has traditionally enjoyed a well deserved international reputation of excellence it also had some well documented deficiencies. These included the lack of planned and structured training programmes. As a result, trainees often spent time duplicating elements of their training or seeking appointments in which to gain specific experience. Compare this with the situation today, in which trainees follow planned training programmes encompassing flexibility, choice, competition, and regular assessments of progress. Trainees now know when they can expect to complete their
1852
Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
Drug therapy for coronary heart disease: the Sheffield table SIR—A F Jones (Oct 18, p 1174)1 is wrong to suggest that targeted primary prevention with statins for individuals with a 3% annual risk of coronary heat disease (CHD) using the Sheffield table,2 as endorsed by the Standing Medical Advisory Committee guidance, is arbitrary or based on costeffectiveness alone. The recommendation was also based on individual benefit, population implications, and the total cost of treatment.2,3 The evidence on these variables is arguably stronger for statins than for any treatment in wide use. He is correct to point out that the Sheffield table, which is based on total cholesterol,2 and uses population mean values for high-density lipoprotein (HDL) cholesterol, will underestimate the risk of CHD in patients with type II diabetes. But the error is small on average. In the Framingham population,4 diabetics had lower HDL
concentrations than non-diabetics, by an average of 4·3% in men and 6·9% in women. Because of this, the Sheffield table targets an annual mean CHD risk of about 3·1% in diabetic men and 3·2% in women, rather than the 3·0% intended. This error is negligible compared with that of not using any formal method of CHD-risk assessment. The Sheffield table will be more inaccurate in individuals whose HDL cholesterol differs substantially from the population mean, and this is stated clearly in the footnotes to the table. A Sheffield table based on the total/HDL cholesterol ratio5 is available on request for those who wish a more precise assessment of CHD risk. We have not advocated wide use of the total/HDL cholesterol ratio in the Sheffield table because of concern that non-specialist doctors may be uncomfortable with this ratio, and because many laboratories do not report the ratio routinely. Perhaps Jones is jesting when he suggests that laboratories might calculate the risk of CHD from the lipids and clinical information. Our understanding is that most clinicians are reluctant to write the patient’s name on the laboratory request form—will they really provide age, sex, smoking habit, blood pressure, and the presence or absence of diabetes or left-ventricular hypertrophy? *E J Wallis, L E Ramsay, P R Jackson, W W Yeo, R Williamson Section of Clinical Pharmacology and Therapeutics, Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK 1
2
3
4
5
Jones AF. Statins and hypercholesterolaemia: UK Standing Medical Advisory Committee guidelines. Lancet 1997; 30:1174–75. Ramsay LE, Haq IQ, Jackson PR, Yeo WW, Pickin DM, Payne JN. Targeting lipidlowering drug therapy for primary prevention of coronary disease: an updated Sheffield table. Lancet 1996; 348: 387–88. Haq IU, Ramsay LE, Pickin DM, Yeo WW, Jackson PR, Payne JN. Lipid-lowering for prevention of coronary heart disease: what policy now?. Clin Sci 1996; 91: 399–413. Kannel WB. Lipids,diabetes, and coronary heart disease: insights from the Framingham Study. Am Heart J 1985; 110: 1100–07. Haq IU, Jackson PR, Yeo WW, Ramsay LE. A comparison of methods for targeting CHD risk for primary prevention. Heart 1997; 77 (suppl 1): 36.
