Ischemic Stroke overview

DefinitionEtiologyEpidemiologyPathophysiologyClinical Presentation
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Abrupt on set of persistent neurological deficit resulting from reduced cerebral blood flow most often due to a thrombo-embolic vaso-occlusive event; approximately 80-85% of all stokes are ischemic.


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Approximately 80-85% involves the anterior circulation (carotids and associated intracranial vessels), ~15-20% involve the posterior circulation (vertebrobasilar and posterior cerebral arteries).


Main causes:

1) Arterial thrombo-embolic events (~75-80%)

  • Primarily due to atherosclerosis
  • Large vessel infractions due to:
    • Artery - artery emboli
    • Thrombosis in situ
    • - Extra or intracranial large or medium seized
    • vessels
    • - Small vessel infractions (lacunes)


2) Cardioemboli (~20-25%)

  • Atrial fibrillation (most common)
  • Post MI
  • Low ejection fraction
  • Mechanical valves
  • Atrial myxoma
  • Subacute bacterial endocarditis


3) Other important but less common causes:

  • Hypoperfusion
    • Focal: Due to severe arterial stenosis
    • Global: Due to systemic hypoperfusion and includes
    • - Myocardial infraction
    • - Heart failure, poor LV function
    • - Cardiac arrhythmias
    • - Blood loss, severe anemia
    • - Pericardial effusion
    • - Medication induced (hypotension)
  • Arterial Dissections
    • May cause thrombo-embolic or hypoperfusion stroke or both
  • Potential hypercoagulable states
    • Antiphospholipid antibody syndrome
    • Protein C and S deficiency
    • Antithrombin III deficiency
    • Factor V Leiden mutation
    • JAK-2 mutation
    • Other pro-coagulable conditions
    • - Neoplasm
    • - Peri-partum


  • Peripartum sagital sinus thrombosis/cerebral venous thrombosis (CVT) during or after pregnancy
    • Increased risk of venous thromboembolic events during pregnancy and for ~6 to 8 weeks post-partum
    • ~2% of pregnancy-associated strokes are attributable to CVT
    • Advancing age, caesarean delivery and presence of infections, hypertension and excessive vomiting during pregnancy increases risk of peripartum CVT
  • Hematological disorders
    • Thrombocytosis
    • Sickle cell
    • Polycythemia
  • Hormone therapy/oral contraceptives
  • Migraine
  • Vasculitis
  • Paradoxical emboli
  • Compression (mass effect) on intracranial vessels
    • Structural lesions (neoplasm), edema
    • Infections (abscesses, basilar meningitis)
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  • Stroke is the third leading cause of death in Canada and fourth leading cause of death in USA
  • After the age of 55, risk of stroke doubles every 10 years
  • Stroke survivor has a 20% chance of having recurrent stroke within 2 years
  • Every year >50,000 Canadians and approximately 795,000 Americans suffer a stroke
  • Approx: 315,000 Canadians are living with stroke or its effects
  • Stroke kills almost 130,000 Americans each year-that's 1 death every 4 minutes



Of every 100 people who have a stroke

  • 15 die (15%)
  • 10 recover completely (10%)
  • 25 recover with a minor impairment or disability (25%)
  • 40 are left with a moderate to severe impairment (40%)
  • 10 are so severely disabled they require long-term care (10%)



  • Stroke costs approximately $2.7 billion/year in Canada and approximately $36.5 billion/year in the US
Reference: Heart and stroke foundation of Canada; Center of disease control and prevention-2012


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Risk factors for ischemic stroke:

  • Atherosclerosis
    • Underlies most thrombo-occlusive events
    • Develop within extra- or intra-cranial vessels affecting large or small vessels
    • Occlusion of small blood vessel via thrombosis in situ or from proximal emboli causes subcortical infarctions (lacunes)
    • Exacerbated by age, hypertension, diabetes, smoking, hyperlipidemia
    • Plaques often occurs at bifurcations
    • Plaque rupture triggers platelet aggregation and thrombosis in situ or distal embolization
  • Putative causes of cardioembolism
  • Cardioemboli lodged within cerebral vessels causes flow obstruction leading to ischemia/infarction. The composition of cardioemboli differs depending upon the cause:

