Read Time: 5 mins

Primary Prevention of Ischaemic Stroke

Copy Link
Published Online: Jun 4th 2011 European Neurological Review, 2007;(1):24-28 DOI:
Authors: Andria L Ford, Allyson R Zazulia
Quick Links:
Article Information

Stroke is the second most common cause of death worldwide and a leading cause of long-term neurological impairment, with as many as 30% of survivors permanently disabled.1–3 Of all strokes, approximately 70% are first-time events, thus primary-care physicians have a great opportunity to identify patients who may benefit from risk factor modification.2 Furthermore, neurologists frequently evaluate non-stroke patients who carry modifiable stroke risk factors. In these settings, initiation of primary prevention strategies may have the greatest impact on the disease and its enormous toll on the healthcare system.

Risk Factors for Ischaemic Stroke

Numerous factors contribute to the risk of first stroke. The non-modifiable risk factors include increasing age, sex, race/ethnicity, family history, genetic factors and low birth weight. While not modifiable, these risk factors may identify those who are at highest risk of stroke and who may benefit from aggressive treatment of any modifiable risk factors. Regarding age, each decade above 55 years of age leads to a doubling of stroke risk.4 Men carry an overall higher risk of stroke than women at younger ages, but women are at greater risk over the age of 85 years.5 This relatively greater risk in older women may reflect changing hormonal status and/or the use of hormone replacement therapy (HRT), as well as the fact that men with stroke risk factors may die earlier from cardiovascular disease.6–7 Race and ethnic contributions to stroke risk are difficult to separate from other risk factors such as hypertension and diabetes, which are more prevalent in certain populations. Even taking into account these risk factors, however, stroke incidence rates remain higher among some racial–ethnic groups (e.g. African-Americans).8,9 Unidentified genetic risk factors may predispose these groups to stroke and may eventually help to explain the contribution of family history to stroke risk. Stroke is a manifestation of a variety of rare genetic disorders, but the association between most inherited coagulopathies – e.g. protein C and S deficiency – and arterial events is weak.10–12 Finally, stroke incidence and stroke mortality are increased among individuals with low birth weight.13,14
The long list of modifiable stroke risk factors is best separated into two groups:
• those that clearly contribute to risk and, if modified, reduce the risk of incident stroke; and
• those that are associated with stroke, but have not been well studied or do not reduce the risk of stroke when treated.
Well-documented risk factors that clearly benefit from specific management include hypertension, cigarette smoking, atrial fibrillation, dyslipidaemia, diabetes mellitus and asymptomatic carotid stenosis (see Table 1).15–17 The discussion and treatment of these risk factors will be the focus of this article. Other well-documented risk factors are cardiovascular and peripheral arterial disease, sickle cell disease and obesity. Less well documented or potentially modifiable risk factors include metabolic syndrome, hyperhomocysteinaemia, hypercoagulability, oral contraceptive use, inflammatory processes, migraine headache and sleep apnoea, among others.18


Blood pressure is a powerful determinant of stroke risk and, because hypertension is the most prevalent of the modifiable stroke risk factors throughout middle and older age, its treatment would produce the greatest impact on reducing the burden of stroke.19 Recent evidence-based guidelines on management of hypertension recommend antihypertensive agents and lifestyle modification to keep blood pressure <140/90, with even tighter control recommended for those with additional vascular risk factors such as diabetes and chronic kidney disease (see Table 2).20 Overall, across multiple classes of antihypertensive therapy, blood pressure reduction is associated with approximately 30–40% reduction in the incidence of stroke, with more intensive lowering superior to less.21–22 Placebo-controlled studies have demonstrated the efficacy of thiazide diuretics, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers and calcium-channel blockers in reducing stroke and cardiovascular outcomes.21–22 In general, the choice of a particular class of agents is less important than the degree of blood pressure reduction achieved.

