Transient Ischemic Attack

History

• Focus on characteristics of the event; symptoms typically resolve before patient presentation
  • If symptoms have not resolved, assume that patient is having stroke or other stroke mimic and urgently treat accordingly
  • Ascertain onset abruptness and symptom duration
    • Transient ischemic attack onset is typically sudden and without prodrome ^c1
    • Most transient ischemic attacks are brief, often lasting less than 1 hour with complete resolution of symptoms within 24 hours ^r6
  • Witnesses to event may provide useful information
• Symptoms are usually focal, reflecting anatomic location of ischemic vessel (80% anterior and 20% posterior circulation) ^r8
  • Nonfocal signs and symptoms (eg, loss of consciousness, confusion, generalized weakness, lightheadedness, incontinence) are rarely caused by transient ischemic attacks ^r4c2c3c4c5c6
• In general, negative symptoms (eg, loss of function) suggest ischemia and positive findings (eg, stimulated or increased function) suggest alternative diagnosis (eg, migraine, seizure)
  • Negative symptoms suggestive of ischemia include:
    • Motor: loss of movement (ie, hemiparesis, hemifacial weakness in upper motor neuron distribution) ^c7c8c9
    • Speech: altered or decreased (ie, aphasia) ^c10c11
    • Visual: loss of vision (ie, amaurosis fugax) ^c12c13
    • Sensation: anesthesia (ie, hemisensory loss) ^c14c15
  • Positive symptoms (eg, involuntary motions, dysesthesias, visual flashes) suggest alternative diagnosis
    • Exception: vertigo may be associated with posterior circulation ischemia ^c16
• Pain is unlikely to be a symptom of transient ischemic attack, although unilateral neck pain with focal neurologic signs and symptoms may occur with cervical artery dissection ^c17c18

Physical examination

• Physical examination findings at time of presentation may be entirely normal; treat presence of new neurologic deficits as stroke until proven otherwise
• Focus of comprehensive examination is to detect any neurologic deficits, define the cause of the event, and assess for vascular risks
  • Complete neurologic assessment (eg, strength, sensation, coordination, balance, speech, language)
    • NIH stroke scale may be useful to document baseline neurologic findings ^r9
  • Neck and heart auscultation may find carotid bruits (stenosis), irregular heart rhythm (atrial fibrillation), or murmurs (valvular disease) ^c19c20c21
  • Ocular fundi may show evidence of emboli (Hollenhorst plaques), retinal artery occlusion, or chronic hypertensive vascular changes; vision testing may find loss or defects ^c22c23c24
  • Skin examination may find signs of trauma, coagulopathies, platelet disorders, or embolic lesions (Janeway lesions or Osler nodes) ^{c25c26c27c28c29}

Causes

• Transient ischemic attack and stroke share the same cause and pathophysiology: focal hypoperfusion with impaired cerebral oxygenation and metabolism
• Causes (classification based on presumed mechanism and type and location of vascular lesion):
  • Cardioembolic (approximately 34% of cases^r1), including: ^c30
    • Cardiac dysrhythmia (atrial fibrillation, atrial flutter) ^c31c32
    • Valve disease and mechanical valve prosthesis ^c33c34
    • Cardiac thrombi
    • Patent foramen ovale; other atrial or ventricular septal defects ^c35c36c37
    • Dilated cardiomyopathies ^c38
    • Impaired left ventricular dysfunction (eg, recent myocardial infarction) ^c39c40
    • Infective endocarditis, septal aneurysms, and myxomas ^c41c42c43c44
  • Large artery atherosclerosis (9%-13% of cases^r1) ^c45
    • May result in plaque emboli or stenosis with flow reduction or complete obstruction ^c46c47
    • Location may be intracranial or extracranial (eg, carotid or vertebral artery stenosis, aortic atherosclerosis) ^c48c49c50
  • Small artery occlusion/disease (lacunar; 10%-18% of cases^r1) ^c51
    • Lacunar strokes are most commonly result of poorly controlled hypertension, diabetes, and hyperlipidemia ^c52
  • Other causes (3%-6% of cases^r1), for example:
    • Dissection of vertebral or carotid artery ^c53c54
    • Hypercoagulable states ^c55
    • Vasculitis ^c56
    • Sympathomimetic drugs (eg, cocaine, amphetamines) ^c57c58c59
  • Undetermined causes (25%-50% of cases^r1) ^c60