Type of cardioemboli and its causes


  • Hypoperfusion - Border zone or watershed infarcts [between vascular zones e.g. middle cerebral artery (MCA) and posterior cerebral artery (PCA) or middle cerebral artery (MCA) and anterior cerebral artery (ACA) can occur from reduced cardiac output or hypotension particularly in the setting of severe stenosis]

Border zone or watershed infracts



  • Paradoxical emboli
    • Shunting of venous emboli into the arterial circulation most often via:
    • - Patent foramen ovale
    • - Atrial septal defect
    • - Pulmonary fistulae (very rare)


  • Dissection
    • Can occur at any age but is a common cause of stroke in "young" adults <50 years of age
    • May follow minor trauma
    • May be associated with vascular disorders such as collagen vascular disease; fibromuscular dysplasia
    • Tear may occlude vessel or narrow lumen leading to hypoperfusion or thrombo-embolic events


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Clinical Presentation:
  • Abrupt onset of persistent neurological deficit


Clinical presentation of ischmeic stroke


  • Clinical Features suggestive of cardioembolic cerebral infarction:
    • Co-occurrence of cerebral and systemic emboli and/or stroke distributing into different vascular territories
    • A valsalva manoeuvre (straining) at the time of stroke onset may suggest paradoxical emboli


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Differential Diagnosis:
  • Seizures with Todd's paralysis
    • Todd paralysis- transient but sometimes prolonged neuro-deficits (weakness, numbness, speech disruption) following a seizure
  • Space occupying lesion
    • Neoplasm, abscess
  • Migraine with aura (classic or complicated)
  • Syncope - lightheaded, dizzy, unsteady, visual blurring
  • Vertigo/dizziness secondary to vestibulopathy
  • Radiculopathies (focal numbness/weakness)
  • Neuropathies focal e.g. carpal tunnel syndrome, or diffuse numbness ± weakness
  • Dementia (e.g. with speech/language impediment or dyspraxia
  • Metabolic derangement
    • Hypoglycemia
    • Hypomagnesemia
  • Conversion reaction/neuroses/stress, anxiety/malingering
  • Head trauma


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Investigation and Workup:


  • Symptom presentation - rapid onset vs. stuttering course vs. gradual
  • Time of onset (crucial if thrombolysis being considered)
  • Collapse ±trauma at time of event (assess bleeding risk)
  • Trauma just prior to event (consider arterial dissection)
  • History of bleeding/ anemia
  • Recent surgery
  • Recent MI
  • Seizure at time of event




Usual Investigations in ED:


- Blood work (all patients)

  • Glucose, electrolytes, renal function tests
  • Complete blood count (CBC)
  • Activated partial thromboplastin time (APTT)
  • Prothrombin time (PT)/ International normalized ratio (INR)
  • Oxygen saturation
  • Cardiac biomarkers (if MI suspected)
  • Type and screen (for tPA cases)


- Blood work (selected patients)

  • Thrombin time (TT) and/or ecarin clotting time (ECT) if it is suspected the patient is taking direct thrombin inhibitors or direct factor Xa inhibitors
  • Liver function tests
  • Creatine kinase (CK) (if rhabdomyolysis suspected)
  • Toxicology screen
  • Blood alcohol level
  • Pregnancy test
  • Arterial blood gas tests (if hypoxia is suspected)


- Cardiac monitoring

  • Blood pressure
  • ECG/ telemetry


- Imaging

  • CT brain ±CTA neck and head
  • MRI brain (if available)
  • CT perfusion and MRI perfusion and diffusion imaging, may help identify select for thrombolysis beyond the accepted time window or with unknown time of onset
  • Chest radiography (if indicated)


Post ED investigations might include:


- Blood work

  • CBC, glucose, electrolytes
  • Partial thromboplastin time (PTT), INR
  • Liver function tests (LFTs)
  • Fasting cholesterol and lipid profile
  • Hypercoagulable state screen (if indicated)
    • Protein C and S
    • Antithrombin III
    • Anticardiolipin antibody
    • Lupus anticoagulant
    • Factor V Leiden
    • JAK-2
  • Vasculitis
    • Antinuclear antibody (ANA)
    • Rheumatoid factor (RF)


- Imaging

  • Carotid and vertebral doppler ±transcarnial doppler
  • Repeat CT brain ±CTA
  • Diffusion MRI ±MR-angiogram (MRA)
  • Conventional (catheter) angiography
    • More invasive than CTA/MRA, used less often
  • Chest x-ray