Cigarette Smoking

Multiple studies have demonstrated that cigarette smoking independently increases the risk of ischaemic stroke approximately two-fold and places individuals at even greater risk of haemorrhagic stroke.23–25 Moreover, smoking may act synergistically with other stroke risk factors such as oral contraceptive pills. Smoking is thought to promote stroke by increasing thrombus generation in narrowed arteries and chronically hastening atherosclerosis. In the Framingham Study of 4,255 middle-aged men and women who were free of stroke or transient ischaemic attacks (TIAs), the risk of stroke in heavy smokers (more than 40 cigarettes per day) was twice the risk of light smokers (fewer than 10 cigarettes per day).26 The stroke risk had decreased significantly by two years after smoking cessation and reached the level of nonsmokers by five years after smoking cessation. Another prospective study of young, healthy registered nurses found that smoking yielded a 2.58 relative risk of first stroke.27 This excess risk largely disappeared between two and four years after smoking cessation.

Atrial Fibrillation

Nonvalvular atrial fibrillation (NVAF) confers a nearly five-fold increase in the age-adjusted risk of stroke.28 The prevalence of NVAF increases markedly with age, as does the proportion of strokes attributable to the dysrhythmia: nearly a quarter of strokes in octogenarians can be ascribed to NVAF.28 Multiple trials have shown that medical therapy is efficacious in the primary prevention of stroke in patients with NVAF. Overall, oral anticoagulation with warfarin reduces the risk of stroke in moderate- to high-risk patients by about 60% and aspirin by about 20%.29 Several risk-stratification methods have been developed to guide choice of treatment in NVAF. One such scheme that has been validated in clinical trials is the CHADS2, which evaluates stroke risk based on the presence of five vascular risk factors (see Table 3).30 Medical therapies other than warfarin have been investigated. Ximelagatran, a direct thrombin inhibitor, was demonstrated to be equally efficacious as warfarin in reducing stroke in NVAF.31 While ximelagatran resulted in fewer minor bleeding complications, it produced significant elevations in liver enzymes and at least one case of fatal hepatic failure – thus the drug has not been approved by either European or American regulatory agencies. The National Study for Prevention of Embolism in Atrial Fibrillation (NASPEAF) trial demonstrated the superiority of combination therapy with warfarin and the antiplatelet agent triflusal over warfarin or antiplatelet therapy alone.32 It is important to remember that chronic and paroxysmal atrial fibrillation carry similar stroke risk and that rhythm control is not superior to rate control in reducing the risk of stroke.33


Prospective studies in men and women have shown that ischaemic stroke rates increase up to 25% for every 1mmol/l increase in total cholesterol above 5.2mmol/l.34 Low high-density lipoprotein (HDL) cholesterol level is a risk factor for stroke in men and possibly women as well.35,36 While the association between low-density lipoprotein (LDL) cholesterol and risk of stroke is not clear, the prevention of vascular events seen in the lipid-lowering therapy trials appears to be directly proportional to the degree of LDL reduction regardless of entry-level LDL.37,38 Two large primary prevention studies have shown that 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors (statins) are effective in reducing stroke. The Heart Protection Study included over 20,000 adults with either occlusive arterial disease or diabetes mellitus who were randomly allocated to receive simvastatin 40mg or a placebo.39 Simvastatin treatment was associated with a 25% relative reduction (1.4% absolute risk reduction) in the event rate for first non-fatal and fatal stroke. This benefit was apparent even among those with low pre-treatment LDL cholesterol below 3.0mmol/l. In the lipid-lowering arm of the Anglo–Scandinavian Cardiac Outcomes Trial, over 10,000 hypertensive patients with at least three other cardiovascular risk factors and a non-fasting total cholesterol of 6.5mmol/l were randomised to atorvastatin 10mg or placebo.40 Fatal and non-fatal stroke were significantly reduced in the treatment group by 27% (0.7% absolute risk reduction). Meta-analyses of multiple statin trials show an overall 21% relative risk reduction for stroke with the magnitude of reduction being largely proportional to the degree of LDL reduction.41 The Treating to New Targets (TNT) trial enrolled 10,001 patients with coronary heart disease and LDL <3.4mmol/l who were assigned to 10mg or 80mg of atorvastatin daily.42 At five-year follow-up, the high-dose atorvastatin group had 30% fewer fatal and non-fatal strokes than the low-dose group (1.1% absolute risk reduction).