Risk factors and/or associations

Genetics

• Parental family history of stroke is a risk factor; no specific genetic factor is clearly established ^r10c64

Primary diagnostic tools

• Accurate history and complete physical examination provide basis for clinical diagnosis ^c79
• Conduct initial diagnostic evaluation promptly; complete thorough evaluation within 48 hours ^r11
  • Identify unsuspected infarction and exclude nonischemic causes
  • Identify high-risk, modifiable conditions that have effective therapeutic interventions (eg, carotid stenosis, atrial fibrillation)
• Obtain fingerstick blood glucose measurement to exclude hypoglycemia, a mimic of transient ischemic attack and stroke
• Perform brain and vasculature imaging in all patients with suspected transient ischemic attack ^r2
  • Obtain neuroimaging within 24 hours of symptom onset or as soon as possible after an event ^r2
    • Identify vascular origin and mechanism of event to prevent future stroke; may provide alternative diagnosis for patient symptoms
    • MRI, including diffusion-weighted imaging, is preferred brain imaging modality ^r2
      • Diffusion-weighted imaging is useful to predict short-term risk of stroke ^r12
    • Obtain head CT if MRI is not available
  • Noninvasive cervical vessel imaging
    • Predicts higher short-term risk for stroke (symptomatic carotid stenosis with narrowing more than 50%) ^r5r12
    • Doppler ultrasonography, magnetic resonance angiography, or CT angiography
      • Selection depends on local availability, practitioner expertise, and patient characteristics (eg, pacemaker presence, renal failure)
      • Use of supraaortic magnetic resonance and CT angiography can provide assessment of both carotid bifurcation and intracranial circulation ^r2
• Noninvasive imaging (CT angiography or magnetic resonance angiography) of intracranial vasculature
  • Obtain when knowledge of intracranial vascular disease will alter management
  • Exclude presence of proximal intracranial stenosis and/or occlusion
    • Consider catheter cerebral angiography (gold standard^r13) to confirm reliable diagnosis of abnormalities (presence and degree of stenosis or vasculitis) when detected on noninvasive testing ^r2
• Obtain laboratory tests
  • Order CBC, chemistry panel, and basic coagulation studies at time of initial presentation ^r2
    • Provides baseline and aids in identifying less common causes
  • Screening tests for vascular risk factors ^r7
    • Dyslipidemia: obtain fasting or nonfasting lipid profile ^r7
    • Diabetes: obtain fasting blood glucose level, hemoglobin A1C level, or oral glucose tolerance tests (choice of test and timing are guided by clinical judgment)
  • Specialized coagulation studies may be useful in younger patients without vascular risk factors or known underlying cause ^r2
  • Obtain other laboratory tests on case-by-case basis (eg, pregnancy test, toxicologic screening) in relation to suspected cause and pretest risk assessment ^r1
  • Diagnostic and prognostic markers of transient ischemic attack are being studied, but none have been solidly identified as useful in clinical practice ^r1
• Obtain ECG in all patients ^r2
  • Assess for cardioembolic mechanism (eg, atrial fibrillation, ventricular hypertrophy, cardiac ischemia) ^r2
    • Patients with atrial fibrillation are at high risk for stroke ^r14
  • Cardiac monitoring (inpatient telemetry or Holter monitor) is useful for patients in whom the origin of transient ischemic attack remains uncertain after brain imaging and ECG ^r2
• Obtain echocardiography when a cardiac cause is suspected or when no other cause has been identified in the workup ^r2
  • Includes transthoracic echocardiography or transesophageal echocardiography
• Consider prolonged cardiac rhythm monitoring (approximately 30 days)
  • May be useful to screen for atrial fibrillation when no other cause is apparent ^r7