SIR—We were delighted to receive formal governmental approval and the recommendations provided by the Standing Medical Advisory Committee that statins should be used routinely in clinical practice for the prevention of cardiovascular disease. Whilst we generally agree with the recommendations on the use of statins for secondary prevention, we do not
Vol 350 • December 20/27, 1997
THE LANCET
believe that it is appropriate for the Sheffield tables1 to be used as the benchmark to decide if and when patients should receive lipid-lowering therapy in the context of primary prevention. Primary prevention studies (eg, WOSCOPS)2 have shown benefit from statin therapy for a large proportion of society. Therefore, for financial reasons, some method of selection should be applied to distinguish patients most suitable to receive statins. The Sheffield tables are inadequate and misleading for this purpose. According to the tables, all women with diabetes and men with diabetes younger than 58 years should not have their lipids measured. This contradicts all national and international guidelines and optimum medical practice for managing diabetes. The tables also suggest that all women with hypertension and all men with hypertension younger than 60 years should not have their lipids measured. Again, this contradicts all national and international guidelines and optimum medical practice for managing hypertension. The tables are also limited in terms of the number of relevant and important indices compared with other scores. As A F Jones3 points out, the exclusion of high-density lipoprotein (HDL) cholesterol is particularly important since it has a major impact on risk, especially in the context of diabetes and as part of the insulin-resistance syndrome.4 The tables imply that lipid concentrations are only important in the presence of other major risk factors, which is no more or less true for dyslipidaemia than for hypertension or diabetes. The tables are based on estimates of absolute risk of a coronary event of 30% in the next 10 years. More appropriate evaluations of risk should also consider risk among people of the same age and sex, that is, the relative risk. For example, the score suggests that a 70year-old man who is a smoker should have his lipids treated if his total cholesterol is 5·5 mmol/L. Such a patient’s risk, relative to the average 70year-old, is hardly raised. Taken to its logical conclusion, we would treat all 80-year-old men with a statin, irrespective of their lipid concentration, because they all have an annual risk of 3%. We are only protected from such a nonsensical approach because we do not have trial data to show the benefits of lipid lowering in 80-year-olds—yet! Ideally, therefore, such a table should be weighted for potential life-years gained. That is to acknowledge that, for example, men aged 70 and 40 years have on average about 11 and 33 years,
Vol 350 • December 20/27, 1997
respectively, to live. Furthermore, the 3% level of annual risk on which the tables are based is at odds with other previously published guidelines which recommend that a 2% per annum risk merits intervention.5 Such conflicting information merely adds to the current confusion about lipid lowering. The New Zealand guidelines, referenced in the recent Standing Medical Advisory Committee report, allow six risk factors stratified by age and sex to be used in assessment of risk. These guidelines do not pre-empt the decision to measure lipids, allow the patient and doctor to consider the degree of risk, and are more userfriendly than the Sheffield tables. *N R Poulter, K G M M Alberti, D G Beevers, D J Betteridge, R W F Campbell Cardiovascular Studies Unit, Department of Clinical Pharmacology and Therapeutics, Imperial College School of Medicine, London W2 1PG, UK 1
2
3
4
5
Ramsey LE, Haq IQ, Yeo WW. The Sheffield table for primary prevention of coronary heart disease: corrected. Lancet 1996; 348: 1251–52. Shepherd J, Cobbe SM, Ford I, et al. West of Scotland Prevention Group (WOSCOPS). Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia. N Eng J Med 1995; 333: 1301–07. Jones AF. Statins and hypercholesterolaemia: UK Standing Medical Advisory Committee guidelines. Lancet 1997; 30:1174–75. Assman G, Schulte H. Relation of highdensity lipoprotein cholesterol and tryglicerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience). Prospective Cardiovascular Munster Study. Am J Cardiol 1992; 70: 733–37. Pyorala K, de Racher G, Graham I, PooleWilson P, Wood D. Prevention of coronary heart disease in clinical practice. Recommendations of the Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Euro Heart J 1994; 15: 1300–31.
SIR—The UK Department of Health’s recent guidelines on statins suggest that a major coronary event rate of 3% or more per annum, based on the Sheffield risk table, should be used as guide to prescribing statins for the primary prevention of coronary heart disease (CHD). The laudable purpose of the Sheffield table is to provide a simplified, user-friendly means of rationalising who should receive preventive therapy for the primary prevention of CHD which is “acceptably accurate”.1 We agree with A F Jones2 on the limitations of the Sheffield table for diabetic patients. The table suggests that event rates in male non-smokers with diabetes and hypertension aged 50 years or younger are too low to warrant treatment. We used data from the WHO Multinational
Study of Vascular Disease in Diabetes3 to calculate that such men aged 45–50 years had an event rate of 3·0% per annum when their total cholesterol was just 6·8 mmol/L, much lower than is recommended for intervention, even up to age 60, in the Sheffield table. Furthermore, diabetes-specific risk factors, such as glycaemic control and diabetic nephropathy, have a substantial effect on CHD risk in patients with diabetes. Any risk equation that does not take these, routinely available, clinical data into consideration is likely to be inaccurate. The Sheffield table assumes that the proportional benefit from statin treatment is constant whatever the initial CHD risk and irrespective of the origin of a given risk. However, in the Cholesterol and Recurrent Events (CARE) Study4 there was a significant interaction between the treatment effect and low-density lipoprotein (LDL) at entry (p<0·03). Patients whose LDL concentration was above 3·9 mmol/L at entry had a relative-risk reduction of 35% compared with a non-significant relative-risk reduction of 15% in those with LDL of less than 3·36 mmol/L at entry and a higher event rate in the treated group in those with LDL less than 3·2 mmol/L at entry (p>0·05). Patients in the CARE study whose triglycerides were above the median at entry had half the relative-risk reduction of those with triglycerides below the median. This is particularly important for diabetes because it implies that the numbers needed to treat to prevent an event could be much higher in individuals with high triglycerides compared with non-diabetic patients with the same initial degree of CHD risk. Conversely, the Scandinavian Simvastatin Survival Study5 showed that diabetic patients (with higher cholesterol concentrations than in CARE) had a greater relative-risk reduction than nondiabetic patients. A valid argument is that in the absence of better data, the Sheffield table is a reasonable approach and that for treatment guidelines to be feasible they must oversimplify. However, collection of data to allow more accurate estimates of risk and benefits of treatment, is needed, particularly at low LDL concentrations. A diabetes-specific risk table would also be useful. *Helen Colhoun, John Fuller Eurodiab Co-ordinating Centre, Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK 1
Ramsay LE, Haq IU, Jackson PR, Yeo WW. The Sheffield table for primary prevention of coronary heart disease: connected. Lancet 1996; 348: 1251–52.
