Transient ischemic attack

Transient ischemic attack

I. What every physician needs to know.

The American Heart Association/American Stroke Association defines transient ischemic attack (TIA) as “a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.” In the past, TIA was defined simply as a focal ischemic neurologic event lasting less than 24 hours. However, it has become clear that an arbitrary, time-based definition of TIA is inadequate to differentiate TIA from stroke, as modern neuroimaging techniques have allowed detection of acute cerebral infarction even in patients whose symptoms completely resolve within hours of onset. This has led to a shift in emphasis from a time-based definition of TIA to a tissue-based definition that relies more heavily on neuroimaging as well as clinical data.

The major mechanisms of TIA are the same as stroke: large vessel atherosclerosis, cardioembolic, and small vessel occlusion/lacunar. In TIA, by definition, the obstruction to blood flow is temporary and resolves before tissue infarction occurs. It may be useful to think of TIA and stroke as conditions on the same clinical spectrum, similar to the relationship between unstable angina and acute myocardial infarction. Accurately diagnosing and risk stratifying patients who present with TIA is important since more than 10% of patients with TIA will go on to have an ischemic stroke in the next 3 months, and as many as half of these strokes occur within the first 48 hours following a TIA.

II. Diagnostic Confirmation: Are you sure your patient has Transient Ischemic Attack?

Clinical signs and symptoms of TIA can include any focal neurologic deficit (as opposed to global brain dysfunction as seen in delirium or encephalopathy). The specific symptoms depend on the vascular territory affected and the location of cerebral ischemia. TIA symptoms are transient by definition, and often (but not always) resolve within a matter of a few hours.

A. History Part I: Pattern Recognition:

The presenting symptoms of TIA can be any focal neurologic deficit with acute onset, such as unilateral weakness, numbness or paresthesia, drooping face, slurred speech, aphasia or dysarthria, dysphagia, double vision, monocular blindness, vertigo, or ataxia. Alterations of consciousness, tonic-clonic seizure, syncope, and/or generalized confusion are less common in TIA, and are more characteristic of other conditions in which brain dysfunction is global rather than focal.

B. History Part 2: Prevalence:

It is estimated that the incidence of TIA in the United States is between 200,000 and 500,000 per year, with a prevalence of 2.3%, or approximately 5 million people. The risk of TIA increases exponentially with age, regardless of gender or race. Other risk factors for TIA include diabetes, hypertension, smoking, hyperlipidemia, atrial fibrillation/flutter, alcohol or illicit drug use (e.g., cocaine), and hypercoagulable states.

C. History Part 3: Competing diagnoses that can mimic Transient Ischemic Attack.

The differential diagnosis for TIA includes seizure, migraine, hypoglycemia, and peripheral nerve conditions (e.g., Bell’s palsy, nerve root compression, or vestibular neuritis). Other conditions such as multiple sclerosis, subdural hematoma, and CNS infection or malignancy can mimic TIA, as can psychiatric conditions such as conversion disorder. In elderly patients and in patients with existing cerebrovascular disease, systemic illness (e.g., pneumonia, UTI, C. diff) can worsen or unmask existing neurologic deficits that were previously mild or less apparent. A careful history and physical exam, including a complete neurologic exam, can often provide clues that help differentiate TIA from other conditions.

D. Physical Examination Findings.

The physical exam findings in TIA will depend on the vascular territory affected and the location of cerebral ischemia. Unilateral weakness, sensory deficits, or cranial nerve deficits are common exam findings in TIA. A patient with TIA will typically have a focal neurologic deficit rather than generalized confusion or alteration of consciousness.

E. What diagnostic tests should be performed?

Due to the high risk of stroke following TIA, all patients suspected of having TIA should be evaluated promptly, usually in an inpatient setting. Outpatient evaluation is reasonable in some instances if the appropriate tests can be obtained expeditiously (within 24-48 hours), but this is often not feasible.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Routine labs, such as a CBC, basic chemistries, INR, and PTT, should be ordered on all patients with suspected TIA, along with a fasting lipid panel and fasting blood glucose. A hemoglobin A1c may be useful in patients suspected of having undiagnosed diabetes mellitus. Other tests, such as urinalysis, blood/urine toxicology screens, ABG, BNP, or ammonia, may be useful depending on the clinical setting. While these tests do not help make the diagnosis of TIA they may identify coexisting conditions or TIA mimics that may help with diagnosis or management of the patient.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