Laboratory ^c80

• Laboratory tests for all patients with suspected transient ischemic attack ^r1r2
  • Serum glucose and electrolyte levels (including renal function tests) ^c81c82
    • Provide baseline information of renal function and metabolic state
    • Hypoglycemia may mimic stroke
  • CBC with platelet count ^c83
    • Evaluates for inflammation, thrombocytosis, and myelodysplastic disease
    • Abnormal results may indicate cause of symptoms (eg, thrombocytosis, polycythemia, leukocytosis, thrombocytopenia)
  • Coagulation studies (eg, prothrombin time with INR, partial thromboplastin time) ^c84c85c86c87
    • Establish baseline for possible anticoagulation, patients on known anticoagulants, or patients with liver disease
• Diabetes screening tests and fasting or nonfasting lipid profile ^{r7c88c89c90c91c92}
  • Aid in identifying diabetes and dyslipidemia, known risk factors for stroke
• Optional coagulation screening tests (useful for younger patients with transient ischemic attack without vascular risk factor or known cause) ^r2
  • Protein C, protein S, and antithrombin III activities ^c93c94c95
  • Activated protein C resistance/factor V Leiden ^c96c97
  • Fibrinogen and D dimer ^c98c99
    • High D-dimer levels may be associated with the risk of stroke and adverse clinical outcomes in patients with transient ischemic attack ^r15
    • There is not an established dose-dependent relationship ^r15
  • Anticardiolipin antibody ^c100
  • Lupus anticoagulant ^c101
  • Anti–β₂-glycoprotein antibody ^r16c102
  • Homocysteine ^c103
  • F2 gene (prothrombin) mutation G20210A ^c104
  • Factor VIII activity ^c105
  • Von Willebrand factor ^c106
  • Plasminogen activator inhibitor ^c107
  • Endogenous tissue plasminogen activator ^c108
• Toxicologic screening may detect sympathomimetic drug use in absence of typical stroke risk factors ^c109

Imaging

• Neuroimaging
  • CT scan of head (without contrast material) ^c110
    • Useful for identifying intracranial hemorrhage and mass lesions ^r12
    • Not a reliable predictor of short-term risk for stroke ^r12
    • Early signs of cerebral ischemia include:
      • Loss of gray-white differentiation
      • Swelling of gyri, producing sulcal effacement
    • Relatively insensitive in detecting acute, small cortical or subcortical infarctions, especially in posterior fossa
    • Advantages over MRI
      • More widely available
      • Relatively easy to interpret
    • Limitations
      • Less sensitive than MRI in detecting ischemic lesions
      • Exposure to ionizing radiation
  • MRI of brain ^c111
    • Differentiates between temporary ischemia (transient ischemic attack) and infarction (stroke), especially in early hours after symptom onset; excludes other nonvascular causes ^r17
    • Diffusion-weighted MRI is preferred; very sensitive in detecting small areas of brain ischemia ^r2c112
      • Useful for predicting short-term stroke risk ^r12
        • Patients with diffusion-weighted lesions have higher risk of recurrent ischemic events ^r2
        • Presence of large-vessel occlusion is a predictor of new events ^r2
      • Increased sensitivity for ischemia over CT
        • Sensitivity to identify stroke using diffusion-weighted MRI within the first 12 hours of symptoms is 99%, whereas sensitivity of CT is only 39% ^r1
    • Advantages over CT
      • Distinguishes acute and small cortical, deep, and posterior fossa infarcts
      • Distinguishes acute from chronic ischemia
      • Identifies subclinical satellite ischemic lesions, providing information on stroke mechanism
      • Improves spatial resolution
      • Avoids ionizing radiation
    • Limitations
      • More limited availability
      • Increased cost
      • Patient contraindications (eg, pacemakers, defibrillators, patient confusion or claustrophobia, extreme obesity)
• Vessel imaging