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I agree with Barber that the Royal Colleges need to be more supportive of their ordinary fellows and members and more aware of their concerns. I hope there will be a flood of letters in response to Barber’s refreshing opening shot and that copies will be sent to the relevant bodies. I suspect, however, that it is far too late and we are now all too weary. Bill Alexander Western General Hospital, Edinburgh EH4 2XU, UK 1
Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
Sir—You announced Sir Kenneth Calman’s resignation as chief medical officer, Department of Health (Oct 11, p 1084)1 one week after Philip Barber’s commentary2 pointing out the problems resulting from the Calman reforms. I wonder if this means that he has now realised the terrible damage he has done to the hospital service. Calman will be remembered for destroying the spirit and structure of the consultant body in UK hospitals. Doubtless, he will be rewarded with a peerage for succeeding where successive governments have failed. Peter Daggett Staffordshire General Hospital, Stafford ST16 3SA 1 2
Anon. Calman to move on. Lancet 1997; 350: 1084. Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
training—when the objectives of their training programmes have been met and they have demonstrated clinical skills to an agreed standard. Although time in the training grades is diminishing overall, the minimum time prescribed by college training programmes has, by and large, not altered in most specialties. Of course, the reforms of specialist training are not being achieved effortlessly. However, the scale of change already achieved has been substantial. Concerns regarding the impact of the reforms, particularly in respect of uncertainties about the characteristics of new certificate holders and the balance between education and service provision have been raised, and these need to be properly and thoroughly evaluated. That is why the Department of Health has commissioned the Joint Centre for Education in Medicine to carry out a full evaluation of the reforms over a 2-year period. The centre’s evaluation, which involves every deanery in England and Wales, will address these concerns and others resulting from the introduction of the reforms. A paper will be published in the new year, charting the reform process and considering its impact in more detail. Kenneth C Calman Department of Health, Richmond House, London SW1A 2NS, UK 1
Kenneth Calman replies SIR—Philip Barber’s commentary1 on the reforms of higher specialist training, and the subsequent correspondence that it has prompted, raise several important issues that challenge everyone involved with introducing the reforms. Although it would not be appropriate to address these in detail here, I would like to offer one or two initial observations. I do not accept, as Barber seems to suggest, that structured training with progressive assessment is worthless. Although British postgraduate medical education has traditionally enjoyed a well deserved international reputation of excellence it also had some well documented deficiencies. These included the lack of planned and structured training programmes. As a result, trainees often spent time duplicating elements of their training or seeking appointments in which to gain specific experience. Compare this with the situation today, in which trainees follow planned training programmes encompassing flexibility, choice, competition, and regular assessments of progress. Trainees now know when they can expect to complete their
1852
Barber P. The colleges, Calman, and the new deal. Lancet 1997; 350: 974.