Type 2 diabetes is independently associated with a 1.8- to 6-fold increased stroke risk.18 Moreover, these patients have an increased prevalence of hypertension, dyslipidaemia and obesity. Multiple studies have demonstrated the benefit of tight blood pressure control in diabetics. The UK Prospective Diabetes Study (UKPDS-36) stratified diabetic patients by 10mmHg increments of systolic blood pressure ranging from <120mmHg to >160mmHg and found that each 10mmHg decrement in mean systolic blood pressure was associated with a significant reduction in risk for any complication related to diabetes, including stroke.43 No threshold of risk reduction was observed for any end-point. Specific classes of antihypertensive agents may offer better prevention in the diabetic population. For example, in the Losartan Intervention for End-point Reduction in Hypertension (LIFE) study, angiotensin II receptor blocker treatment resulted in a significant 24% relative risk reduction (5% absolute risk reduction) in major vascular events and a nonsignificant 21% reduction (2% absolute risk reduction) in stroke compared with beta-blocker therapy.44 The benefit of statin therapy in diabetic patients was demonstrated in the Heart Protection Study (HPS), as discussed above.39 Furthermore, in the Collaborative Atorvastatin Diabetes Study (CARDS), treatment with atorvastatin resulted in a 48% reduction (1.3% absolute risk reduction) in stroke among type 2 diabetics with at least one additional vascular risk factor and an LDL cholesterol <4.14mmol/l but no history of cardiovascular disease.45 While tight blood pressure control has been proved to reduce stroke risk in diabetic patients, tight glycaemic control has not. The UKPDS-33 showed that intensive glycaemic control with sulfonylureas and insulin reduced microvascular, but not macrovascular, complications of diabetes.46 Certain diabetic medications may offer protection through other mechanisms. In the UKPDS-34, metformin significantly reduced macrovascular events without providing tighter glycaemic control relative to the conventional treatment group.47

Asymptomatic Carotid Stenosis

Among the elderly in Western populations, the prevalence of extracranial carotid stenosis is as high as 10%.18 The risk of stroke from asymptomatic carotid artery stenosis >50% is 1–3.4% per year.48–50 Factors associated with higher risk include male sex, stenosis >75% and heart disease.48 Two large trials have studied endarterectomy in asymptomatic carotid disease of >60% stenosis: the Asymptomatic Carotid Atherosclerosis Study (ACAS) and the Asymptomatic Carotid Surgery Trial (ACST).51,52 The studies found strikingly similar benefits with surgical treatment compared with medical therapy alone with a 53 and 45% relative risk reduction, respectively, corresponding to a 5.9 and 5.3% absolute risk reduction, respectively. Interestingly, after subgroup analysis, the same benefit was not seen in women, largely due to a higher rate of peri-operative complications.53 As with many surgical trials, the benefits seen depend highly on peri-operative risk, which was approximately 3% for men in both the ACAS and ACST.51,52 In patients with medical co-morbidities placing them at high surgical risk or in centres with less experienced surgeons, the risk–benefit ratio must be reassessed. Importantly, the observational studies on asymptomatic carotid disease as well as the endarterectomy trials were performed before the widespread use of statin medications. As primary preventative strategies with medical therapy continue to improve, the benefits of endarterectomy may need to be re-evaluated. Although carotid artery angioplasty/stenting is less invasive and possibly less costly than endarterectomy, its noninferiority to endarterectomy has not been established and thus it cannot be recommended for use outside of a trial setting. Most recently, the Endarterectomy Versus Angioplasty in Patients with Severe Symptomatic Caroid Stenosis (EVA-3S) study was stopped prematurely after interim analysis revealed that the rates of stroke and death at one and six months in patients with symptomatic stenosis (60%) were significantly higher in the stenting group.54

