INTRODUCTION

It was recently shown that initiating stroke prevention treatment within a day of initial neurological symptoms rather than waiting for a few days can reduce stroke by 80% over waiting for a few days or weeks.¹ As we gather more information about how best to protect against stroke, it has become evident that an early and aggressive approach, with interventions aimed at each component of an individual’s risk of stroke is most effective.

The burden of stroke will continue to increase because of the increasing numbers of the elderly population. ² Treatment of stroke once it has occurred is extremely limited because of the need to start therapy within a few hours of onset. ³   Of all stroke patients presenting to the emergency department, less than 3% of patients currently receive intravenous tissue plasminogen activator (TPA), the standard therapy. ⁴ Thus the best means of treating stroke is through prevention.

Strokes are often of ischemic origin, meaning there is a lack of blood flow to an area of the brain; in the majority of cases, that restricted blood supply can be attributed to atherothrombosis. ⁵ Atherothrombosis is a systemic disease of the multiple vascular beds and stroke patients frequently have co-existent coronary artery disease and peripheral arterial disease, ⁶ and are at risk for a variety of vascular events. ^{7, 8}  The short-term risk of recurrent stroke or other serious morbidity can be as high as 18.5% over the three months following an initial stroke or transient ischemic attack (TIA). ⁹ The 30-day mortality rate after a first-ever stroke is approximately 25%, but is even higher for a second stroke. ^{10, 11}  This reinforces the idea that early and aggressive treatment of risk factors with medical treatments and lifestyle modifications would be most effective approach towards preventing stroke in at-risk populations. ^{8, 12}

ISCHEMIC STROKE RISK FACTORS

The first step in any approach to stroke prevention is the identification of predisposing risk factors (Table 1). Certain stroke risk factors such as age, male gender, and race are not modifiable and therefore cannot be the target of intervention. ¹³  The most important modifiable stroke risk factors are hypertension (high blood pressure), diabetes, smoking, and dyslipidemia (over-production or deficiency in lipoproteins, including LDL and HDL, common measures of cholesterol levels).

High blood pressure is the single most important modifiable risk factor for stroke, accounting for up to 50% of all strokes. ^{14, 15}  Blood pressure is strongly and directly related to stroke; the higher your blood pressure, the higher your risk of stroke.  Reducing blood pressure  can reduce risk of stroke and vascular mortality in a continuous manner all the way down to a level of 115/75 mm Hg.¹⁶  Elevated serum low-density lipoprotein cholesterol (LDL) and high-density lipoprotein (HDL) cholesterol also are emerging as established risk factors for stroke, and in particular atherosclerotic stroke due to thickening and hardening of the arteries.¹⁷ Cigarette smoking is a well-established risk factor for ischemic stroke. ¹⁸ The risk for stroke in diabetics has been estimated to be up to six times higher than that found in the normal population. ¹⁹

As the number and severity of risk factors increases, so does the risk of an individual having a first-ever stroke.  This was best demonstrated by the Framingham Study in which stroke-free subjects were monitored prospectively over the long-term and periodically evaluated for a variety of vascular risk factors. ^{20, 21} Based on the Framingham heart study, cardiovascular risk calculators have been developed to better assist clinicians in the stratification of individual’s risk of heart disease and stroke. ²² Understanding the risk factors facilitates a more comprehensives stroke prevention strategy, one that can address each stroke risk factor for every patient without focusing on only one particular aspect.  Measures can include medications, lifestyle changes, and education at the earliest possible time, often while hospitalized.

MEDICATION THERAPIES

            Three main categories of medications have been shown to reduce cardiovascular and stroke risk.  They are antithrombotic agents (such as antiplatelet therapy), antihypertensive agents, and cholesterol agents/statins. The benefits of these treatments are not unique to stroke, but extend to all forms of atherosclerosis such as coronary artery disease and peripheral vascular disease.

