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Am Fam Physician. 2023;108(1):70-77

Patient information: See related handout on stroke prevention.

This clinical content conforms to AAFP criteria for CME.

Author disclosure: No relevant financial relationships.

Ischemic stroke is a major cause of morbidity and mortality worldwide. Ischemic stroke and transient ischemic attack exist on a continuum of the same disease process. Ischemic stroke is common, and more than 85% of stroke risk is attributed to modifiable risk factors. The initial management of acute stroke is usually performed in the emergency department and hospital settings. Family physicians have a key role in follow-up, ensuring that a complete diagnostic evaluation has been performed, addressing modifiable risk factors, facilitating rehabilitation, and managing chronic sequelae. Secondary prevention of ischemic stroke includes optimization of chronic disease management (e.g., hypertension, type 2 diabetes mellitus, dyslipidemia), nonpharmacologic lifestyle interventions (e.g., diet changes, exercise, substance use counseling), and pharmacologic interventions. Dual antiplatelet therapy with aspirin and clopidogrel is generally indicated for minor noncardioembolic ischemic strokes and high-risk transient ischemic attacks and should be converted to single antiplatelet therapy after 21 to 90 days. Secondary prevention of cardioembolic stroke requires long-term anticoagulation. Direct oral anticoagulants are preferred over warfarin for patients with nonvalvular atrial fibrillation. Poststroke problems with mobility, balance, cognition, dysphagia, and depression are common. Rehabilitation involves a multidisciplinary, multimodal approach that includes physical therapy, speech therapy, and treatment of chronic pain and poststroke depression.

Ischemic stroke is the result of a sudden blockage of blood flow to the central nervous system due to thrombotic or embolic phenomena, and it is a major cause of morbidity and mortality worldwide. In 2019, stroke was the fifth leading cause of death in the United States.1 Although stroke can be hemorrhagic or ischemic, approximately 87% of strokes in the United States are ischemic.2 Almost 800,000 strokes occur annually in the United States, often leading to long-term disability.2

Clinical recommendation Evidence rating Comments
Patients with hypertension and a previous ischemic stroke or TIA should be treated to an ambulatory blood pressure of 130/80 mm Hg, if tolerated.3 C Expert consensus guideline based on large clinical trials showing reduction of future cardiovascular events
Patients with atherosclerotic ischemic stroke and a low-density lipoprotein cholesterol level greater than 100 mg per dL (2.59 mmol per L), with or without known coronary artery disease, should be treated with high-intensity statin therapy.3 C Expert consensus guideline based on trials showing reduction of stroke incidence and cardiovascular events with atorvastatin
Patients with minor noncardioembolic ischemic stroke or high-risk TIA should be treated with dual antiplatelet therapy (aspirin plus clopidogrel) for 21 to 90 days, followed by single antiplatelet monotherapy indefinitely for secondary prevention. Continued use of dual antiplatelet therapy for more than 90 days should be avoided due to increased bleeding risk.3,1618 A A Cochrane review and meta-analysis of randomized controlled trials showing that the benefit of decreased stroke risk outweighs the risk of major bleeding when treated for at least 21 days but not for longer than 90 days after a minor noncardioembolic stroke or high-risk TIA
Long-term antiplatelet therapy for secondary prevention of TIA or ischemic stroke should include aspirin, 50 to 325 mg, once per day; clopidogrel, 75 mg, once per day; or aspirin, 25 mg, and extended-release dipyridamole, 200 mg, twice per day.3,1921 B Multiple randomized controlled trials showing a consistent decrease in the risk of recurrent ischemic stroke, myocardial infarction, and vascular death in patients treated with antiplatelet therapy after stroke (secondary prevention)

Transient ischemic attack (TIA) is defined as a transient neurologic dysfunction caused by ischemia without infarction on imaging. Because the subsequent risk of stroke after TIA is similar to that of an initial stroke, TIA is treated similarly to a minor, nondisabling stroke. In this article, TIA is included with ischemic stroke, except where noted.