Hormone Replacement

The observation that the rate of vascular events in women dramatically increases post-menopause has led to many studies on primary and secondary prevention with HRT. The Women’s Health Initiative was a primary prevention study of the effect of hormone therapy on cardiovascular disease among post-menopausal women in which stroke was a pre-specified end-point.55,56 Two groups of women were randomised: those with an intact uterus received combined estrogen and progesterone therapy, while those with a hysterectomy received only estrogen. Both groups had a small but significant increase in vascular events with HRT compared with placebo. Thus, HRT cannot be recommended and is discouraged for prevention of ischaemic stroke.

Antiplatelet Therapy

Although antiplatelet therapy has a well-established role in secondary stroke prevention for both men and women, its value in primary prevention varies by sex and vascular risk profile. Among men, use of aspirin offers no benefit for primary prevention of ischaemic stroke or death, but, because it reduces the incidence of myocardial infarction, it is recommended for men with moderate to high risk of developing cardiovascular disease.57,58 It has no role in primary prevention for those at low cardiovascular risk. The Women’s Health Study randomised 39,876 asymptomatic women aged 45 years or older to aspirin or placebo on alternate days followed over 10 years. The results showed a nonsignificant reduction of 9% for the primary end-point of major cardiovascular events and a significant 17% reduction in the risk of stroke (24% reduction of ischaemic stroke and a non-significant increase in haemorrhagic stroke).59 Subgroup analysis showed that aspirin reduced the risk of ischaemic stroke and myocardial infarction largely among women aged 65 years and older. Women younger than 65 years old are unlikely to benefit from empiric antiplatelet therapy unless they carry stroke risk factors.


Substantial evidence supports the importance of a variety of modifiable stroke risk factors whose treatment offers the potential to reduce the considerable socioeconomic burden of stroke. Control of blood pressure, cessation of smoking and use of anticoagulation to prevent cardioembolism in atrial fibrillation offer the greatest impact at the population level because of the prevalence of these risk factors. The use of statins and antiplatelet agents, avoidance of HRT in older women and treatment of carotid stenosis in men contribute modest benefits to stroke risk reduction. ■