 Antiplatelet Therapy

Antiplatelets include aspirin, clopidogrel, ticlopidine, and dipyridamole. A meta-analysis by the Antithrombotic Trialists' Collaboration assessed the effect of antiplatelet therapy in over 200,000 patients with various manifestations of atherosclerosis. ²³ This meta-analysis of many smaller studies found that, overall, antiplatelet therapy reduces the combined odds of having a stroke, heart attack (myocardial infarction or MI), or vascular death by 22%, and the odds of a non-fatal stroke by 25%. These benefits were seen over a wide range of patients with or without a previous stroke.²³

Aspirin is the most commonly used medication in this class and prevents platelet activation by inhibiting the enzyme cyclooxygenase, thereby blocking the generation of thromboxane (a blood clotting substance) and reducing the relative risk of stroke recurrence by 13–18%. ²⁴  There were no important differences for preventing stroke and other vascular events for various doses aspirin between 30 mg and 1,300 mg per day.^24-27 A dose of 81 mg per day is very commonly prescribed for stroke prevention.

Aspirin may be a better treatment option than anticoagulation with warfarin for the vast majority of patients without cardiac origins of stroke. The Warfarin Aspirin in Recurrent Stroke Study (WARSS) found no difference between aspirin and warfarin for prevention of recurrent ischemic stroke, death, or major hemorrhage in patients with non-cardioembolic stroke²⁸ – stroke not caused by a blood clot traveling from the heart to the brain.  Another study comparing aspirin and warfarin in stroke due to critical narrowing of the cranial arteries found that warfarin was associated with significantly higher rates of adverse events and provided no benefit over aspirin. ²⁹

Adenosine diphosphate (ADP)-receptor antagonists such as clopidogrel inhibit ADP-induced fibrinogen binding to platelets, a necessary step in the platelet aggregation (clotting) process.  Studies have demonstrated that clopidogrel effectively prevents stroke in patients with evidence of vascular disease. The Clopidogrel vs. Aspirin in Patients at Risk of Ischemic Events (CAPRIE) study was comprised of 19,185 patients with recent ischemic stroke, myocardial infarction, or peripheral arterial disease and showed an 8.7% relative risk reduction in the combination of ischemic stroke, myocardial infarction or vascular death.³⁰  The safety profile of clopidogrel is superior to that of ticlopidine (another ADP receptor antagonist), which is rarely used today due to cases of hematologic (blood) problems, such as agranulocytosis (a reduction of white blood cells) and anemia (low hemoglobin levels). ³¹

The combination of aspirin and long-acting dipyridamole has been tested and found to be more effective than aspirin alone in stroke prevention in the Second European Stroke Prevention Study (ESPS-2) and European/Australasian Stroke Prevention in Reversible Ischaemia Trial (ESPRIT) studies. ^{24, 32}  An analysis of six published trials compared 3888 patients treated with the combination of aspirin and dipyridamole to 3907 treated with aspirin alone.  There were a total of 1158 strokes and vascular events recorded with an overall risk reduction of 18% in favor of the combination over aspirin.³²

Not all combinations of antiplatelets are better than single antiplatelet in stroke prevention. The first study of the combination of aspirin with clopidogrel, the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) study, demonstrated a benefit for the combination in patients with recent heart attacks, leading to speculation as to the benefit of this approach in stroke.  Unfortunately, follow-up studies in patients who did not have recent heart symptoms, including stroke patients, demonstrated no significant benefit for this combination.^{33, 34} Most relevant was the Management of Atherothrombosis with Clopidogrel in High-risk patients (MATCH) study which included only individuals with a recent stroke or TIA.³³  This study found that the combination of aspirin and clopidogrel was no better than clopidogrel alone in preventing secondary stroke or vascular events, but was associated with more bleeding.

Data from the MATCH and the Clopidogrel for High Atherothrombotic Risk, Ischemic Stabilization, Management, and Avoidance (CHARISMA) studies argue against routine use of combination aspirin and clopidogrel over the long-term for secondary prevention of stroke. This combination may have a small benefit when started during the acute phase of stroke and continued for a short duration,³⁵  but this approach is not recommended at this time.³⁶

Blood Pressure Reduction

Antihypertensive treatment has been shown to reduce the risk of initial and second stroke in hypertensive individuals substantially. ³⁷ Many individuals whose blood pressure is not considered within the hypertensive range (less than or equal to 140/90 mm Hg) with stroke risk factors may also benefit from antihypertensive medication treatment. ³⁸ The overall effect of treating hypertension is a 30% reduction in the risk of secondary stroke.^{39, 40}