Drug therapy for coronary heart disease: the Sheffield table SIR—A F Jones (Oct 18, p 1174)1 is wrong to suggest that targeted primary prevention with statins for individuals with a 3% annual risk of coronary heat disease (CHD) using the Sheffield table,2 as endorsed by the Standing Medical Advisory Committee guidance, is arbitrary or based on costeffectiveness alone. The recommendation was also based on individual benefit, population implications, and the total cost of treatment.2,3 The evidence on these variables is arguably stronger for statins than for any treatment in wide use. He is correct to point out that the Sheffield table, which is based on total cholesterol,2 and uses population mean values for high-density lipoprotein (HDL) cholesterol, will underestimate the risk of CHD in patients with type II diabetes. But the error is small on average. In the Framingham population,4 diabetics had lower HDL
concentrations than non-diabetics, by an average of 4·3% in men and 6·9% in women. Because of this, the Sheffield table targets an annual mean CHD risk of about 3·1% in diabetic men and 3·2% in women, rather than the 3·0% intended. This error is negligible compared with that of not using any formal method of CHD-risk assessment. The Sheffield table will be more inaccurate in individuals whose HDL cholesterol differs substantially from the population mean, and this is stated clearly in the footnotes to the table. A Sheffield table based on the total/HDL cholesterol ratio5 is available on request for those who wish a more precise assessment of CHD risk. We have not advocated wide use of the total/HDL cholesterol ratio in the Sheffield table because of concern that non-specialist doctors may be uncomfortable with this ratio, and because many laboratories do not report the ratio routinely. Perhaps Jones is jesting when he suggests that laboratories might calculate the risk of CHD from the lipids and clinical information. Our understanding is that most clinicians are reluctant to write the patient’s name on the laboratory request form—will they really provide age, sex, smoking habit, blood pressure, and the presence or absence of diabetes or left-ventricular hypertrophy? *E J Wallis, L E Ramsay, P R Jackson, W W Yeo, R Williamson Section of Clinical Pharmacology and Therapeutics, Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK 1
2
3
4
5
Jones AF. Statins and hypercholesterolaemia: UK Standing Medical Advisory Committee guidelines. Lancet 1997; 30:1174–75. Ramsay LE, Haq IQ, Jackson PR, Yeo WW, Pickin DM, Payne JN. Targeting lipidlowering drug therapy for primary prevention of coronary disease: an updated Sheffield table. Lancet 1996; 348: 387–88. Haq IU, Ramsay LE, Pickin DM, Yeo WW, Jackson PR, Payne JN. Lipid-lowering for prevention of coronary heart disease: what policy now?. Clin Sci 1996; 91: 399–413. Kannel WB. Lipids,diabetes, and coronary heart disease: insights from the Framingham Study. Am Heart J 1985; 110: 1100–07. Haq IU, Jackson PR, Yeo WW, Ramsay LE. A comparison of methods for targeting CHD risk for primary prevention. Heart 1997; 77 (suppl 1): 36.
SIR—We were delighted to receive formal governmental approval and the recommendations provided by the Standing Medical Advisory Committee that statins should be used routinely in clinical practice for the prevention of cardiovascular disease. Whilst we generally agree with the recommendations on the use of statins for secondary prevention, we do not
Vol 350 • December 20/27, 1997
THE LANCET
believe that it is appropriate for the Sheffield tables1 to be used as the benchmark to decide if and when patients should receive lipid-lowering therapy in the context of primary prevention. Primary prevention studies (eg, WOSCOPS)2 have shown benefit from statin therapy for a large proportion of society. Therefore, for financial reasons, some method of selection should be applied to distinguish patients most suitable to receive statins. The Sheffield tables are inadequate and misleading for this purpose. According to the tables, all women with diabetes and men with diabetes younger than 58 years should not have their lipids measured. This contradicts all national and international guidelines and optimum medical practice for managing diabetes. The tables also suggest that all women with hypertension and all men with hypertension younger than 60 years should not have their lipids measured. Again, this contradicts all national and international guidelines and optimum medical practice for managing hypertension. The tables are also limited in terms of the number of relevant and important indices compared with other scores. As A F Jones3 points out, the exclusion of high-density lipoprotein (HDL) cholesterol is particularly important since it has a major impact on risk, especially in the context of diabetes and as part of the insulin-resistance syndrome.4 The tables imply that lipid concentrations are only important in the presence of other major risk factors, which is no more or less true for dyslipidaemia than for hypertension or diabetes. The tables are based on estimates of absolute risk of a coronary event of 30% in the next 10 years. More appropriate evaluations of risk should also consider risk among people of the same age and sex, that is, the relative risk. For example, the score suggests that a 70year-old man who is a smoker should have his lipids treated if his total cholesterol is 5·5 mmol/L. Such a patient’s risk, relative to the average 70year-old, is hardly raised. Taken to its logical conclusion, we would treat all 80-year-old men with a statin, irrespective of their lipid concentration, because they all have an annual risk of 3%. We are only protected from such a nonsensical approach because we do not have trial data to show the benefits of lipid lowering in 80-year-olds—yet! Ideally, therefore, such a table should be weighted for potential life-years gained. That is to acknowledge that, for example, men aged 70 and 40 years have on average about 11 and 33 years,
