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Stroke prevention

Prevention of stroke may be classified as primary prevention if there is no previous history of stroke or transient ischaemic attack and secondary prevention if there has been such an event. Usually, secondary prevention is management of a much higher risk.

About 80% of stroke is ischaemic from thrombosis or embolism but 20% is due to haemorrhage. The aetiology is usually atherosclerotic but in younger patients another cause must be sought. Sometimes there is incomplete arterial occlusion but the Circle of Willis is not such a good system of anastomoses as is classically taught by anatomists. The problem may be an inadequate rather than a totally occluded circulation. Sometimes, prevention of stroke involves trying to support the circulation in shock, perhaps with hypovolaemia. Occasionally stroke may follow a period of inadequate circulation when a patient has been on and off cardiopulmonary bypass.

Epidemiology: Stroke affects between 174 and 216 per 100,000 population in the UK each year.¹ It tends to be thought of as a disease of the elderly and incidence certainly rises with age but about 30% occurs under the age of 65. In the younger age group, aetiology other than atheroma should be sought and stroke rehabilitation produces different challenges from in the elderly. Stroke accounts for 11% of all deaths in England and Wales. The incidence doubles for every decade after 45 years. It rises from 104 per 100,000 per year age 45 to 54 to 1113 per 100,000 per year age 75 to 84.

Subarachnoid haemorrhage(SAH) affects 6 to 12 people in each 100,000 of the population per year and constitutes about 6% of first strokes. Most patients are under 60 years old. Approximately 85% of patients bleed from intracranial arterial aneurysms, 10% from a non-aneurysmal peri-mesencephalic haemorrhage and 5% from other vascular abnormalities including arteriovenous malformation.² The arterial aneurysms are often called berry aneurysms because they look like little berries.

Intracranial venous thrombosis tends to present as headache followed by stroke, perhaps some time later. It tends to be much slower in origin than stroke of arterial origin. There is much more detail in the article. The risk factors are for hypercoagulation. It represents no more than 1 or 2% of all strokes but may be unrecognised when it occurs amidst other serious illness.

Primary Stroke Prevention: By and large, the risk factors for stroke are the risk factors for atherosclerosis and so a history of acute myocardial infarction, angina pectoris or peripheral vascular disease should be seen as proof of existing arterial disease. Hence the risk of stroke should be seen as high. Compared to risk of coronary heart disease, hyperlipidaemia is slightly less important for stroke and hypertension is even more important. Risk factors for atherosclerosis are discussed in more detail in the article. Risk calculators for CHD have been developed. They are purely for use in primary prevention and should not be used for secondary prevention. Some calculators also give a risk of stroke. Although the figures for risk of stroke tend to be rather lower than for CHD, often around 10-fold lower, patients are so much more frightened by the prospect of a stroke that this may be the more potent figure in terms of prompting to make changes in lifestyle.

• Smoking, hypertension, hyperlipidaemia and diabetes mellitus, especially type 2 diabetes, are all strong risk factors that have been extensively discussed elsewhere. As discussed under atherosclerosis, inflammatory conditions such as rheumatoid arthritis also have high risk.
• Stroke can result from embolism. The origin may be atrial fibrillation, a mural thrombus on a myocardial infarct, vegetations from atrial myxoma or bacterial endocarditis or arising from the arteries along the way. The commonest site is near the bifurcation of the carotid. Paradoxical embolism may also occur with a right to left shunt.
• Haemorrhagic stroke may result from vascular anomalies such as berry aneurysm. High blood pressure increases risk. It may also follow trauma.
• Conditions that increase the risk of sludging in the vessels predispose to stroke. These include polycythaemia rubra vera in which a high haematocrit increases viscosity but platelets are also raised. There are many other causes of thrombophilia and they are discussed elsewhere.
• In antiphospholipid syndrome and related disease including systemic lupus erythematosis, there is increased risk of both venous and arterial thrombosis and hence risk of stroke.
• Migraine, especially with aura, increases the risk of stroke. Migranous infarction is when a cerebral infarction occurs during the course of a typical attack of migraine with aura. The aura lasts over an hour and neuroimaging shows ischaemic infarction. Migraine is associated with increased risk of ischaemic but not haemorrhagic stroke. A meta-analysis of 14 studies showed that the relative risk of ischaemic stroke was 2.16 (confidence interval 1.89 to 2.48). This meta-analysis also showed that oral contraceptive use increased risk of ischaemic stroke approximately eight-fold compared with non-users.³ The article about migraine covers the question of migraine and risks of oral contraceptive use in much more detail. In those without migraine, there is a very slight increase in risk of stroke in those who use oral contraceptives but the absolute risk in women of this age is tiny. A large study of women taking HRT found no increased risk of stroke⁴ whilst another that looked at HRT after stroke⁵ found no benefit but no disadvantage either.
• Such matters as stress and PTSD may seem rather nebulous compared with criteria than can be quantified but the American Department of Veteran Affairs have accepted the stress of having been a prisoner of war as a risk factor for atherosclerotic disease in terms of acknowledging the possible contribution of military service to subsequent illness.⁶ Papers from Serbia⁷ and Croatia⁸ have associated civil conflict with risk of stroke.