There are four groups of antihypertensive agents which have been shown to reduce vascular morbidity and stroke.  These are the ABCD drugs, Angiotensin converting enzyme (ACE) inhibitors/ angiotensin receptor blockers (ARBs), beta (b)-blockers, Calcium channel blockers (CCBs), and Diuretics.  Other agents such as direct-acting smooth muscle relaxants and direct-acting α2 adrenergic agonists may reduce blood pressure, but have not been shown to reduce strokes and should not be routinely used.⁴¹

ACE inhibitors and ARBs are medications that weaken the effects of the rennin-angiotensin system. The renin-angiotensin system is involved in vascular remodeling, oxidative stress, and inflammation.  Several large studies have evaluated the role of ACE inhibitors and ARBs for stroke prevention in different populations (Table 2). These classes of agents may have benefits for stroke prevention above and beyond blood pressure lowering. In head-to-head trials with b-blockers and CCBs in select populations, these agents have been associated with lower stroke occurrence despite similar blood pressure lowering.^{42, 43}

No study has so far shown a difference between ACE inhibitors and ARBs with regard to stroke prevention, however the selective actions of ARBs have been associated with fewer side effects.  Furthermore, early initiation (within 48 hours) of the ARB candesartan in patients hospitalized for stroke with hypertension was shown to be safe, and provided greater vascular protection compared to antihypertensive initiation one week after stroke onset. ⁴⁴

b-blockers antagonize the b-adrenergic receptors of the heart muscle and vasculature.  b-blockers have been used for the treatment of hypertension for four decades and are considered to be appropriate for initial antihypertensive therapy.^{41, 45} The efficacy of b-blockers in patients who have coronary artery disease such as myocardial infarction, angina, congestive heart failure, or cardiomyopathy has been demonstrated thorough many prospective randomized trials.^46-48 The recent Joint National Committee (JNC) 7 guidelines consider congestive heart failure and secondary cardioprotection in hypertensive patients an indication for the use of β-blockade. The evidence behind routine use of b-blockers for secondary stroke prevention is not as robust.

            In the LIFE study, the b-blocker atenolol was compared with the ARB losartan in patients with hypertension and LVH.⁴² The ARB was found to be consistently superior to the b-blocker therapy alone or in combination in hypertensive patients with or without diabetes, with 25% fewer strokes and superior reduction of left ventricular hypertrophy. In the group of patients with isolated systolic hypertension, the stroke risk was reduced by 40% with losartan compared with atenolol.  Given the less desirable side-effect profile of b-blockers, these agents are usually reserved for patients at risk of stroke with established cardiac disease.

CCBs reduce blood pressure by inhibiting entry of calcium into cells by antagonizing the alpha-1c subunit of the L-type calcium channel, which is the main pore-forming unit of the channel. The recently reported MOSES trial (MOrbidity and mortality after Stroke, Eprosartan compared with nitrendipine for Secondary prevention) randomized hypertensive patients with a history of stroke to antihypertensive therapy with either the ARB eprosartan or the CCB nitrendipine.  Despite equal blood pressure reductions in both arms, there was a significant 23% risk reduction in recurrent stroke for patients treated with the ARB over the CCB. ⁴³

The most commonly used diuretic, thiazides, acts by reducing tubular re-absorption of sodium and chloride ions in the ascending loop of Henle and early distal tubule of the kidney.  This results in excretion of water, sodium, and chloride.  The net effect is a decrease in peripheral vascular resistance - blood pressure.  Thiazides have been associated with decreased rates of stroke in many studies of various populations. In the randomized, placebo-controlled trial PATS (The Post-stroke Antihypertensive Treatment Study), the thiazide diuretic indapamide was evaluated in secondary stroke prevention in 5665 people.⁴⁹ Treatment with thiazides was associated with a 5mm/2mm reduction in blood pressure and a 29% relative reduction of stroke at three years compared to placebo. The PROGRESS trial found that combined therapy with a thiazide diuretic, indapamide, and an ACE inhibitor, perindopril, but not perindopril alone significantly reduced the risk for recurrent stroke.³⁸

            Alpha-blockers act by antagonizing the central nervous system α-2 receptor.  This causes blood pressure to be lowered by a negative feedback mechanism at the presynaptic neurons.  Based on the results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) study, treatment with a-blockers was inferior to all other treatment groups and this class of agents is not recommended for treatment of hypertension in stroke patients.⁵⁰ 

When evaluating the best antihypertensive regimen for stroke prevention, one has to take into account the impressive results of the PROGRESS trial, which led the JNC 7 to recommend the combination of thiazide-type diuretic and ACE inhibitors for patients with cerebrovascular disease. ⁵⁰ In patients with very elevated blood pressure meeting a diagnosis of stage 2 hypertension (systolic blood pressure greater than or equal to 160 mm Hg or diastolic blood pressure greater than or equal to100 mm Hg), the JNC-7 guidelines indicate treatment with a combined two-drug antihypertensive regimen should be initiated.  We routinely initiate combination therapy with thiazides and ACE inhibitors or ARBs for all stable stroke patients with elevated blood pressure.