  • Doppler ultrasonography ^c113
    • Carotid Doppler ultrasonography ^c114
      • Images carotid bifurcation and measures blood velocities
      • Useful initial screening tool to exclude severe carotid stenosis; accuracy is similar to that of magnetic resonance or CT angiography ^r12r13
        • More readily available, less expensive, avoids need for IV contrast material
      • Ultrasonography is slightly less sensitive than magnetic resonance angiography for detecting severe carotid stenosis; specificity appears to be similar ^r12
        • No studies directly compared ultrasonography and CT angiography
      • Insensitive in detecting arterial dissection and non–flow-limiting lesions; unable to evaluate intracranial portion of internal carotid artery
      • Difficult to assess the stenosis of posterior circulation vessel (vertebral and basilar arteries)
    • Transcranial Doppler ultrasonography ^c115
      • Use to evaluate intracranial vessel abnormalities, occlusions, and stenosis
      • Less accurate than CT and magnetic resonance angiography for steno-occlusive disease
  • Angiography ^c116
    • Magnetic resonance angiography ^c117
      • Noninvasive; can depict intracranial and extracranial circulation
      • Contrast-enhanced magnetic resonance angiography is more accurate ^r2
      • Allows visualization of vertebrobasilar system
      • Limitations
        • Patients with claustrophobia, extreme obesity, or incompatible implanted devices (eg, pacemakers, defibrillators)
        • Increased patient cost with limited availability
    • CT angiography ^c118
      • Rapid, noninvasive visualization of both extracranial and intracranial vessels
      • Provides direct imaging of arterial lumen; high accuracy for determining severity of lumen stenosis ^r13
      • Supraaortic vessel CT (or magnetic resonance) angiography is recommended when other carotid imaging is inconclusive or when endarterectomy is planned
      • Requires administration of contrast material
    • Catheter angiography ^c119
      • Gold standard for diagnosis and grading of cerebrovascular lesions and disease ^r13
        • Confirms presence and degree of intracranial stenosis detected on noninvasive studies ^r2
        • May not be required if noninvasive imaging provides firm diagnostic findings
        • Use to diagnose central nervous system vasculitis and other types of arteriopathies (eg, moyamoya disease)
      • For extracranial vascular imaging (cervical carotid and vertebral arteries)
        • Gold standard for establishing degree of stenosis and determining patient eligibility for carotid endarterectomy, angioplasty, or stenting ^r13
          • Rarely used; reserved for patients when noninvasive imaging is contraindicated, inconclusive, or yields discordant results
          • May use 2 concordant noninvasive studies (eg, ultrasonography, CT angiography, magnetic resonance angiography), avoiding catheterization risk
      • Invasive test; risks include contrast material use (eg, allergic reaction, kidney dysfunction), femoral artery injuries, injection site infection or hematoma, stroke, or death ^r13
        • Rate of serious complications is less than 1 in 1000 and less than 5% for minor events
• Echocardiography ^c120
  • Useful for patients without clear cause for transient ischemic attack after initial evaluation and vessel imaging, or those with suspicion of cardiac cause ^r3
    • Transthoracic echocardiography ^c121
      • Assess for cardiac hypertrophy, ventricular hypokinesis or thrombus, valve disease, and endocarditis ^r12
    • Transesophageal echocardiography ^c122
      • More sensitive than transthoracic echocardiography for aortic arch atheroma and interatrial septum abnormalities (eg, patent foramen ovale) ^r2
      • Better visualization of the left atrium and the left atrial appendage

