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At the heart of general practice since 1960

TOATT ­ tooled off all the time

New guidelines from the Royal College of Physicians

urge GPs to go further than the nGMS targets.

Dr Andrew Mimnagh explains why it's worth

the effort


is a major cause of mortality

and morbidity in the United Kingdom, affecting over 130,000 people each year. Of these 10,000 are under 55 years of age, 1,000 are under 30, with a strong preponderance of women in this lower age range. Much of the responsibility for delivering effective secondary prevention, and managing long-term problems associated with stroke, falls to the primary care team.

The risk of having a second or third vascular event is well documented. The Oxford Community Stroke Project (OCSP) provides data applicable to general practice to quantify this risk (see box, left).

As you can see from the box there is a substantial overlap of mortality which allows GPs the chance to deal with patients following stroke in a pragmatic manner, in a unified cardiovascular clinic, perhaps even an 'atherothrombosis clinic'.

Secondary prevention

The clinical discrimination between stroke and TIA remains useful for prognosis in acute care; clinical imaging of TIA patients blurs the boundary. Scans reveal evidence of infarction in those patients with a TIA whose neurological symptoms lasted more than a few seconds, and for the purposes of secondary prevention the management of stroke and TIA is identical.

The new National Clinical Guidelines for Stroke state: 'There should be a high priority given to rapid delivery of evidence-based secondary prevention.'2

The three key interventions in secondary prevention are exactly the same as ischaemic heart disease prevention, but their relative worth is different:

·Control of blood pressure levels

·Anticoagulation or antiplatelet agents (in ischaemic stroke only)

·Statin-based antilipid therapy (almost regardless of serum cholesterol).

Blood pressure control


With the mainly elderly population the effect of sodium restriction is particularly beneficial. At the age of 75, sodium restriction alone produces a fall in blood pressure of approximately 15mmHg, an effect comparable with thiazide type antihypertensive therapy.

This is of some significance, as meta-analysis of trials of blood pressure lowering suggest that the relatively modest reduction of 7mmHg halves the stroke risk; therefore dietary sodium restriction in this group could reduce the risk of stroke by 75 per cent.

The downside is that the effects are less marked in the younger age group, perhaps 5mmHg at 40 years of age, and the restriction has to be significant.

To achieve these beneficial levels an exclusion of ready-made meals is necessary. Unfortunately salt added to food during processing appears less salty-tasting than salt added at table or at the end of preparation. Hence two slices of white bread have more salt than a standard packet of ready salted crisps. (Do not ignore the fat content if you think this is a recommendation to change your diet!)


Exercise is useful, producing falls in blood pressure if it is regular and sustained. The small downside is that the rise in blood pressure during the activity may trigger a stroke, but even so, the reduction in risk during the longer periods of rest produces a net positive gain.

A full explanation of the risk/benefits is obviously helpful, especially in areas offering 'exercise on prescription', to reduce the inevitable tendency for litigation if your patient experiences a fatal stroke while undertaking the exercise you recommended!

Choosing a target

Stroke risk is an exponential function, with a doubling for every 7mmHg. Although the graph will mathematically include no strokes at 0mmHg this is clearly not clinically useful.

An individual's target blood pressure is the lowest blood pressure that an individual can safely function with. This should include assessment of postural variation in blood pressure.

The GMS quality indicators should not be regarded as target levels, and as the contract allows these to be altered in future, applying the clinical standard of lowest tolerated blood pressure is to be recommended.

This will serve you well financially in any future reduction of quality marker for blood pressure levels, and if the maximally tolerated medication level does not achieve the GMS quality levels, you can code the patient as an exemption to allow payment.

General weight reduction will be beneficial in altering any adverse factors for metabolic syndrome.

Smoking cessation

The adverse effects of smoking produce not only an increased coagulability of the blood in smokers, but also a rise in blood pressure caused by tobacco ingestion. Any of the standard cessation methods are suitable for patients who have had a stroke.


The important issue in secondary prevention is to remember to increase therapy if further events occur on an existing therapy. Aspirin has an excellent cost benefit ratio, but remember any anticoagulation should not be commenced after a haemorrhagic stroke.

For a patient already on aspirin who suffers a further event, consideration should be given to aspirin/dipyridamole combination, which will lower stroke risk further; or clopidogrel which will confer both stroke and cardiac prevention.

This choice has polarised the experts and no current cost benefit studies give a clear advantage, so provided the therapy is escalated in response to further events you are doing as much as the evidence supports.

An interesting area is aspirin/clopidogrel combinations because of their differing mode of action on platelet function, but evidence was lacking at the time of publication of the guidance.

Warfarin therapy is indicated in all patients who exhibit atrial fibrillation regardless of whether it is chronic or paroxysmal, valvular or non-valvular.

The risk exceeds the benefit in patients in sinus rhythm, unless investigation has shown a significant intracardiac source of emboli.This will usually require secondary care.

Statin-based antilipid therapy

It has been established that there is no statistically significant correlation to be found between serum cholesterol, its subfractions and stroke. The 4S study was initially criticised because of a reduction in stroke in the treatment group, some commentators stating the benefit of statin was not as marked, and that control of hypertension in the trial reduced heart attack and stroke.

The WOSCOPS study was designed to engineer out this irregularity but subsequently confirmed the existence of this real but currently not understood effect. American based studies have shown a stroke reduction (and heart attack reduction) even in individuals with low overall risk and cholesterols in the normal range. The methodology of these studies excluded individuals with serum cholesterol below 3.5mmol/litre in case this was a marker of occult existing disease, hence a lower limit in stroke guidance of 3.5mmol.

As the mechanism of statin action is unclear, GPs may wish to take the pragmatic step of using a statin following a stroke, regardless of cholesterol level, but this is definitely not in the current royal college guidelines.

There is no evidence to support a target level of cholesterol in stroke prevention, unlike ischaemic heart disease, but clearly it would be helpful to exceed GMS quality indices to maximise practice income.

Outcomes from the Oxfordshire Community Stroke Project1

In one OCSP study, 675 patients with first stroke were followed for up to 6.5 years to establish their long-term prognosis. The results showed a 31 per cent risk of death in the first year. This has been as high as 43 per cent

in other studies.

For patients who died, cause of death was classified into five groups:

·First stroke

·Recurrent stroke

·Other cardiovascular event

·Non-vascular disease


Of those who survived more than 30 days after a stroke, but who died within the first 6 years:

·35 per cent of deaths after a first stroke are due to other cardiovascular events,

·17 per cent died from late effects of the first stroke

·16 per cent died of a further stroke.2


1 Dennis MS et al. Long-term survival after first-ever stroke: The Oxfordshire Community Stroke Project. Stroke 1993; 24: 796-800.

2 The Intercollegiate Working Party for Stroke, Royal College of Physicians. National Clinical Guidelines for Stroke, 2nd edition. London, 2004.

Useful websites

Northern Ireland Chest, Heart & Stroke Association,

Chest, Heart and Stroke Association, Scotland,

Andrew Mimnagh is a full time GP in Waterloo, Liverpool and member of the Action For Stroke group which has produced an abbreviated version of the full national guidelines. Copies of this desktop guidance are available by emailing: guidelines or by writing to P.O. Box 50331, London W4 1Y

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