All patients suspected of having TIA should undergo neuroimaging as soon as possible. Magnetic resonance imaging (MRI) with diffusion weighted imaging is the preferred modality given its superior sensitivity in detecting cerebral ischemia or infarction, although in practice non-contrast head computed tomography (CT) is the most commonly ordered initial imaging study due to its lower cost and greater availability. Non-contrast CT has limited ability to detect cerebral ischemia or infarction, but it is useful to rule out hemorrhage or mass effect.

In patients with pacemakers or AICDs, or who have intolerance or other contraindications to MRI, a second non-contrast CT may be performed 24-48 hours after the initial study if symptoms are still present or if the diagnosis is unclear. Cerebral infarction not seen on the initial CT often shows up later as local tissue changes and edema develop at the site of the infarction. CT perfusion is another modality that can detect cerebral ischemia or infarction, but it has been better studied in stroke and is not often employed in TIA.

Other recommended imaging studies in patients with TIA include an evaluation of the extracranial vasculature with either Duplex ultrasound, CT angiography (CTA), or MR angiography (MRA). Detecting a lesion such as a high-grade carotid stenosis can alter management in patients with TIA and can help prevent subsequent stroke.

Evaluation of the intracranial vasculature by CTA, MRA, or trans-cranial Doppler is also recommended by the 2009 AHA/ASA guidelines, although its effect on patient management may be limited. There are no effective interventions for treating intracranial stenotic lesions other than standard medical therapy and risk factor reduction. The SAMMPRIS trial, the only published, randomized, controlled trial to address the efficacy of stenting intracranial stenotic lesions, suggested that intracranial stenting was inferior to medical therapy in preventing recurrent stroke.

An EKG should be obtained on all patients with suspected TIA to evaluate for arrhythmias, such as atrial fibrillation or atrial flutter, which can be associated with TIA. Continuous cardiac monitoring should be carried out for the duration of the hospitalization, and prolonged 30-day cardiac monitoring in the outpatient setting is recommended for patients in whom no clear etiology for their TIA was determined.

Up to 20% of patients with cryptogenic stroke or TIA will be found to have occult atrial fibrillation or atrial flutter on 30-day cardiac monitoring, and identifying these patients is important as they would be candidates for anticoagulation rather than antiplatelet therapy. There is growing recognition of the utility and cost-effectiveness of extended cardiac monitoring in stroke and TIA evaluation, and the practice has been more widely adopted in recent years.

Echocardiography is commonly performed in the evaluation of TIA under the rationale of looking for cardiac sources of embolism. The utility of echocardiography in the evaluation of TIA is discussed in greater detail below.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.


As many as 20% of TIA/stroke patients are cardioembolic, and consequently many experts recommend echocardiography as part of the initial evaluation of TIA. The AHA/ASA guidelines give echocardiography a class IIa recommendation (level of evidence B) and state that “echocardiography (at least TTE) is reasonable in patients with suspected TIAs, especially in patients in whom no cause has been identified by other elements of the work-up.”

In practice, transthoracic echocardiography (TTE) is ordered routinely as part of the initial evaluation of TIA. However, multiple studies have demonstrated that the sensitivity of TTE in detecting cardiac sources of embolism is quite low, except for left ventricular thrombus, a rare cause of embolic TIA/stroke. Transesophageal echocardiography (TEE) has been shown to be significantly more sensitive than TTE in detecting most cardiac sources of embolism, especially left atrial appendage thrombus, the most common cause of embolic TIA/stroke. However, TEE is limited by cost, associated risks, and availability, and is not commonly ordered for TIA unless the patient has recurrent episodes of TIA and a negative TTE.

Multiple studies have demonstrated that both TTE and TEE findings rarely change the management of patients with stroke or TIA. Many sources of embolism detected by either TTE or TEE (e.g., PFO, atrial septal aneurysm, aortic atheromas, mitral annular calcifications) have no defined therapy, or therapy that does not differ from the standard medical therapy for TIA. Therefore, detecting these conditions does not typically alter management of the patient. In addition, given the increasing penetrance of EHR order sets and an increased emphasis on standardization of care, it is not uncommon for patients who have had a recent TTE, or who already have an indication for anticoagulation, or who are not candidates for anticoagulation, to have a TTE ordered and performed despite the fact that the test is unlikely to add anything to the work-up other than cost and increased length of stay. Hospitalists should recognize these instances of low/no-value care and strive to avoid them.