Statins (HMG-CoA reductase inhibitors)

Over the past decade many large trials of cholesterol treatment with statins have shown a reduction in vascular events, including stroke (Table 43). The mechanisms by which statins protect from stroke and vascular disease are many and include cholesterol/lipoprotein-mediated alterations (increasing the LDL cholesterol receptor activity with less entry of LDL, the bad cholesterol, into the circulation), improved function of the cells lining the blood vessels (upgrading endothelial nitric oxide synthase), stabilization of atherosclerosis plaque, blocking coagulation, reducing inflammation responses, and antioxidant effects. In addition, statins may also directly protect the brain cells.

The American Stroke Association/ American Heart Association (ASA/AHA) recommend that a statin be initiated during hospitalization for ischemic strokes caused by or in the presence of atherosclerosis (Table 4).⁵¹ This guideline can be applied to ischemic strokes caused by small vessel disease or large vessel atherosclerosis. Treatment dose should depend on an individual’s vascular risk; for most patients an LDL cholesterol goal of less than 100 mg/dL should be targeted.  Some patients at very high risk should have an LDL cholesterol goal of less than 70 mg/dL.  ⁵²

LIFESTYLE MODIFICATION

Smoking causes increased artery wall stiffness resulting in reduced vessel wall mobility and increased inflammation within the vessel. The stroke risk associated with quitting smoking has been shown to substantially decrease as the time since quitting increases, ultimately returning to the risk level of nonsmokers at five years from cessation in the Framingham study. ¹⁸ Prospective studies assessing modification of smoking habits showed that 21.7% gave up smoking at six months after having inpatient counseling.⁵³ All stroke patients should be screened for this risk factor and receive counseling. 

            High daily dietary intake of fat is associated with obesity and is an independent risk factor for stroke or may affect other risk factors such as hypertension, diabetes, dyslipidemia, and cardiac disease. The AHA diet guidelines (http://americanheart.org/presenter.jhtml?identifier=851) are an important resource for initiating a diet that will lead to weight loss, improved quality of life, and less stroke.⁵⁴ Patients with prior stroke should eat fewer high fat/high cholesterol foods and should lose weight to achieve normal weight based on the calculation of basal metabolic index (BMI). 

Physical activity prevents stroke in part through its role in controlling known risk factors like hypertension, cardiovascular disease, diabetes, and body weight. Other possible mechanisms include reductions in fibrinogen and platelet activity as well as elevations in plasma tissue plasminogen activator activity leading to less clots forming, and improving the cholesterol profile.  Guidelines endorsed by the Centers for Disease Control and Prevention and the National Institutes of Health recommend that Americans should exercise for at least 30 minutes of moderately intense physical activity on most, and preferably all days of the week.^{55, 56}

Education

Education about stroke and risk factors can lead to empowerment of individuals and increased motivation to comply with guidelines. Education of the importance of risk factor and lifestyle modification can be especially effective when a person is admitted to the hospital and focused on their health.  Secondary stroke prevention initiatives with a high emphasis on patient education, such as the PROTECT program, ⁵⁷ have consistently demonstrated better outcomes ⁵⁸.

SURGERY AND ENDOVASCULAR TREATMENT

Carotid Endarterectomy (CEA)

CEA is a surgical procedure where the carotid artery (the artery that supplies the head and neck with oxygenated blood) is opened and cleared of plaque.  Internal carotid artery (ICA) narrowing/stenosis is an important cause of TIAs and stroke, accounting for up to 20% of cases. ICA stenosis of greater than 50% is present in about 4% to 8% of the population aged 50 to 79 years. The most common cause of ICA stenosis is atherosclerosis.