- Cardiovascular workup

  • Holter monitor/telemetry
  • Echocardiography
    • Transthoracic (TTE) (commonly used, low yield)
    • Transesophageal (TEE) (better visualization of anatomy, thrombus detection)


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Acute Ischemic Stroke


Stroke algorithm:



"Is to examine and begin fibrinolytic therapy within 60 minutes of the ischemic stroke patient's arrival in the emergency department"


General Considerations:

  • Time
  • Ensure hemodynamic stability plus mechanical ventilation as required
  • Cardiac monitoring (assess for arrthymia including brady- and tacy- arrthymias as well as AF)
  • Hypertension:
    • Caution: Avoid overly aggressive blood pressure lowering if possible unless signs of HTN crisis/ encephalopathy or tPA use being considered
    • BP up to ~220/115 may be allowed to encourage cerebral perfusion
    • Decrease BP to <185/110 mmHg as required for tPA administration and maintain for at least 24hr post tPA
  • Intravenous fluids:
    • Both hyper and hypovolemia could potentially exacerbate brain injury
    • Treat hypovolemia leading to hypoperfusion
  • Blood glucose:
    • Treat hypo- or hyperglycemia
  • Fever:
    • Treat hyperthermia (acetaminophen)
    • Consider septic work-up
    • - Blood/ urine culture
    • - Chest x-ray
  • Oral intake:
    • NPO until swallowing assessment to avoid aspiration
  • Ins/Out:
    • Avoid dehydration but avoid excess fluid and glucose infusion
    • Bladder - catheterize prn to avoid bladder distension or use Foley catheter



Intravenous rtPA fibrinolytic therapy:

  • Thrombolysis within 4.5 hours, remains the mainstay of treatment of ischemic strokes
  • There are other intravenous fibrinolytic agents such as; tenecteplase, reteplase, desmoteplase, urokinase, but their use are not well established and should not be used apart from clinical trials
  • Intravenous rtPA (0.9 mg/kg, maximum dose 90 mg) is recommended for administration to eligible patients who can be treated in the time period of ≤4.5 hours of stroke onset


Intra-arterial rtPA fibrinolytic therapy:

  • IA tPA considered in select cases <6 hours duration caused by intracranial occlusions typically MCA) who are otherwise not ideal candidates for intravenous rtPA


Mechanical clot disruption/ extraction:

  • Mechanical thrombectomy is a consideration as both a primary reperfusion strategy and in conjunction with pharmacological fibrinolysis for achieving recanalization in patients with acute ischemic stroke
  • Intra-arterial embolectomy ±IV tPA may be considered in select cases. The recently presented Mr. Clean Trial (Berkhemer OA et al. A Randomized Trial of Intra-arterial Treatment for Acute Ischemic Stroke. The article was published on December 17, 2014, at suggest superiority in stroke volume reduction and clinical outcome with modern clot retrieval devices above the use if IV tPA alone


Acute angioplasty and stenting:

Intracranial acute angioplasty and stenting

  • The efficacy of urgent angioplasty with adjunctive stent deployment with or without fibrinolysis or clot extraction is unknown. May be considered in select cases as decided by a stroke specialist and neuro-interventionalist


Antiplatelet therapy:

  • Aspirin: Recommended to begin within 24-48 hours following an acute non-tPA treated stroke or 24 hours after tPA was administered provided there are no bleeding complications
  • The combination of aspirin and clopidogrel might be considered for initiation within 24 hours of a minor ischemic stroke or TIA and continued for 90 days prior to reverting to monotherapy



  • Heparin: No data to support use in acute stroke, however use in select cases might be considered by a stroke specialist


DVT prophylaxis:

  • Subcutaneous administration of anticoagulants is recommended for treatment of immobilized patients to prevent DVT


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Fibrinolytic agents:

Fibrin selective agents:

  • ➢ Alteplase (rt-PA)



  • These agents stimulates plasminogen activator à forms a complex by binding with fibrin and plasminogen
  • This complex → converts residual plasminogen into plasmin, a proteolytic enzyme capable of hydrolyzing fibrin
  • Unopposed plasmin digests fibrinogen and other plasma proteins, including factors V and VIII



