Coronary and cardiovascular risk estimation for primary prevention:validation of a new Sheffield table in the 1995 Scottish health survey populationBMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7236.671 (Published 11 March 2000) Cite this as: BMJ 2000;320:671
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Editor - The New Sheffield Table1 and it's alternatives make little
use of a cardinal risk factor that is easy to assess. A family history of
coronary artery disease, especially when premature, is a powerful and
independent indicator of an individual's risk. Failure to include this
element will cause these tables to underestimate the 10 year risk of
cardiovascular disease, and cannot be corrected for by simply adding 6
years to the patients age, as suggested in the Sheffield table. The
increase in risk is variable depending on the exact details of the family
history, the age, and the sex of the patient.
The GISSI-EFRIM investigators2 showed that a family history of MI is an
independent risk factor for MI, with the number of relatives and the age
at which they were affected influencing the strength of the association.
Compared with subjects without a family history, those with one or two
affected first-degree relations had relative risks for MI of 2.0 and 3.0
The danger seems to be greater for women than for men, and is especially
high if a sister is affected. In one study of MI patients under 60 years3,
the cumulative risk to women of IHD before 65 years is almost twice as
high if a sister, rather than a brother is affected (26% vs. 16%).
Using more precise definitions of a positive family history allows for a
more accurate assessment of coronary risk. An Australian survey4 found
that compared with an affected parent, an affected sibling carries a
relative risk of 2.5 for coronary artery disease, regardless of age. Hence
any females defined by the Sheffield table to have a 10 year CHD risk of
15%, but who have an affected sister of similar age, may actually have a
risk of >30%.
Family history of coronary artery disease cannot be ignored and should
feature prominently in all guidelines for primary prevention of
Dr. John Younger
John Hunter Hospital,
1. Wallis EJ, Ramsay LF, Iftikhar UH, Ghahramani P, Jackson PR,
Rowland-Yeo K, Yeo W. Coronary and cardiovascular risk estimation for
primary prevention : validation of a New Sheffield table in the 1995
Scottish health survey population. BMJ 2000; 320: 671-676 (11 March)
2. Roncagliono MC, Santoro L, D'Avanzo B, et al. Role of family
history with Myocardial Infarction. An Italian case-control study. GISSI-
EFRIM Investigators. Circulation 1992; 85(6) : 2065-72
3. Pohjola-Sintonen S, Rissanen A, Liskola P, Luomanmaki K. Family
history as a risk factor of coronary heart disease in patients under 60
years of age. Eur-Heart-J. 1998; 19(2): 235-239
4. Silberberg J, Wlodarczyk J, Fryer J, Robertson R, Hensley MJ. Risk
associated with various definitions of family history of coronary artery
disease. The Newcastle Family History Study II. Am-J-Epidemol. 1998;
Competing interests: No competing interests
Wallis and her colleagues are to be congratulated on the new
Sheffield tables  which by the inclusion of HDL cholesterol are
considerably more accurate than the earlier version . We continue,
however, to disagree with their means of assessing the accuracy of risk
prediction methods by applying them to the whole population when such
methods are intended to identify high risk populations.
Inevitably when a
whole population approach is employed the majority of people will have a
risk which is substantially below the threshold CHD risk for which the
tables are designed (in this case 15% over the next 10 years). Accuracy
should be tested in people who are closer to this threshold, because they
represent the type of patient for whom the clinical decision about drug
therapy is to be made in practice. We have therefore compared the accuracy
of the new Sheffield tables and the Joint British Societies chart for CHD
risk  and the New Zealand charts for cardiovascular risk  with the
Framingham risk equation on which they are based  in a series of 386
patients referred to our Lipid Clinic by their physicians for advice about
whether drug therapy was justified. The Joint British Societies charts
identified correctly 88% of the patients to whom they could be applied,
the new Sheffield table 81%, but the New Zealand charts only 63% .
Thus, in terms of accuracy the Sheffield tables performed similarly
to the Joint British Societies charts. We were surprised by the inaccuracy
of the New Zealand tables, which stems from their use of both systolic and
diastolic blood pressure on the same axis when the curves for CHD risk
generated by these two measurements of blood pressure relative to the
total serum to HDL cholesterol ratio are not parallel . This is not
really overcome by the use of boxes rather than curves. We appreciate that
many clinicians are reluctant to abandon diastolic blood pressure, but it
is less accurately measured than systolic and does not predict risk as
The new Sheffield tables were considered by the Joint British
Societies for inclusion in their guidelines , but were not adopted
because they do not allow practitioners to judge the level of risk between
15% and 30% and the Joint British Guidelines recommend that, as statins
become cheaper and more resources are available, people at lower risk will
progressively be targeted for cholesterol-lowering treatment. It would now
appear that this decision was further justified by the findings of the
study by Isles and colleagues that nurses and doctors found the New
Sheffield tables more difficult to use than the charts adopted in the
Joint British recommendations . Rather than tables or charts, for those
physicians with access to a computer, the programme produced by the Joint
British Societies available from us, the British Heart Foundation or on
the British Hypertension Society and Family Heart Association websites
( www.hyp.ac.uk/bhs or www.familyheart.org respectively) was considered
preferable in the Joint British Guidelines. This provides both CHD and
stroke risk for both systolic and diastolic blood pressure so that
physicians can obtain a more comprehensive understanding of an
individual's cardiovascular risk and plan antihypertensive or lipid-
lowering drug therapy accordingly.