  1. Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002, World Health Organization, World Health Report 2003: Statistical Annex 2.
  2. Wolf PA, et al., Prevalence of stroke-related disability: US estimates for the Framingham Study, Neurol, 1998;4(Suppl 4): A55–6.
  3. American Heart Association,Heart Disease and Stroke Statistics 2004 update, 2003.
  4. Wolf PA, et al., Secular trends in stroke incidence and mortality: the Framingham Study, Stroke, 1992;23:1551–5.
  5. Sacco RL, et al., Stroke incidence among white, black, and Hispanic residents of an urban community; the Northern Manhattan Stroke Study, Am J Epidemiol, 1998;147:259–68.
  6. Kittner SJ, et al., Pregnancy and the risk of stroke, N Engl J Med, 1996;335:768–74.
  7. Mosca L, et al., Cardiovascular disease in women: a statement for healthcare professionals from the American Heart Association, Circulation, 1997;96:2468–82.
  8. Rosamond WD, et al., Stroke incidence and survival among middle-aged adults: nine-year follow-up of the Atherosclerosis Risk in Communities (ARIC) cohort, Stroke, 1999;30:736–43.
  9. Giles WH, et al., Determinants of black–white differences in the risk of cerebral infarction: the National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, Arch Intern Med, 1995;155:1319–24.
  10. Rubattu S, et al., Genetic susceptibility to cerebrovascular accidents, J Cardiovasc Pharmacol, 2001;38(Suppl. 2):S71–4.
  11. Nicolaou M, et al., Genetic predisposition to stroke in relatives of hypertensives, Stroke, 2000;31:487–92.
  12. Ortel TL, Genetics of coagulation disorders. In: Armonk NY, Alberts MJ (eds), Genetics of Cerebrovascular Disease, Futura Publishing Co, 1999:129–56.
  13. Barker DJ, Lackland DT, Prenatal influences on stroke mortality in England and Wales, Stroke, 2003;34:1598–602.
  14. Lackland DT, Egan BM, Ferguson PL, Low birth weight as a risk factor for hypertension, J Clin Hypertens, 2003;5:133–6.
  15. Wolf PA, et al., Probability of stroke: a risk profile from the Framingham Study, Stroke, 1991;22:312–18.
  16. D’Agostino RB, et al., Stroke risk profile: adjustment for antihypertensive medication: The Framingham Study, Stroke, 1994;25:40–43.
  17. Wang TJ, et al., A risk score for predicting stroke or death in individuals with new-onset atrial fibrillation in the community: the Framingham Heart Study, JAMA, 2003;290:1049–56.
  18. Goldstein LB, et al., Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Stroke, 2006;37:1583–1633.
  19. Lewington S, et al., Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies, Lancet, 2002;360:1903–13.
  20. Chobanian AV, et al., The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report, JAMA, 2003;289:2560–72.
  21. Neal B, MacMahon S, Chapman N, Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs, results of prospectively designed overviews of randomized trials, Lancet, 1998;351:1755–62.
  22. Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of ACE inhibitors, calcium antagonists, and other bloodpressure lowering drugs: results of prospectively designed overviews of randomised trials, Lancet, 2000;355:1955–64.
  23. Manolio TA, et al., Short-term predictors of incident stroke in older adults: the Cardiovascular Health Study, Stroke, 1996;27:1479–86.
  24. Rodriguez BL, et al., Risk of hospitalized stroke in men enrolled in the Honolulu Heart Program and the Framingham Study: a comparison of incidence and risk factor effects, Stroke, 2002;33:230–36.
  25. Kurth T, et al., Smoking and risk of hemorrhagic stroke in women, Stroke, 2003;34:2792–5.
  26. Wolf PA, et al., Cigarette smoking as a risk factor for stroke: The Framingham Study, JAMA, 1998;259(7):1025–9.
  27. Kawachi I, et al., Smoking cessation and decreased risk of stroke in women, JAMA, 1993;269(2):232–6.
  28. Wolf PA, Abbot RD, Kannel WB, Atrial fibrillation as an independent risk factor for stroke: The Framingham Study, Stroke, 1991;22(8):983–8.
  29. Hart RG, et al., Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis, Ann Intern Med, 1999;131:492–501.
  30. Gage BF, et al., Validation of clinical classification schemes for predicting stroke; results from the national registry of atrial fibrillation, JAMA, 2001;285:2864–70.
  31. Sportif Executive Steering Committee for the SPORTIF V Investigators: Ximelagatran vs warfarin for stroke prevention in patients with nonvalvular atrial fibrillation, a randomized trial, JAMA, 2005;293:690–98.
  32. Perez-Gomez F, et al., Comparitive effects of antiplatelet, anticoagulant, or combined therapy in patients with valvular and nonvalvular atrial fibrillation, J Am Coll Cardiol, 2004;44:1557–66.