Acute ischemic stroke

  • Intravenous rtPA 0.9 mg/kg (maximum dose 90 mg) infused over 60-minutes with 10% of the total dose administered as an initial intravenous bolus over 1 minute is recommended for administration to eligible patients who can be treated in the time period of 3 to 4.5 hours after stroke onset



  • ➢ Aspirin
  • ➢ Clopidogrel





  • Works through cyclooxygenase pathway (COX 1-2 )
  • Inhibits platelet aggregation
  • Antipyretic, anti-inflammatory and analgesic action
  • Antiplatelet effects last ~7-10 days



  • Binds to adenosine diphosphate (ADP) → impairs activation of receptor complex → inhibits platelet aggregation
  • Antiplatelet effects last ~7-10 days




TIA and secondary prevention of atherothrombotic cerebral infarction:


  • 80-325 mg daily according to the individual needs of the patient, as determined by the physician


Recent MI/ Recent stroke/ Peripheral arterial disease (PAD)


  • Oral: 75 mg PO once daily

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  • ➢ Heparin (unfractionated)
  • ➢ Enoxaparin (LMWH)
  • ➢ Dalteparin (LMWH)
  • ➢ Fondaparinux


Oral anticoagulants (OAC)

  • ➢ Warfarin
  • ➢ Dabigatran
  • ➢ Rivaroxaban
  • ➢ Apixaban


Mechanism for anticoagulants:

  • Inhibits thrombus formation
  • May prevent propagation of existing thrombi
  • No direct lytic effect on established thrombi
  • Prolongs activated partial thromboplastin time (aPTT)




Prevention of venous thromboembolism (fixed-dose therapy):


  • The usual prophylactic dose is 5000 units SC every 8 to 12 hours. Prophylaxis should begin on hospital admission if indicated, or 1 to 2 hours preoperatively


Note: Heparin should continue until the patient is fully ambulatory, or until hospital discharge [Chest 2008;133(6 Suppl):381S-453S].


Typical use for IV heparin:

AF with concomitant TIA or minor/small ischemic stroke


  • Initial IV bolus of ~60-80 IU/kg or 5000 IU
  • Followed by an infusion of 12 IU/kg/hr; Max. 1000 IU/hr
  • Adjusted to maintain an APTT to 1.5 - 2 times normal (usually 50 to 70 seconds)


Caveat: For patients with moderate or large strokes, the above may be modified to a low initial exposure for avoidance of supra-therapeutic PTT and potential risk of bleeding:

  • - Initial IV bolus of ~30-40 IU/kg or 2500 IU or no
  • bolus
  • - Followed by an infusion of 12 IU/kg/hr;
  • Max. 1000 IU/hr
  • - Adjusted to maintain an APTT to 1.4-1.8 times
  • normal (suggested, but adjusted at discretion of
  • treating physician)


Low-molecular-weight heparins (LMWHs):

Prophylaxis of deep vein thrombosis

  • Dalteparin: 5000 IU SC once daily. In clinical trials, the usual duration of administration was 12-14 days


  • Enoxaparin: 40 mg (4000 IU) SC once daily. The usual duration of administration is 6-11 days
  • - Dosage in renal impairment: (CrCl <30 mL/min)
  • Recommended dosage is 20 mg (2000 IU) or
  • 30 mg (3000 IU) once daily based on individual
  • risk/benefit assessment


  • Fondaparinux: 2.5 mg SC once daily if body weight ≥50 kg
  • Note: Prophylactic use contraindicated in patients <50 kg.


Oral anticoagulants:


Prevention/Treatment of thrombosis/embolism

  • Start 2-10 mg PO once daily for 1-2 days then; adjust dose according to INR results
  • Desired INR 2-3 for non-mechanical valves. May be acceptable for aortic bileaflet mechanical valve without thromboembolism risk factors
  • OR

  • INR 2.5-3.5, if concomitant mitral mechanical valve or aortic mechanical valve
Reference: Bonow Ro, Carabello BA, Chatterjee K et al. Circulation. 2008; 118: e523-e661

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Prevention of stroke and systemic embolism in patients with atrial fibrillation


Canada labelling:

  • Age <80 year: 150 mg twice daily if creatinine clearance >30 mL/min
  • Age >80 years: 110 mg twice daily if creatinine clearance >30 mL/min
  • Contraindicated in creatinine clearance <30 mL/min