P.N. Durrington MD FRCPath FRCP
PROFESSOR OF MEDICINE
1. Wallis, E.J., Ramsay, L.E., Haq, I.U., Ghahramani, P., Jackson, P.R.,
Rowland-Yeo, K., Yeo, W.W. Coronary and cardiovascular risk estimation for
primary prevention: validation of a new Sheffield table in the 1995
Scottish health survey population. Brit. Med. J. 2000; 320: 671-6.
2. Durrington, P.N., Prais, H., Bhatnagar, D., France, M., Crowley,
V., Khan, J., Morgan. J. Indications for cholesterol-lowering medication:
comparison of risk-assessment methods. Lancet. 1999; 353: 278-281.
3. Wood, D., Durrington, P.N., Poulter, N., McInnes, G., Rees, A.,
Wray, R. Joint British Recommendations on prevention of coronary heart
disease in clinical practice. Heart 1998; 80 Suppl 2: S1-S29.
4. Dyslipidaemia Advisory Group, on behalf of the Scientific
Committee of the National Heart Foundation of New Zealand. 1996 National
Heart Foundation Guidelines for the Assessment and Management of
Dyslipidaemia. N.Z. Med. J. 1996; 109: 224-32.
5. Anderson, K.M., Odell, P.M., Wilson, P.W.F., Kannel, W.B.
Cardiovascular disease risk profiles. Am. Heart J. 1990; 121: 293-8.
6. Durrington, P.N., Prais, H. Methods for the prediction of coronary
heart disease risk. Heart 2000. In press.
7. Isles, C.G., Ritchie, L.D., Murchie, P., Norrie, J. Risk
assessment in primary prevention of coronary heart disease: randomised
comparison of three scoring methods. Brit. Med. J. 2000; 320: 690-1.
Competing interests: No competing interests
According to the prevailing theory of atherogenesis (1) the response-
to-injury hypothesis, atherosclerosis is caused by a repetitive insult to
the vascular endothelium, which eventually leads to an excessive
inflammatory fibro-proliferative response to the endothelium and smooth
muscle to the arterial wall. Injury may be induced by a variety of factors
such as modified low-density lipoproteins, mechanical force, immunological
factors or viruses.
One of the earliest events observed following the endothelial insult
is an increased monocyte adhesion to the endothelial surface, which is a
critical component of atherogenesis. This is followed by recruitment of
monocytes into the sub-endothelial space and ingestion of modified LDL by
these cells, leading to the formation of foam cells. Accumulation of the
modified LDL such as oxidized LDL and lyso-phosphatidylcholine (LysoPC) in
turn stimulates endothelial cells to induce the expression of pro-
inflammatory molecules such as ICAM-1 and VCAM-1 which further promote
monocyte migration and development of atherosclerotic lesions. T-
lymphocytes also migrate into the intima, and together with the foam cells
they form fatty streaks. Subsequently, the vascular smooth muscle cells
also infiltrate into the intima and proliferate, leading to the formation
of atherosclerotic plaques.
Miyasaka et al (2) observed that while monocyte attachment to the
endothelial surface appears to be the initiator of a cascade of events
that leads to the development of atherosclerosis, the molecular mechanism
of such a process needs to be fully elucidated. It has also been suggested
that the vascular endothelium directs the accumulation of leukocytes into
the inflamed tissue by expressing appropriate receptors, namely selectins,
which mediate the first step of leukocyte extravasation or rolling.
Different types of adhesion molecules expressed by the activated
endothelial cells are involved in mediating the inflammatory process. In
particular, the E-, L- and P- selectins are thought to play a pivotal role
in mediating the process, bringing leukocytes in close proximity to the
endothelial lining of the inflamed vessel (3).
In short, the Sheffield Risk Table may have a 97% sensitivity and 95%
selectivity for screening of primary prevention of coronary and
cardiovascular risk estimates (4). Bit it does not highlight the primary
event in atherogenesis which is considered to be one of the foremost of
risk factors that lead to coronary events.
1. Ross R. The pathogenesis of atherosclerosis, a perspective for the
1900s. Nature 1993; 362: 801-809
2. Miyasaka M et al. Involvement of selectins in atherogenesis: a
primary or secondary event? Ann New Y Acad Sci. 1996; 811: 25-35
3. Yoshida M & Gibrone MA. Novel roles for E-selectin in
endothelial-leukocyte adhesion. Ann New Y Acad Sci. 1996; 811: 493-97
4. Wallis E et al. Coronary and cardiovascular risk estimates and
primary prevention. BMJ 2000; 320: 671-676
Competing interests: No competing interests