It is estimated that 87% of stroke risk is attributable to modifiable risk factors.2 Risk factors for ischemic stroke are listed in Table 1.3,4

Embolic
Arrhythmia (atrial fibrillation/flutter)
Artery-to-artery embolization
Bacterial endocarditis
Bioprosthetic or mechanical heart valve
Dilated cardiomyopathy
Heart failure with ejection fraction of less than 30%
Myocardial infarction within the past month
Patent foramen ovale
Rheumatic mitral or aortic valve disease
Thrombotic
Aortic dissection
Arteritis/vasculitis
Atherosclerosis
Diabetes mellitus
Fibromuscular dysplasia
Hypercoagulable states
Hyperlipidemia
Hypertension
Polycythemia vera
Thrombocytosis

Similar to many conditions, stroke is associated with health disparities. Compared with White people, Black people in the United States have strokes at younger ages and have more poststroke disability, much of which is related to modifiable risk factors.5 Increasing age and female sex are associated with greater poststroke disability.5 Stroke risk also varies with education level, income, zip code, health insurance, and social isolation, and assessing these factors is important for the primary and secondary prevention of stroke.6

Diagnostic Evaluation

Although the initial management of acute stroke usually occurs in the emergency and hospital settings, the outpatient follow-up evaluation is critical to ensure that the appropriate testing has been completed, reviewed, and discussed with the patient.7 Certain parts of the evaluation to determine the cause of the stroke may be deferred until outpatient follow-up. Table 2 summarizes the evaluation of stroke on the basis of pathogenesis.3,7,8

EvaluationPurposeComments
Cervical carotid artery imaging with ultrasonography, computed tomography angiography, or magnetic resonance angiographyScreen for carotid stenosisMagnetic resonance angiography can identify less common etiologies of stroke (e.g., vasculitis, dissection)
EchocardiographyScreen for cardiac source of emboli and intracardiac defects (e.g., patent foramen ovale)Transesophageal echocardiography may be indicated when an embolic stroke has occurred and the etiology has not been determined; a bubble study may be useful to identify a left ventricular thrombus or patent foramen ovale with right-to-left shunt
Long-term cardiac rhythm monitoring (e.g., 30-day event monitor, implantable loop recorder)Screen for atrial fibrillation when the etiology has not been determined and embolic stroke is suspectedApproximately 9% of patients with cryptogenic stroke will exhibit atrial fibrillation on long-term rhythm monitoring
Laboratory evaluation: complete blood count, prothrombin time, partial thromboplastin time, glucose, A1C, creatinine, lipid panelScreen for risk factors and inform therapeutic goals (e.g., dyslipidemia and lipid treatment goals)
Expanded laboratory evaluation with blood and cerebrospinal fluid testsScreen for hypercoagulable states; infection; vasculitis; drug use; and connective tissue, inflammatory, and genetic disorders if etiology has not yet been determined or based on medical, social, or family historyHypercoagulable states include prothrombin gene mutation, factor V Leiden, protein C and S deficiencies, and antithrombin deficiency

At the first primary care visit after stroke, diagnostic imaging should be reviewed to confirm the diagnosis.3 Although computed tomography (CT) and magnetic resonance imaging (MRI) are both used to diagnose stroke, MRI has 99% sensitivity for stroke, compared with 39% with CT, and can diagnose acute ischemic strokes missed by CT.8 If initial imaging was negative for stroke despite characteristic symptoms, follow-up CT or MRI may be indicated to confirm the diagnosis.3,7

Atrial fibrillation is estimated to cause approximately 1 in 7 strokes.9 In addition to electrocardiography performed during the initial evaluation of stroke, continuous cardiac rhythm monitoring is often performed during hospitalization.3 Long-term cardiac rhythm monitoring (e.g., 30-day event monitor, implantable loop recorder) increases the detection of atrial fibrillation and is useful in the evaluation of cryptogenic stroke.3,10

The initial evaluation of stroke includes laboratory testing to identify underlying risk factors and determine therapeutic targets.3 Complete blood count, prothrombin time, partial thromboplastin time, glucose, A1C, creatinine, and lipid profile are recommended to identify risk factors such as diabetes, dyslipidemia, chronic kidney disease, and blood cell dyscrasia. If stroke is determined to be cryptogenic based on the initial evaluation, expanded laboratory assessment, including testing for hypercoagulable states (e.g., prothrombin gene mutation, factor V Leiden, protein C and S deficiencies, antithrombin deficiency), infection, drug use, and connective tissue, inflammatory, and genetic disorders, may be indicated.

Polysomnography can also be considered to evaluate for obstructive sleep apnea. This condition is both a risk factor for stroke and a common comorbidity in patients with previous stroke (approximately 40% of stroke cases); however, it is unclear whether treatment with continuous positive airway pressure prevents recurrent vascular events.3

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