Some experts recommend an individualized, case-by-case approach to echocardiography in TIA/stroke, and this is probably the best and most cost-conscious strategy. Rather than ordering TTE routinely on all patients with TIA, it is reasonable to: assess the likelihood of an embolic event in each patient based on age, cardiac history, and other risk factors; consider whether the patient already has an indication for anticoagulation or whether they would be a candidate for anticoagulation should a source of embolism be found; determine if they have had a recent echocardiogram and if so whether it is necessary to repeat the study; and then order either a TTE, TEE, or no echocardiography accordingly.

Intracranial vascular imaging

Intracranial imaging (CTA or MRA) is commonly ordered as part of the initial work-up of patients with TIA. As compared to extracranial vascular imaging, which is an important component of the initial evaluation of TIA and can have a large impact on management of the patient, imaging of the intracranial vasculature is often a lower value test in many patients with TIA.

In certain populations with higher rates of intracranial large artery atherosclerosis (African-American, Hispanic, and Asian patients) the diagnostic yield of intracranial imaging may be higher, but the impact on patient management is less clear. This is in contrast to patients with acute ischemic stroke, in whom detection of an intracranial thrombus might be an indication for thrombolysis or mechanical thrombectomy.

For patients with TIA but not acute ischemic stroke, detecting an intracranial stenosis will likely not change management given the SAMMPRIS trial findings discussed above, which demonstrated that stenting intracranial lesions was inferior to medical therapy for secondary prevention of TIA and stroke.

There is weak evidence that short-term, dual antiplatelet therapy with aspirin and clopidogrel for 90 days can confer some benefit in certain populations with TIA due to high-grade intracranial lesions (70-99% stenosis), but this approach was given a Class IIb, level of evidence B recommendation by the most recent AHA/ASA guidelines, reflecting the weakness of the recommendation and the low quality of the data.

CTA and MRA, the most common modalities for evaluating intracranial vasculature, are relatively costly tests that are not without risk. Given the relatively low diagnostic yield, questionable impact on patient management, and relatively high cost of intracranial imaging, it may be a more cost-conscious strategy to defer intracranial imaging to later in the evaluation or even forgo it altogether in certain patients if it is clear that the results of the tests would not alter management of the patient.

Homocysteine and lipoprotein(a)

Elevated homocysteine and lipoprotein(a) levels are associated with an increased risk of cerebrovascular disease. However, there is no evidence that lowering either of these levels has any effect on either primary or secondary prevention of TIA or stroke, and therefore they should not be routinely ordered during the evaluation of TIA.

Autoimmune testing

In the absence of a history or clinical evidence of active lupus, tests such as ESR, ANA, and other auto-antibodies are unlikely to be useful in the initial evaluation of TIA.

Hypercoagulable testing

Antiphospholipid antibody testing or tests for other inherited thrombophilias may be indicated in specific patients (e.g., young patients with an otherwise negative evaluation, or patients with a personal or family history of thrombosis, lupus, or antiphospholipid syndrome) but should not be routinely ordered as part of the initial evaluation of TIA.

III. Default Management.

A. Immediate management.

Initial management in the emergency department should include basic labs, EKG, cardiac monitoring, and urgent neuroimaging (MRI or CT). A bedside swallow study should be performed, and once hemorrhagic stroke has been ruled out, aspirin (oral or rectal) should be given to all patients who do not have a contraindication. Admission to the hospital is usually advised to expedite the work-up. Permissive hypertension is generally recommended, although specific parameters for this are not well defined. The benefit of permissive hypertension is likely greater in patients with acute ischemic stroke as compared to patients with TIA. If a patient is taking a beta-blocker it may be reasonable to continue it even if other antihypertensives are held, in order to reduce the risk of myocardial infarction while in the hospital.