Functional testing

• ECG ^c123
  • Assesses for cardioembolic mechanism (eg, atrial fibrillation, ventricular hypertrophy) or signs of cardiac ischemia ^r1
  • Approximately 2% of patients have new-onset atrial fibrillation ^r17
• Prolonged cardiac monitoring/Holter monitoring ^c124
  • Identifies patients with suspected paroxysmal arrhythmias (eg, atrial fibrillation)
    • More likely to detect arrhythmias than continuous cardiac telemetry ^r18
    • Consider 24-hour telemetry to investigate for paroxysmal atrial fibrillation ^r1
    • Additional 4 days of Holter monitoring can detect paroxysmal atrial fibrillation in additional 14% of patients ^r17
    • Can extend up to 30 days for suspected embolic or cryptogenic cause ^r1

Other diagnostic tools

• Risk stratification tools
  • Developed to help identify patients with high short-term risk for stroke and to assist in determining urgency of follow-up or need for hospitalization
  • No perfect scoring system has been developed, and clinical judgment, based on thorough history and physical examination, must be incorporated into clinical decision making ^r1
  • ABCD² score (age, blood pressure, clinical features, duration of transient ischemic attack, and presence of diabetes) ^r19c125
    • Most often used; provides framework for decision making
    • Score is determined by the following:
      • Age 60 years or older: 1 point
      • Blood pressure 140/90 mm Hg or higher: 1 point
      • Clinical features (choose 1)
        • Unilateral weakness: 2 points
        • Speech impairment without unilateral weakness: 1 point
      • Duration of transient ischemic attack
        • 60 minutes or longer: 2 points
        • 10 to 59 minutes: 1 point
      • Diabetes present: 1 point
    • Classification by score ^r19
      • Low risk: less than 4 points (stroke risk 1% at 2 days, 1.2% at 7 days, and 3.1% at 90 days)
      • Moderate risk: 4 to 5 points (stroke risk 4.1% at 2 days, 5.9% at 7 days, and 9.8% at 90 days)
      • High risk: greater than 5 points (stroke risk 8.1% at 2 days, 11.7% at 7 days, and 17.8% at 90 days)
    • Limitations ^r20
      • Does not reliably discriminate those at low and high risk for early recurrent stroke ^r20
        • Approximately one-third of patients with stroke mimic had score of 4 points or higher; approximately one-third of patients with true transient ischemic attack had score of less than 4 points ^r20
      • Does not identify patients with carotid stenosis or atrial fibrillation requiring urgent intervention ^r20
      • Does not include posterior circulation symptoms (ataxia, dysmetria, homonymous hemianopia) ^r21
      • Should not be relied upon to identify patients who can safely be discharged from the emergency department ^r12
  • Other risk stratification tools (eg, ABCD, ABCD³, ABCD²-I, California score) have also been evaluated and not found useful alone as risk stratification instruments ^{r12c126c127c128c129}

Most common

• Migraine with aura (complicated) ^c130d2
  • Reflects cortical spreading depression; spreading onset corresponds to adjacent cortical regions over minutes ^r22
    • Usually resolves within 30 minutes (rarely more than 1 hour)
  • Visual disturbances are most commonly reported; positive symptoms include teichopsia (zigzag) and geometric patterns
  • Can include sensory, motor, or speech disturbances
    • These often occur sequentially with migraine but simultaneously with transient ischemic attack
  • Typically associated with headache, either immediate or delayed; frequently accompanied by nausea, vomiting, and/or photophobia
  • Differentiation suggested by history of migraines; more common in younger people
    • MRI findings are usually normal
    • Headache may accompany transient ischemic attack; first episode or worst-ever headache warrants brain imaging
• Seizure disorder ^c131
  • Nonepileptic or epileptic seizures ^d3
  • Paroxysmal transient disturbances of brain function
    • Partial seizures can cause episodic neurologic deficits
  • Positive symptoms: limb movements, lip smacking, head turning, dystonic posturing, and/or painful sensory disturbance
    • Symptoms often spread sequentially (jacksonian march); transient ischemic attack symptoms typically have sudden onset without progression
  • Associated symptoms: tongue biting, incontinence, muscle pains, and/or postictal disorientation
    • Altered consciousness is more likely with seizure than with transient ischemic attack
  • Suggestive history and physical examination findings are diagnostic; obtain EEG to confirm
• Hypoglycemia ^c132
  • Serum glucose level less than 70 mg/dL; most common in type 1 diabetes ^d4
  • Symptoms can include anxiety, tremors, weakness, sweating, nausea, seizures, and confusion
    • Blurred vision and focal neurologic signs may occur
  • Diagnosed by low serum glucose level and resolution of symptoms with administration of glucose
• Mass lesions (eg, tumor, subdural hematoma, abscess) ^c133c134c135
  • Symptoms are based on location and may not follow vascular distribution
    • Onset is typically gradual
  • Focal disturbances of cerebral function (eg, weakness, ataxia, cranial nerve deficits, aphasia) may occur abruptly and are likely to persist
  • Consider in patients with primary cancer, fever, immunosuppression, or recent trauma
  • Diagnosed using cerebral imaging studies (CT or MRI)
• Functional anxiety ^c136c137c138
  • Psychogenic conditions (eg, anxiety, panic disorder, conversion reaction) may mimic transient ischemic attack ^d5
  • Diagnosed by history and physical examination; MRI findings are usually normal
    • Symptoms are often stereotypical and recurrent; findings are nonanatomic or inconsistent

Admission criteria

Patients with transient ischemic attack require urgent evaluation (preferably within 24 hours^r3); no clear guidelines exist on hospitalization

Disposition (inpatient or outpatient) varies based on local resources, risk assessment, clinical acumen, and patient access to follow-up