According to the AHA recommendations, CEA is beneficial for persons who have had a recent non-disabling stroke or TIA on the same side as a 70% to 99% carotid narrowing.⁵⁹ CEA is not beneficial for patients with less than 30% stenosis. There is yet uncertainty about the benefits of CEA for symptomatic patients with 30% to 69%. CEA for ICA stenosis greater than 60% and not associated with neurological symptoms is an acceptable option for patients when performed in a center with a surgical risk less than 3% and when the life expectancy of the treated person is at least five years.⁵⁹ Patients with less than 60% asymptomatic stenosis do not benefit from CEA. 

Carotid Angioplasty with Stenting (CAS)

Carotid artery stenosis may be treated non-surgically using an endovascular approach to open up the artery. The procedure involves percutaneous transluminal balloon angioplasty with or without stent (a metal or plastic tube) insertion – or primary stenting. Endovascular treatment may be a useful alternative to CEA, particularly for lesions not suitable for surgery.

The AHA guidelines state that with few exceptions, use of CAS should be limited to well-designed, well-controlled randomized studies with careful, dispassionate oversight.⁶⁰ These guidelines may soon be updated and should incorporate recent clinical trial data.  The Carotid Revascularization Endarterectomy Versus Stent Trial (CREST), and the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS II), are currently in progress.^{61, 62} In our institution we will only use CAS in the rare patient who is at a very high risk for surgery and has had recent symptoms.  All other CAS procedures are performed within a clinical trial setting.

IN-HOSPITAL INITIATION STRATEGY

Disease-management programs initiated at the time of acute hospitalization result in higher compliance over the long-term with more patients continuing therapy.  This was shown in studies comparing hospital initiation with routine recommendations to the primary-care doctors, which is often the case. ⁶³ This strategy is not just a strong predictor of patients continuing the treatments, ⁶⁴ but also results in better clinical outcomes like fewer hospitalizations and adverse events. ^{63, 65} In-hospital initiation of secondary prevention therapies as the standard of care for hospitalized stroke patients could dramatically improve compliance with treatment and benefit society as a whole.

CONCLUSIONS

In summary, a multimodal stroke prevention strategy addresses each stroke risk factor for every patient without focusing on only one particular aspect. This approach includes medications, lifestyle changes, and education at the earliest possible time-point, often while hospitalized. The effects in stroke prevention for each individual intervention are additive and complementary. (Table 5) As our knowledge of atherosclerosis and stroke increases, we need to put this information to use immediately to benefit at-risk individuals.  Though using evidence-based stroke risk reduction treatments effectively and efficiently may prove to be a challenge, with close attention to new research and the ready incorporation of this evidence into routine care of stroke patients, the societal toll that stroke exerts may be mitigated.

 

 

 

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TABLES

Table 1.  Established Modifiable Stroke Risk Factors

 

Established Modifiable Risk Factors

Prior TIA or Stroke

Hypertension

Cardiac Disease

Atrial Fibrillation

Hyperlipidemia

Carotid Stenosis

Diabetes

Cigarette Smoking

Physical Inactivity

Heavy Alcohol Use

 

 

 

 

 

Table 2. Major Trials of Angiotensin-Modifying Antihypertensive Agents 

 

Trial	Year	N	Population Studied	Intervention	Follow-up	Superior Agent	RRR	Comments
PROGRESS38	2001	6105	History of stroke or TIA	Perindopril-based (n=3051) vs. placebo-based (n=3054)	4 y	Perindopril	28% for stroke	43% for perindopril plus indapamide
LIFE42	2002	9193	Essential HTN and LVH	Losartan-based (n=4605) Vs. atenolol-based (n=4588)	4.8 y	Losartan	13% for stroke	Equal BP reduction  in groups
ACCESS44	2003	342	Acute ischemic stroke	Candesartan vs. Placebo	12 mo	Candesartan	53% for mortality and vascular events.	BP equal in both groups
HOPE66	2002	9297	Vascular disease or DM + one vascular RF	Ramipril vs. Placebo	4.5 y	Ramipril	32% for stroke	Modest  reduction in BP (3.8/2.8)
ALLHAT50	2002	33,357	HTN + one other coronary risk factor	Chlorthalidone vs. Amlodipine vs. Lisinopril	4.9 y	None	Not significant for stroke	Most required multi-drug regimen
MOSES67	2004	>1400	Hypertensives with history of stroke	Eprosartan vs. Nitrendipine		Erposartan	23% for stroke	Equal BP reductions in groups