  33. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM): a comparison of rate control and rhythm control in patients with atrial fibrillation, N Engl J Med, 2002;347(23):1825–33.
  34. Zhang X, et al., Asia Pacific Cohort Studies Collaboration. Cholesterol, coronary heart disease, and stroke in the Asia Pacific region, Int J Epidemiol, 2003;32:563–72.
  35. Wannamehee SG, Shaper AG, Ebrahim S, HDL-cholesterol, total cholesterol, and risk of stroke in middle-aged British men, Stroke, 2000;31:1882–8.
  36. Soyama Y, et al., High-density lipoprotein cholesterol and risk of stroke in Japanese men and women: the Oyabe Study, Stroke, 2003;34:863–8.
  37. Shahar E, et al., Plasma lipid profile and incident ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) study, Stroke, 2003;34:623–31.
  38. Cholesterol Treatment Trialists’ (CTT) Collaborators, Efficacy and safety of cholesterol-lowering treatment, prospective metaanalysis of data from 90,056 participants in 14 randomised trials of statins, Lancet, 2005;366:1267–78.
  39. Heart Protection Study Collaborative Group, MRC/BHF heart protection study of cholesterol-lowering with simvastatin in 5963 people with diabetes, a randomized placebo controlled trial, Lancet, 2003;361:2005–16.
  40. Sever PS, et al., Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lowerthan- average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial, Lancet, 2003;361:1149–58.
  41. Amerenco P, et al., Statins in stroke prevention and carotid atherosclerosis: systematic review and up-to-date metaanalysis, Stroke, 2004;35:2902–9.
  42. LaRosa JC, et al., Intensive lipid lowering with atorvastatin in patients with stable coronary disease, N Engl J Med, 2005;352(14):1425–1535.
  43. Adler AI, et al., Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study, BMJ, 2000;321:412–19.
  44. Lindholm LH, et al., Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomized trial against atenolol, Lancet, 2002;359:1004–10.
  45. Calhoun HM, et al., Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial, Lancet, 2004;364:685–96.
  46. UK Prospective Diabetes Study (UKPDS) Groups: Intensive bloodglucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33), Lancet, 1998;352:837–53.
  47. UK Prospective Diabetes Study (UKPDS) Groups: Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34), Lancet, 1998;352:854–65.
  48. Chambers BR, Norris JW, Outcome in patients with asymptomatic neck bruits, N Engl J Med, 1986;315(14):860–65.
  49. Mackey AE, et al., Outcome of asymptomatic patients with carotid disease, asymptomatic cervical bruit study group, Neurology, 1997;48(4):896–903.
  50. Meissner I, et al., The natural history of asymptomatic carotid artery occlusive lesions, JAMA, 1987;258(19):2704–7.
  51. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis, JAMA, 1995;273:1421–8.
  52. MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. Prevention of disabling fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomized controlled trial, Lancet, 2004;36; 1491–1502.
  53. Rothwell PM, Goldstein LB, Carotid endarterectomy for asymptomatic carotid stenosis asymptomatic carotid surgery trial, Stroke, 2004;35:2425–7.
  54. Mas JL, et al., Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis, N Engl J Med, 2006;355(16):1660–71.
  55. Rossouw JE, et al., Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial, JAMA, 2002;288:321–33.
  56. Anderson GL, et al., Women’s Health Initiative Steering Committee. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial, JAMA, 2004;291(14):1701–12.
  57. Hayden M, et al., Aspirin for the primary prevention of cardiovascular events: a summary of the evidence for the US Preventive Services Task Force, Ann Intern Med, 2002;136:161–72.
  58. Steering Committee of the Physicians Health Study Research Group. Final report on the aspirin component of the ongoing physicians’ health study, N Engl J Med, 1989;321:129–35.
  59. Ridker PM, et al., A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women, N Engl J Med, 2005;352(13):1293–1304.
  60. Whisnant JP, et al., A population-based model of risk factors for ischemic stroke: Rochester, Minnesota, Neurology, 1996;47:1420–28.
  61. Bonow RO, et al., ACC/AHA guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines, J Am Coll Cardiol, 1998;32(5):1486–1588.
  62. Go AS, et al., Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study, JAMA, 2001;285:2370–75.
  63. Wilterdink JL, Easton JD, Vascular event rates in patients with athersosclerotic cerebrovascular disease, Arch Neurol, 1992;49:857–63.

