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EDITORIALS:
Fiona Bradley and Margaret E Cupples
Reducing the risk of recurrent coronary heart disease
BMJ 1999; 318: 1499-1500 [Full text]
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Rapid Responses published:

[Read Rapid Response] Misinterpretation of research
Tom Marshall   (8 June 1999)
[Read Rapid Response] Homocysteine and Cardiovascular Disease
Donald G Weir, John M Scott   (1 July 1999)
[Read Rapid Response] Reducing the risk of recurrent coronary heart disease - a model from Carrick PCG in Cornwall
H M Dalal   (1 July 1999)
[Read Rapid Response] A tax on saturated fats?
Martin Breach   (7 July 1999)

Misinterpretation of research 8 June 1999
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Tom Marshall,
Honorary Clinical Lecturer in Public Health Medicine
University of Birmingham

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Re: Misinterpretation of research

Bradley and Cupple's editorial states of the POST study: "there were no differences between the two groups in the main outcome measures (prescribing of beta-blockers and cholesterol lowering drugs)".

This is simply not the case. The POST study clearly reports changes in prescribing of beta-blockers: 38% in the intervention group compared to 27% in the control group. It also showed changes in the prescribing of statins: 28% and 23% in intervention and control groups respectively. These changes are clearly large enough to be clinically important.

The differences failed to reach statistical significance. The correct interpretation of this is that the study was too small (had insufficient power) to rule out the possibility that this result was due to chance. Bradley and Cupple draw from this the mistaken conclusion that the intervention was ineffective.

The correct inference to draw from the results is that there the POST study provides some evidence that this is an effective intervention but that the case is not proven beyond reasonable doubt. This is quite different to the interpretation implied by Bradley and Cupple's description of the study's results as "disappointing".

Yours sincerely,

Tom Marshall

Conflicts of interest: none.

Homocysteine and Cardiovascular Disease 1 July 1999
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Donald G Weir,
Regius Professor of Physic and Professor of Experimental Nutrition
Department of Clinical Medicine, Trinity College Dublin,
John M Scott

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Re: Homocysteine and Cardiovascular Disease

We read with interest the leading article on "Reducing the risk of recurrent coronary heart disease" June 5th by Drs F Bradly and ME Cupples. While accepting the thrust of their arguments concerning the mechanisms of delivering secondary preventive care, it was suprirsing that no mention was made to hyperhomocysteinaemia as a risk factor for coronary heart disease (1,2,3). Since this can be easily rectified by taking low dose oral folic acid either as a tablet (4) or as fortification of a food staple (5), it would seem sensible to include it as one of the preventative mechanisms.

References

1. Wald NJ, Watt HC, Law MR, Weir DG, McPartlin J, Scott JM. Homocysteine and ischaemic heart disease. Arch Int Med 1998, 158: 862-6.

2. Weir DG, Scott JM. Homocysteine as a risk factor for cardiovascular disease and related disease: nutritional implications. Nutr Res Rev 1998; 11: 311-38.

3. Nygard O, Nordehaug JE, Refsum H, Ueland FM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. New Eng J Med 1997, 337: 230-6.

4. Daly S, Mills JL, Molloy AM, Conley M, Lee YJ, Kirke PN, Weir DG, Scott JM. Minimum effective dose of folic acid for food fortification to prevent neural tube defects. Lancet 1997, 350: 1666-9.

5. Tucker KL, Mahnken B, Wilson PWF, Jacques P, Selhub J. Folic acid fortification of the food supply. Potential benefits and risks for the elderly population. JAMA 1996; 276: 1879-85.

Reducing the risk of recurrent coronary heart disease - a model from Carrick PCG in Cornwall 1 July 1999
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H M Dalal,
Principal in General Practice
18 Lemon Street Surgery,Truro,Cornwall TR1 2LZ

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Re: Reducing the risk of recurrent coronary heart disease - a model from Carrick PCG in Cornwall

Sir,

Bradley and Cupples end their editorial (June 5th) with the question - "Has anyone got a better idea to improve our performance in this area?"(1)

Earlier they make the point that adequate resources would be needed to ensure a systematic approach to the secondary prevention of coronary heart disease in primary care - and that primary care groups would be well placed to implement this. In one area, that of the Carrick Primary Care Group in Cornwall, such a scheme has begun.

For the next two years the British Heart Foundation is funding two liaison nurses to ease the discharge of coronary patients from the Royal Cornwall Hospital into the community and the training of a lead nurse from each practice. The PCG has then been persuaded to give extra monies to each of their 13 practices for a scheme which includes creating a register of coronary patients, starting a call and recall system and developing improved links with acute care, ie structured long-term care.

Campbell et al(2) have shown us that nurse run secondary prevention clinics in primary care can reduce risk factors for the recurrence of coronary events. The widespread adoption of such clinics will need the same level of funding as that currently provided for the management of those other, perhaps less deserving, chronic diseases - asthma and diabetes.

Three cheers for Carrick PCG which is doing what the government should have done when it initiated payment for some chronic disease management in general practice. Let us all try to persuade our own primary care groups to follow their example,if necessary using innovative methods of joint funding.

Yours faithfully

Dr H M Dalal General Practitioner 18 Lemon Street TRURO TR1 2LZ

Dr Hugh Bethell Chairman - Secondary Prevention and Rehabilitation Committee Coronary Prevention Group 2 Taviton Street LONDON WC1H 0BT

1. Bradley F, Cupples ME. Reducing the risk of recurrent coronary heart disease. BMJ 1999;318:1499-500

2. Campbell NC, Thain J, Deans HG, Ritchie LD, Rawles JM, Squair J Secondary prevention clinics for coronary heart disease: randomised trial of effect on health. BMJ 1998; 316:1434-7

A tax on saturated fats? 7 July 1999
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Martin Breach,
GP
Ormskirk, Lancashire

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Re: A tax on saturated fats?

Dear Sir,

In their editiorial 'Reducing the risk of recurrent coronary heart disease' BMJ 1999;318:1499-1500 ( 5 June ) Fiona Bradley and Margaret Cupples pose the question of how better to improve our performance in the secondary prevention of cardiac disease. It is clear that saturated animal fats are, at least in respect of their effects upon the cardiovascular system, unfit for human consumption. Therefore an essential target must be to reduce the total consumption of these products within the population.

Many sources of saturated fats are, in effect, waste products. Their subsequent presence in common foodstuffs is a consequence of their relative cheapness in comparison to healthier alternatives.

A tax on saturated fats would however be a means of rendering these products uneconomical. The revenue raised could be used for their safe destruction, and for the temporary compensation of affected industries. Most importantly a change in pricing would promote the use of safer unsaturated fat alternatives, or of non-fat products.