 

 

 

Table 3. ATP III LDL-C Treatment Recommendations in Light of Recent Clinical Trial Evidence

Overall Risk Category	LDL-C Goal
High risk:  Stroke in the setting of CHD° or CHD equivalents*. (10-year risk >20%)#	<100 mg/dL or <70 mg/dL (optional goal)
Moderately high risk: Stroke in the setting of 2 or more risk factors, 10-year risk 10-20%#	<130 mg/dL or <100mg/dL (optional goal)
Moderate risk: Stroke in the setting of 2 or more risk factors, 10-year risk <10%#	<130 mg/dL
Low risk: Stroke in the setting of 0-1 risk factors^	<160 mg/dL
° CHD includes myocardial infarction, unstable angina, coronary artery procedures, or evidene of myocardial ischemia. * CHD equivalents include clinical manifestations of noncoronary forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease), and diabetes. ^ Risk factors include cigarette smoking, hypertension (BP 140/90 mm Hg or on antihypertensive medication), low HDL cholesterol (<40 mg/dL), family history of premature CHD (CHD in male first-degree relative <55 years of age; CHD in female first-degree relative <65 years of age), and age (men 45 years; women 55 years). #-10-year risk calculators are available at www.nhlbi.nih.gov/guidelines/cholesterol.

Adapted from: Grundy, S.M., et al., Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. Circulation, 2004. 110(2): table 2. (Permission requested)

 

 

 

 

Table 4 Clinical trials of statins versus placebo: effects on stroke.

Trial	Year	N	Population studied	Statin type and dose	Average follow-(years)	Stroke RRR	Stroke ARR	Comments
SPARCL68	2006	4731	Stroke or TIA	Atorvastatin 80mg	4.9	16%	2.2%	None
ASCOT- LLT69	2003	10305	Hypertension plus three risk factors for stroke	Atorvastatin 10mg	3.3	27%	0.7%	Included many with normal cholesterol
PROSPER70	2002	5804	Age 70–82. Tchol 155–350 mg/dl (4.01–9.07 mmol/l)	Pravastatin 40mg	3.2	3% (NS)	0%	No effect on cognitive decline
ALLHAT-LLT71	2002	10355	Hypertension and age >55	Pravastatin 20–40 mg	4.8	9% (NS)	0.4%	Not double-blind or placebo-controlled
HPS72	2002	20536	Stroke or coronary heart disease	Pravastatin 40mg	5.3	25%	1.4%	Included patients with prior stroke
LIPID73	1998	9014	Post-MI or unstable angina. Tchol 155–271 mg/dl (4.01–7.02 mmol/l)	Pravastatin 40mg	6.0	19%	0.8%	All stroke subtypes, validated by neurologist
CARE74	1996	4159	Post-MI. Tchol < 240 mg/dl (6.22 mmol/l), LDL 115–174 mg/dl (2.98–4.51 mmol/l)	Pravastatin 40mg	5.0	32%	1.2%	All types of stroke, effect additive to aspirin (80% of subjects were on aspirin)
4S75	1994	4444	Post-MI or unstable angina. Tchol >270 mg/dl (6.99 mmol/l)	Simvastatin 10–40mg	5.4	30% for stroke and/orTIA	1.6%	Most of reduction was in TIAs. Only 37% of subjects were on aspirin

Abbreviations: ARR, absolute risk reduction; MI, myocardial infarction; N, number of patients; NS, not significant (p<0.05); RRR, relative risk reduction; Tchol, total cholesterol; TIA, transient ischemic attack.

Table 5. The Number of Patients Who Need to Be Treated For One Year with Each Stroke Prevention Measure To Prevent One Stroke From Occurring

 

Treatment	Relative Risk Reduction	Number Needed to Treat (One stroke/year)
Antihypertensive agents	28%	51
Statins	25%	57
Aspirin	28%	77
Smoking Cessation	33%	43
Carotid Endarterectomy	44%	26

 

 

Adapted from Straus, S.E., S.R. Majumdar, and F.A. McAlister, New Evidence for Stroke Prevention: Scientific Review. JAMA, 2002. 288(11): p. 1388-1395. (Permission requested)