• Inpatient hospitalization ^r12
  • Recommended for high-risk patients, as determined by any of the following:
    • Abnormal initial head CT scan
    • Suspected embolic source (presence of atrial fibrillation, cardiomyopathy, or valvuloplasty)
    • Moderate to severe (greater than 50%) intracranial or extracranial symptomatic stenosis ^r21
    • Previous stroke or transient ischemic attack
    • Crescendo transient ischemic attacks (multiple, recurrent, increasing frequency)
  • Provides decreased time to thrombolysis if stroke occurs; permits cardiac monitoring and timely diagnostic workup
• Outpatient management
  • Outpatient management settings include:
    • Specific outpatient transient ischemic attack clinics where patients referred (based on emergency department diagnostic protocols) receive comprehensive testing and evaluation by stroke expert within 24 to 48 hours ^r3r21
    • Emergency department observation units that provide cardiac monitoring, serial clinical examinations, access to imaging and consultation as needed, and rapid access to emergent therapy and hospital admission when indicated ^r12
  • Transient ischemic attack clinics and observation units are noninferior to inpatient hospitalization in reducing stroke risk after transient ischemic attack in medium- and low-risk patients ^r1r23
    • Timing of workup (preferably within 24 hours of symptom onset) is more important than location
    • Patients not admitted must be fully educated about the need to return immediately if symptoms recur
    • Patients who received treatment in emergency departments without further follow-up have a higher risk of subsequent stroke ^r23

Recommendations from professional organizations

• 2023 American Heart Association scientific statement ^r21
  • Presumed symptomatic (greater than 50%) extracranial or intracranial stenosis warrants hospital admission
  • Acceptable disposition options include:
    • Rapid emergency department transient ischemic attack protocols with expedited referral to specialized cerebrovascular or transient ischemic attack–specific clinics
    • Admission to a 24-hour emergency department observation unit
    • Standard hospital admission
  • To determine disposition of patients with transient ischemic attack, consider:
    • Short-term stroke risk on the basis of presentation and vessel imaging
    • Timeliness of a reliable workup
    • Availability of rapid outpatient follow-up
    • The patient's ability to return for rapid workup in a clinic setting
  • Institutional and regional factors should guide protocols for the decision-making about disposition for patients with transient ischemic attack
• 2009 American Heart Association/American Stroke Association scientific statement ^r2
  • It is reasonable to hospitalize patients with transient ischemic attack who present within 72 hours of symptoms with:
    • ABCD² score of 3 points or higher
    • ABCD² score of 0 to 2 points with evidence of focal ischemia
    • ABCD² score of 0 to 2 points if uncertain that patient can obtain outpatient workup within 2 days
  • The ABCD² score does not sufficiently identify short-term risk for stroke to use alone as a risk stratification tool ^r4r12
• 2006 National Stroke Association guidelines: ^r11
  • Consider hospitalization for patients with first transient ischemic attack within the past 24 to 48 hours to provide:
    • Early intervention with lytic therapy if symptoms recur and progress to stroke
    • Completion of appropriate diagnostic testing
    • Initiation of definitive secondary prevention therapy
  • Crescendo transient ischemic attacks may also justify hospitalization
  • In patients with recent (within 1 week) transient ischemic attack, timely hospital referral with hospitalization is reasonable for:
    • Symptom duration longer than 1 hour
    • Crescendo or stuttering pattern of transient ischemic attacks
    • Symptomatic internal carotid stenosis with narrowing more than 50%
    • Known cardiac source of embolus (eg, atrial fibrillation)
    • Known hypercoagulable state
    • ABCD² score greater than 3 points ^r19

Recommendations for specialist referral

• All patients with suspected transient ischemic attack should be promptly assessed by a neurologist or stroke expert ^r3
• Consider cardiologist consultation for patients with cardiac findings influencing stroke risk (eg, atrial fibrillation, cardiac thrombus, valvular abnormalities)
• Consider consulting vascular surgeon or neurosurgeon for patients with significant vessel stenosis or occlusion