B. Physical Examination Tips to Guide Management.

Frequent neurologic checks by a physician or nurse are important to document the patient’s clinical course during the hospitalization. TIA patients often have rapidly resolving deficits, but they are also at elevated risk of stroke in the time period immediately following the TIA. Progression or evolution of deficits in a patient after an initial negative neuroimaging study would be an indication for urgent reimaging to look for evolving stroke. Physical therapy, occupational therapy, and speech therapy services can be consulted as needed, although typically TIA symptoms will completely resolve prior to hospital discharge and rehab services will not be indicated.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Blood glucose should be monitored while the patient is hospitalized and, if elevated, insulin therapy should be instituted to maintain glycemic control. A fasting lipid panel should be drawn so that response to lipid-lowering therapy can be monitored in the outpatient setting. Changes in neurologic status should prompt urgent reimaging to look for evidence of evolving stroke.

D. Long-term management.

Long-term management of TIA focuses on secondary prevention of TIA or stroke with antiplatelet and statin therapy, and risk-factor reduction (blood pressure management, glycemic control, smoking cessation/substance abuse treatment, treatment of metabolic syndrome, etc.).

Antiplatelet therapy

Antiplatelet agents effective in secondary prevention of TIA include aspirin, clopidogrel (Plavix), and aspirin-dipyridamole (Aggrenox). Clopidogrel and aspirin-dipyridamole are each considered to be superior to aspirin alone, though the additional benefit of each agent is modest and is offset by significantly higher drug costs. Aspirin may actually be the best agent when efficacy, tolerance, and cost are taken into account.

The optimal dose of aspirin is not well-defined, but doses of 50-325 mg/day are recommended by the most recent AHA/ASA guidelines. Short-term combination therapy with aspirin and clopidogrel may be effective in certain populations (Asians, patients with high grade intracranial stenosis) but long-term dual antiplatelet therapy for TIA does not confer any additional benefit while significantly increasing the risk of bleeding complications.

Antihypertensive therapy

In general, the target for long-term blood pressure management in patients with TIA is <140/90. This may be accomplished with a single agent or some combination of a diuretic, ACE inhibitor, angiotensin receptor blocker, calcium channel blocker, or beta-blocker.

Lipid-lowering therapy

Statins are the only class of lipid-lowering agents shown to reduce the risk of TIA or stroke, even in patients with normal or average LDL. High dose atorvastatin (80 mg/day) has the best evidence from the SPARCL trial, and is therefore the agent of choice for secondary prevention of TIA.

Glycemic control

Strict glycemic control has not been shown to decrease macrovascular complications of diabetes, including TIA. However, it is reasonable to use existing guidelines for glycemic control in TIA patients with diabetes.

Smoking cessation

Smoking is associated with an increased risk of TIA and stroke, and all patients with TIA who are smokers should undergo smoking cessation counseling.

E. Common Pitfalls and Side-Effects of Management.

Adverse effects of medications started for secondary prevention of TIA are the most common side-effects of management. These can include bleeding complications from antiplatelet therapy, hypotension from antihypertensives, and LFT abnormalities or muscle pain or weakness from statins. Dose adjustment or changing or discontinuing medications may be required.

Antiplatelet therapy

  • Aspirin – start at 325 mg daily in the acute setting, then 50-325 mg daily thereafter (no clear evidence to recommend a specific dose)

  • Clopidogrel (Plavix) – 75 mg daily

  • Aspirin/ER dipyridamole (Aggrenox) – 25/200 mg twice a day

Antihypertensive therapy (commonly used generic agents)

  • Chlorthalidone (thiazide) – 12.5-25 mg daily (preferred over HCTZ due to longer duration of action and superior outcome data)

  • Lisinopril (ACE inhibitor) – 10-40 mg daily

  • Losartan (angiotensin receptor blocker) – 25-100 mg daily

  • Amlodipine (calcium channel blocker) – 5-10 mg daily

  • Metoprolol (beta-blocker) – 12.5-100 mg twice a day, or 25-200 mg daily ER

  • Carvedilol (alpha-1/beta-blocker) – 3.125-25 mg twice a day

Statins (commonly used agents)

  • Atorvastatin (Lipitor) – 10-80 mg daily (best evidence for secondary prevention from SPARCL trial, now available as generic)

  • Pravastatin (Pravachol) – 10-40 mg at bedtime (relatively less muscle toxicity)

  • Fluvastatin (Lescol) – 20-40 mg at bedtime (relatively less muscle toxicity)

  • Rosuvastatin (Crestor) – 5-40 mg daily (high potency, not generic)

IV. Management with Co-Morbidities.

A. Renal Insufficiency.

Choice of antihypertensive therapy could change in patients with CKD (e.g., furosemide instead of chlorthalidone, or forgoing an ACE inhibitor for another class of drug if the serum creatinine is markedly elevated). Some statins should be dose-adjusted for CKD.