Further Resources

Share this Article
Related Content In Stroke
  • Copied to clipboard!
    accredited arrow-down-editablearrow-downarrow_leftarrow-right-bluearrow-right-dark-bluearrow-right-greenarrow-right-greyarrow-right-orangearrow-right-whitearrow-right-bluearrow-up-orangeavatarcalendarchevron-down consultant-pathologist-nurseconsultant-pathologistcrosscrossdownloademailexclaimationfeedbackfiltergraph-arrowinterviewslinkmdt_iconmenumore_dots nurse-consultantpadlock patient-advocate-pathologistpatient-consultantpatientperson pharmacist-nurseplay_buttonplay-colour-tmcplay-colourAsset 1podcastprinter scenerysearch share single-doctor social_facebooksocial_googleplussocial_instagramsocial_linkedin_altsocial_linkedin_altsocial_pinterestlogo-twitter-glyph-32social_youtubeshape-star (1)tick-bluetick-orangetick-red tick-whiteticktimetranscriptup-arrowwebinar Sponsored Department Location NEW TMM Corporate Services Icons-07NEW TMM Corporate Services Icons-08NEW TMM Corporate Services Icons-09NEW TMM Corporate Services Icons-10NEW TMM Corporate Services Icons-11NEW TMM Corporate Services Icons-12Salary £ TMM-Corp-Site-Icons-01TMM-Corp-Site-Icons-02TMM-Corp-Site-Icons-03TMM-Corp-Site-Icons-04TMM-Corp-Site-Icons-05TMM-Corp-Site-Icons-06TMM-Corp-Site-Icons-07TMM-Corp-Site-Icons-08TMM-Corp-Site-Icons-09TMM-Corp-Site-Icons-10TMM-Corp-Site-Icons-11TMM-Corp-Site-Icons-12TMM-Corp-Site-Icons-13TMM-Corp-Site-Icons-14TMM-Corp-Site-Icons-15TMM-Corp-Site-Icons-16TMM-Corp-Site-Icons-17TMM-Corp-Site-Icons-18TMM-Corp-Site-Icons-19TMM-Corp-Site-Icons-20TMM-Corp-Site-Icons-21TMM-Corp-Site-Icons-22TMM-Corp-Site-Icons-23TMM-Corp-Site-Icons-24TMM-Corp-Site-Icons-25TMM-Corp-Site-Icons-26TMM-Corp-Site-Icons-27TMM-Corp-Site-Icons-28TMM-Corp-Site-Icons-29TMM-Corp-Site-Icons-30TMM-Corp-Site-Icons-31TMM-Corp-Site-Icons-32TMM-Corp-Site-Icons-33TMM-Corp-Site-Icons-34TMM-Corp-Site-Icons-35TMM-Corp-Site-Icons-36TMM-Corp-Site-Icons-37TMM-Corp-Site-Icons-38TMM-Corp-Site-Icons-39TMM-Corp-Site-Icons-40TMM-Corp-Site-Icons-41TMM-Corp-Site-Icons-42TMM-Corp-Site-Icons-43TMM-Corp-Site-Icons-44TMM-Corp-Site-Icons-45TMM-Corp-Site-Icons-46TMM-Corp-Site-Icons-47TMM-Corp-Site-Icons-48TMM-Corp-Site-Icons-49TMM-Corp-Site-Icons-50TMM-Corp-Site-Icons-51TMM-Corp-Site-Icons-52TMM-Corp-Site-Icons-53TMM-Corp-Site-Icons-54TMM-Corp-Site-Icons-55TMM-Corp-Site-Icons-56TMM-Corp-Site-Icons-57TMM-Corp-Site-Icons-58TMM-Corp-Site-Icons-59TMM-Corp-Site-Icons-60TMM-Corp-Site-Icons-61TMM-Corp-Site-Icons-62TMM-Corp-Site-Icons-63TMM-Corp-Site-Icons-64TMM-Corp-Site-Icons-65TMM-Corp-Site-Icons-66TMM-Corp-Site-Icons-67TMM-Corp-Site-Icons-68TMM-Corp-Site-Icons-69TMM-Corp-Site-Icons-70TMM-Corp-Site-Icons-71TMM-Corp-Site-Icons-72