Drug therapy ^c139c140

• Antiplatelet agents ^{c141c142c143c144c145c146c147c148c149c150c151c152c153c154c155}
  • Aspirin ^{c156c157c158c159c160c161c162c163c164c165c166c167c168c169}
    • Aspirin monotherapy
      • Aspirin Oral tablet; Adults: 50 to 325 mg PO once daily.
    • Aspirin used with clopidogrel for dual antiplatelet therapy
      • Aspirin Oral tablet; Adults: 75 to 100 mg PO once daily plus clopidogrel.
    • Aspirin used with ticagrelor for dual antiplatelet therapy
      • Aspirin Oral tablet; Adults: 300 to 325 mg PO loading dose, then 75 to 100 mg PO once daily plus ticagrelor for up to 30 days.
  • Aspirin plus extended-release dipyridamole ^{c170c171c172c173c174c175c176c177c178c179c180c181c182}
    • Aspirin, Dipyridamole Oral capsule, extended-release; Adults: 25 mg aspirin/200 mg dipyridamole PO twice daily.
  • Clopidogrel ^{c183c184c185c186c187c188c189c190c191c192c193c194c195}
    • Clopidogrel Bisulfate Oral tablet; Adults: 75 mg PO once daily.
  • Ticagrelor
    • Ticagrelor Oral tablet; Adults: 180 mg PO loading dose, then 90 mg PO twice daily plus aspirin for up to 30 days.
  • Dipyridamole ^{c196c197c198c199c200c201c202c203c204c205c206c207c208}
• Anticoagulants ^{c209c210c211c212c213c214c215c216c217c218c219c220}
  • Vitamin K antagonist ^{c221c222c223c224c225c226c227c228c229c230c231c232}
    • Nonvalvular atrial fibrillation
      • Warfarin Sodium Oral tablet; Adults 18 to 59 years: 2 to 10 mg PO once daily, initially; 10 mg PO once daily for 2 days may initially be considered in persons eligible for outpatient initiation. Adjust dose to maintain INR 2 to 3.
      • Warfarin Sodium Oral tablet; Adults 60 years and older: 2 to 5 mg PO once daily, initially; 10 mg PO once daily for 2 days may initially be considered in persons eligible for outpatient initiation. Adjust dose to maintain INR 2 to 3.
    • Valvular atrial fibrillation
      • Warfarin Sodium Oral tablet; Adults 18 to 59 years: 2 to 10 mg PO once daily, initially; 10 mg PO once daily for 2 days may initially be considered in persons eligible for outpatient initiation. Adjust dose to maintain INR 2 to 3 for persons with rheumatic mitral stenosis or moderate to severe mitral stenosis and 2.5 to 3.5 for persons with mechanical heart valves.
      • Warfarin Sodium Oral tablet; Adults 60 years and older: 2 to 5 mg PO once daily, initially; 10 mg PO once daily for 2 days may initially be considered in persons eligible for outpatient initiation. Adjust dose to maintain INR 2 to 3 for persons with rheumatic mitral stenosis or moderate to severe mitral stenosis and 2.5 to 3.5 for persons with mechanical heart valves.
  • Direct acting oral anticoagulants
    • Apixaban ^{c233c234c235c236c237c238c239}
      • Apixaban Oral tablet; Adults: 5 mg PO twice daily. Coadministration of certain drugs may need to be avoided or dosage adjustments may be necessary; review drug interactions.
      • Apixaban Oral tablet; Adults with at least 2 of the following criteria: age 80 years or older, body weight 60 kg or less, and/or serum creatinine 1.5 mg/dL or more: 2.5 mg PO twice daily. Coadministration of certain drugs may need to be avoided; review drug interactions.
    • Dabigatran ^{c240c241c242c243c244c245c246}
      • Dabigatran etexilate Oral capsule; Adults: 150 mg PO twice daily. Coadministration of certain drugs may need to be avoided or dosage adjustments may be necessary; review drug interactions.
      • Dosage adjustment is necessary for CrCl of 30 mL/min or less
    • Edoxaban ^{c247c248c249c250c251c252}
      • Edoxaban Oral tablet; Adults: 60 mg PO once daily.
      • Dosage adjustment is necessary for CrCl of 15 to 50 mL/min; use is not recommended if CrCl is more than 95 mL/min or less than 15 mL/min
    • Rivaroxaban ^{c253c254c255c256c257c258c259}
      • Rivaroxaban Oral tablet; Adults: 20 mg PO once daily.
      • Dosage adjustment is necessary for CrCl of 15 mL/min or less

Nondrug and supportive care ^c260

Comorbidities ^c264