Vol 350 • December 20/27, 1997
respectively, to live. Furthermore, the 3% level of annual risk on which the tables are based is at odds with other previously published guidelines which recommend that a 2% per annum risk merits intervention.5 Such conflicting information merely adds to the current confusion about lipid lowering. The New Zealand guidelines, referenced in the recent Standing Medical Advisory Committee report, allow six risk factors stratified by age and sex to be used in assessment of risk. These guidelines do not pre-empt the decision to measure lipids, allow the patient and doctor to consider the degree of risk, and are more userfriendly than the Sheffield tables. *N R Poulter, K G M M Alberti, D G Beevers, D J Betteridge, R W F Campbell Cardiovascular Studies Unit, Department of Clinical Pharmacology and Therapeutics, Imperial College School of Medicine, London W2 1PG, UK 1
2
3
4
5
Ramsey LE, Haq IQ, Yeo WW. The Sheffield table for primary prevention of coronary heart disease: corrected. Lancet 1996; 348: 1251–52. Shepherd J, Cobbe SM, Ford I, et al. West of Scotland Prevention Group (WOSCOPS). Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia. N Eng J Med 1995; 333: 1301–07. Jones AF. Statins and hypercholesterolaemia: UK Standing Medical Advisory Committee guidelines. Lancet 1997; 30:1174–75. Assman G, Schulte H. Relation of highdensity lipoprotein cholesterol and tryglicerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience). Prospective Cardiovascular Munster Study. Am J Cardiol 1992; 70: 733–37. Pyorala K, de Racher G, Graham I, PooleWilson P, Wood D. Prevention of coronary heart disease in clinical practice. Recommendations of the Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Euro Heart J 1994; 15: 1300–31.
SIR—The UK Department of Health’s recent guidelines on statins suggest that a major coronary event rate of 3% or more per annum, based on the Sheffield risk table, should be used as guide to prescribing statins for the primary prevention of coronary heart disease (CHD). The laudable purpose of the Sheffield table is to provide a simplified, user-friendly means of rationalising who should receive preventive therapy for the primary prevention of CHD which is “acceptably accurate”.1 We agree with A F Jones2 on the limitations of the Sheffield table for diabetic patients. The table suggests that event rates in male non-smokers with diabetes and hypertension aged 50 years or younger are too low to warrant treatment. We used data from the WHO Multinational
Study of Vascular Disease in Diabetes3 to calculate that such men aged 45–50 years had an event rate of 3·0% per annum when their total cholesterol was just 6·8 mmol/L, much lower than is recommended for intervention, even up to age 60, in the Sheffield table. Furthermore, diabetes-specific risk factors, such as glycaemic control and diabetic nephropathy, have a substantial effect on CHD risk in patients with diabetes. Any risk equation that does not take these, routinely available, clinical data into consideration is likely to be inaccurate. The Sheffield table assumes that the proportional benefit from statin treatment is constant whatever the initial CHD risk and irrespective of the origin of a given risk. However, in the Cholesterol and Recurrent Events (CARE) Study4 there was a significant interaction between the treatment effect and low-density lipoprotein (LDL) at entry (p<0·03). Patients whose LDL concentration was above 3·9 mmol/L at entry had a relative-risk reduction of 35% compared with a non-significant relative-risk reduction of 15% in those with LDL of less than 3·36 mmol/L at entry and a higher event rate in the treated group in those with LDL less than 3·2 mmol/L at entry (p>0·05). Patients in the CARE study whose triglycerides were above the median at entry had half the relative-risk reduction of those with triglycerides below the median. This is particularly important for diabetes because it implies that the numbers needed to treat to prevent an event could be much higher in individuals with high triglycerides compared with non-diabetic patients with the same initial degree of CHD risk. Conversely, the Scandinavian Simvastatin Survival Study5 showed that diabetic patients (with higher cholesterol concentrations than in CARE) had a greater relative-risk reduction than nondiabetic patients. A valid argument is that in the absence of better data, the Sheffield table is a reasonable approach and that for treatment guidelines to be feasible they must oversimplify. However, collection of data to allow more accurate estimates of risk and benefits of treatment, is needed, particularly at low LDL concentrations. A diabetes-specific risk table would also be useful. *Helen Colhoun, John Fuller Eurodiab Co-ordinating Centre, Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK 1
Ramsay LE, Haq IU, Jackson PR, Yeo WW. The Sheffield table for primary prevention of coronary heart disease: connected. Lancet 1996; 348: 1251–52.
1853