Secondary prevention of stroke: The Royal College of Physicians report on stroke is very committed to secondary prevention after the incident. Most of the following section comes from that report and differing levels of evidence as cited in that report will be given. It says that after a first stroke the risk of recurrence is high in the first year, and remains elevated for the rest of that person's life. All patients will require regular review and appropriate treatment of risk factors for vascular disease all their lives (evidence level B) and practices should keep a register of stroke patients and conduct regular audit of secondary prevention (evidence level C). Patients who have suffered a stroke remain at an increased risk of a further stroke of between 30% and 43% within 5 years. The risk of a complete stroke after a TIA may be as high as 20% within the first month. An individualised strategy for stroke prevention should be implemented within 7 days of acute stroke or TIA.^9,10 Specific recommendations are followed by the level of evidence in parenthesis:

• Stopping smoking (B), regular exercise (D), diet and achievement of satisfactory weight (B), reduced intake of salt (B) and avoiding excess alcohol (D)
• High blood pressure persisting for more than 2 weeks should be treated. The British Hypertension Society guidelines are:
  • In non-diabetic people the goal of treatment should be systolic blood pressure below 140 mmHg and diastolic blood pressure below 85 mmHg
  • For diabetics the optimal goals of control are a BP of 130/80 (A)¹¹
• Antithrombotic treatment is of value.¹² All patients with ischaemic stroke or TIA (not haemorrhagic stroke) who are not on anticoagulation should have antiplatelet therapy such as aspirin (A) or clopidogrel, or a combination of low-dose aspirin and dipyridamole modified release (MR). The most suitable dose of aspirin seems uncertain. Anticoagulation should be started if there is persistent or paroxysmal atrial fibrillation unless contraindicated (A). Anticoagulants should not be used for patients in sinus rhythm unless there is a major source of cardiac embolism. Anticoagulants should not be started before brain imaging has excluded haemorrhage, and usually not until 14 days after the onset of an ischaemic stroke (A).
• Treatment with a statin should be given to patients with ischaemic stroke or TIA, to bring total cholesterol to 3.5 mmol/L or lower unless contraindicated (A).
• Carotid stenosis may produce a carotid bruit but this is very unreliable and carotid duplex ultrasound should be performed after a stroke in the carotid area. Stroke in the carotid area is suggested by hemiplegia or hemiparesis, visual disturbance in one eye, change in sensation such as tingling down one side of the body, difficulty with speech or comprehension and bulbar symptoms such as difficulty swallowing. Findings are confirmed with magnetic resonance angiography (MRA) or with a second ultrasound. Carotid endarterectomy should be considered where carotid stenosis exceeds 70% as measured using the ECST methods, and 50% as measured using the NASCET methods (A). Carotid angioplasty or stenting may be an alternative in specialist centres.

References:

1. Mant J, Wade D, Winner S (2004) 'Health care needs assessment: stroke'. In: Stevens A, Raftery J, Mant J, Simpson S (eds) (2004) Health care needs assessment: the epidemiologically based needs assessment reviews. Second edition. Oxford: Radcliffe Medical Press.
2. van Gijn J, Rinkel GJ; Subarachnoid haemorrhage: diagnosis, causes and management.;Brain. 2001 Feb;124(Pt 2):249-78.[abstract]
3. Etminan M, Takkouche B, Isorna FC, et al; Risk of ischaemic stroke in people with migraine: systematic review and meta-analysis of observational studies.;BMJ. 2005 Jan 8;330(7482):63. Epub 2004 Dec 13.[abstract]
4. Simon JA, Hsia J, Cauley JA, et al; Postmenopausal hormone therapy and risk of stroke: The Heart and Estrogen-progestin Replacement Study (HERS).;Circulation. 2001 Feb 6;103(5):638-42.[abstract]
5. Viscoli CM, Brass LM, Kernan WN, et al; A clinical trial of estrogen-replacement therapy after ischemic stroke.;N Engl J Med. 2001 Oct 25;345(17):1243-9.[abstract]
6. Federal Register Vol. 70, No. 123/Tuesday, June 28, 2005 Rules and Regulations 37041
7. Djokic G, Marjanovic D; ;Vojnosanit Pregl. 2000 Nov-Dec;57(6):641-5.[abstract]
8. Kadojic D, Demarin V, Kadojic M, et al; Influence of prolonged stress on cerebral hemodynamics.;Coll Antropol. 1999 Dec;23(2):665-72.[abstract]
9. Coull AJ, Lovett JK, Rothwell PM; Population based study of early risk of stroke after transient ischaemic attack or minor stroke: implications for public education and organisation of services.;BMJ. 2004 Feb 7;328(7435):326. Epub 2004 Jan 26.[abstract]
10. Lovett JK, Dennis MS, Sandercock PA, et al; Very early risk of stroke after a first transient ischemic attack.;Stroke. 2003 Aug;34(8):e138-40. Epub 2003 Jul 10.[abstract]
11. Williams B, Poulter NR, Brown MJ, et al; Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV.;J Hum Hypertens. 2004 Mar;18(3):139-85.
12. No authors listed; Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients.;BMJ. 2002 Jan 12;324(7329):71-86.[abstract]

Internet:

• Royal College of Physicians National Clinical Guidelines for Stroke, 2nd edition 2004
• Royal College of Physicians Concise Guidelines for Stroke, 2004
• Department of Health, NSF for Older People (chapter 5)
• The Stroke Association

Acknowledgements EMIS is grateful to the Mentor authoring team for writing this article. The final copy has passed peer review of the independent Mentor GP authoring team. ©EMIS 2006.

Last issued 30 Aug 2006