B. Liver Insufficiency.

The FDA recommends that transaminases should be checked prior to initiation of statin therapy, and 12 weeks following initiation. Patients with chronic liver disease should be monitored closely for progressive LFT abnormalities while on statin therapy. Statins should not be used in patients with progressive or decompensated liver disease or hepatic failure.

Antiplatelet agents may increase the risk of bleeding in patients with impaired synthetic hepatic function and coagulopathy.

C. Systolic and Diastolic Heart Failure.

Patients with heart failure may be at higher risk of a cardiac source of embolism (CSE) or cardiac arrhythmia (such as atrial fibrillation) that can increase the risk of TIA. Management is not significantly changed by the presence of either systolic or diastolic heart failure. Antihypertensive therapy for heart failure (ACE inhibitors, beta-blockers, diuretics) aligns well with recommendations for treating hypertension in TIA.

D. Coronary Artery Disease or Peripheral Vascular Disease.

Long-term dual antiplatelet therapy is not recommended for secondary prevention of TIA given the lack of benefit and increased risk of bleeding, but patients with coronary artery stents or a recent myocardial infarction may have indications for dual antiplatelet therapy.

E. Diabetes or other Endocrine issues.

Monitoring of blood glucose or measurement of hemoglobin A1c during a hospitalization for TIA may lead to a new diagnosis of diabetes. Glycemic control according to established guidelines is recommended. Antihypertensive therapy for patients with TIA and diabetes should generally include an ACE inhibitor or angiotensin receptor blocker unless there is a contraindication to both of these agents.

F. Malignancy.

Malignancy is a hypercoagulable state and may increase the risk of TIA. CNS involvement of malignancy should be considered and ruled out in patients with TIA symptoms. Paradoxical embolism from DVT (e.g., via a PFO) should be considered in patients with malignancy who present with TIA.

G. Immunosuppression (HIV, chronic steroids, etc.).

CNS malignancy or infection should be considered and ruled out in immunosuppressed patients who present with TIA symptoms.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

No change in standard management.

J. Hematologic or Coagulation Issues.

Hypercoagulable states increase the risk of TIA, and paradoxical embolism should be considered in these patients. Caution should be exercised in patients with a bleeding diathesis when prescribing antiplatelet therapy.

K. Dementia or Psychiatric Illness/Treatment.

The extent of diagnostic testing may be changed by the presence of advanced dementia. For example, a patient with advanced dementia who is not a candidate for carotid endarterectomy or anticoagulation should probably not undergo evaluation of the extracranial vasculature or echocardiography during an evaluation for TIA. Patients with advanced dementia or active psychiatric conditions may not be able to tolerate MRI. Some psychiatric conditions, such as conversion disorder or tardive dyskinesia from neuroleptic therapy, can mimic TIA.

V. Transitions of Care.

A. Sign-out Considerations While Hospitalized.

An acute change in neurologic status in patients admitted with TIA should prompt urgent reimaging to look for stroke. Uncontrolled blood pressure, hyper/hypoglycemia, and cardiac arrhythmias such as atrial fibrillation are all issues that may come up during hospitalization.

B. Anticipated Length of Stay.

Most patients with TIA can undergo a complete evaluation within 24-48 hours and will not require an extended hospital stay. The availability of imaging modalities such as ultrasound and MRI, especially on nights, weekends, and holidays, can prolong the length of stay.

C. When is the Patient Ready for Discharge.

Patients with TIA are generally ready for discharge once their symptoms have resolved, when they have completed their diagnostic work-up, and when their relevant medical conditions and secondary prevention issues (blood pressure, glycemic control, smoking cessation, etc.,) have been addressed. Patient education regarding TIA/stroke symptoms should be completed prior to discharge. Rehabilitation services (physical/occupation/speech therapy) are generally not required since symptoms will generally have already resolved, but the lack of indication for rehab services should be documented in the medical record to satisfy Joint Commission Quality Measures.

D. Arranging for Clinic Follow-up.

Follow-up with a primary care provider after hospital discharge is important for long-term management of risk factors (blood pressure, lipids, diabetes, smoking cessation).

1. When should clinic follow-up be arranged and with whom.

When possible, a primary care clinic appointment within 7 days of discharge is recommended. For patients with recurrent TIA, or in whom the diagnosis is uncertain (e.g., TIA versus migraine versus seizure), follow-up with a neurologist is reasonable.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

A baseline lipid panel is useful in patients who are starting statin therapy. Hemoglobin A1c should be ordered in patients in whom diabetes is diagnosed or suspected.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Creatinine and potassium should be ordered in patients started on diuretics or ACE inhibitors. It is reasonable to follow LFT’s when starting statin therapy, especially in patients with liver disease or who are taking other medications with the potential for drug-drug interactions.

E. Placement Considerations.

Patients with TIA can generally return to their prior living situation, since their symptoms will have generally resolved by the time of discharge. Rehabilitation services (physical/occupational/speech therapy) are generally not required.

F. Prognosis and Patient Counseling.

Patients with TIA are at increased risk of stroke in the days and weeks following their initial event. All patients and their families should be counseled on signs and symptoms of stroke and should be urged to seek medical attention immediately if they develop these symptoms. Smoking cessation counseling should be performed in patients who have smoked in the past year. Patients should be advised to limit their dietary sodium intake in order to help with blood pressure control. Patients with diabetes should be instructed on glycemic control and a diabetic diet.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.

The Joint Commission requires facilities certified as Primary Stroke Centers to report on eight core quality measures each quarter. These measures generally apply to patients with TIA as well, and should be addressed in physician documentation, especially if a measure is not met. The eight quality measures are:

– Venous thromboembolism prophylaxis

– Discharged on antithrombotic therapy

– Anticoagulation for atrial fibrillation/flutter

– Thrombolytic therapy

– Antithrombotic therapy by the end of hospital day 2

– Discharged on a statin medication

– Stroke education

– Assessed for rehabilitation

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

In-hospital prophylactic measures for TIA include VTE prophylaxis, fall and aspiration precautions in patients whose deficits have not yet resolved, and frequent neurologic checks to detect progression of TIA to stroke. As with other non-ICU medical patients, GI prophylaxis is not indicated in most cases, and may even be harmful by increasing the risk of pneumonia and clostridium difficile infections.

Secondary prevention of TIA consists of prescribing an appropriate medical regimen and addressing modifiable risk factors in patients, as discussed above.

VII. What's the evidence?

Easton, J. “Definition and Evaluation of Transient Ischemic Attack”. Stroke.. vol. 40. 2009. pp. 2276-2293.

Kernan, W. “Guidelines for the Prevention of Stroke in Patients with Stroke and Transient Ischemic Attack”. Stroke.. vol. 45. 2014. pp. 2160-2236. (Updated 2014 AHA/ASA guidelines.)

Chimowitz, M. “Stenting Versus Aggressive Medical Therapy for Intracranial Arterial Stenosis”. N Engl J Med. vol. 365. 2011. pp. 993-1003.

Amarenco, P. “High Dose Atorvastatin After Stroke or Transient Ischemic Attack”. N Engl J Med. vol. 355. 2006. pp. 549-559. (SPARCL)

Wang, Y. “Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack”. N Engl J Med. vol. 369. 2013. pp. 11-19. (First trial showing short-term benefit of dual antiplatelet therapy after TIA/stroke.)

McGrath, E. “Transesophageal echocardiography in patients with cryptogenic ischemic stroke: a systematic review”. Am Heart J.. vol. 168. 2014. pp. 706-712. (Systematic review of TEE and its impact on management of TIA/stroke.)

Gladstone, D. “Atrial fibrillation in patients with cryptogenic stroke”. N Engl J Med. vol. 370. 2014. pp. 2467-2477. (Trial showing significant prevalence of occult atrial fibrillation in stroke patients.)

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