USA labelling:

  • 150 mg PO twice daily if creatinine clearance >30 ml/min
  • 75 mg PO twice daily if creatinine clearance 15-30 ml/min


Conversion from Dabigatran to parenteral anticoagulant


  • Wait 12 hrs after the last dose of dabigatran before switching to a parenteral anticoagulant


Conversion from vitamin K Antagonists (e.g. warfarin) to Dabigatran


  • Dabigatran should only be started after vitamin K antagonists have been discontinued, and the patient's INR found to be <2.0


Conversion from Dabigatran to vitamin K Antagonists (e.g. warfarin)


  • Stop dabigatran for 12 hrs then begin warfarin protocol/nomogram (see above)



Prevention of recurrent DVT and PE

  • 15 mg PO twice daily for 3 weeks, followed by 20 mg once daily for CrCl >50
  • 15 mg PO twice daily for 3 weeks, followed by 20 mg once daily for CrCl 30-49


Prevention of stroke and systemic embolism in patients with atrial fibrillation (ACS)


  • 20 mg PO once daily for CrCl >50
  • 15 mg PO one daily for CrCl 30-49



Stroke prevention in patients with atrial fibrillation

  • GFR >25 ml/min: 5 mg PO twice daily
  • Alternatively 2.5 mg BID may considered in patients with at least 2 of the following:
    • Age ≥80 years
    • Body weight ≤60 kg
    • Serum creatinine ≥133 micromole/L (1.5 mg/dL)


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Clinical Trials:
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Pipeline Agents:
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Physician Resources:
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Core Resources:

  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al eds. Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Jauch EC, Saver JL, Adams HP et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. The Executive Summary is available as an online-only Data Supplement with this article at
  • DOI: 10.1161/STR.0b013e318284056a/-/DC1.
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Kernan et al Stroke Prevention in Patients With Stroke and TIA. The Executive Summary is available as an online-only Data Supplement with this article at
  • DOI: 10.1161/STR.0000000000000024/-/DC1.
  • Longo D, Fauci A, Kasper D, et al. eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • Management of thyroid dysfunction during pregnancy and postpartum. An endocrine society clinical practice guidelines. 2007 J Clin Endocrinol Metab:92 ; S1-S47
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011


Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates


Journals/Clinical Trials:

  • Arboix A and Alió J. Cardioembolic Stroke: Clinical Features, Specific Cardiac Disorders and Prognosis. Current Cardiology Reviews, 2010; 6: 150-161
  • Appelros P, Stegmayr B and Terént A. Sex Differences in Stroke Epidemiology : A Systematic Review. Stroke. 2009;40:1082-1090. doi: 10.1161/STROKEAHA.108.540781
  • Bevan S, Traylor M, Adib-Samii P et al. Genetic heritability of ischemic stroke and the contribution of previously reported candidate gene and genomewide associations. Stroke. 2012 Dec;43(12):3161-7. doi: 10.1161/STROKEAHA.112.665760. Epub 2012 Oct 4
  • Chisholm ME and Campbell DC. Postpartum postural headache due to superior sagittal sinus thrombosis mistaken for spontaneous intracranial hypotension. Can J Anaesth. 2001 Mar;48(3):302-4
  • Connolly SJ, Eikelboom J, Joyner C et al. Apixaban in Patients with Atrial Fibrillation (AVERROES). N Engl J Med 2011; 364:806-17
  • Douen AG, Pageau N and Medic S. Usefulness of Cardiovascular Investigations in Stroke Management : Clinical Relevance and Economic Implications. Stroke. 2007;38:1956-1958. doi: 10.1161/STROKEAHA.106.477760
  • Douen AG, Pageau N and Medic S. Serial Electrocardiographic Assessments Significantly Improve Detection of Atrial Fibrillation 2.6-Fold in Patients With Acute Stroke. Stroke. 2008;39:480-482. doi: 10.1161/STROKEAHA.107.492595
  • Granger CB, Alexander JH, McMurray J J.V et al. for the ARISTOTLE Committees and Investigators. Apixaban versus Warfarin in Patients with Atrial Fibrillation. N Engl J Med 2011; 365:981-992
  • Jickling GC, Stamova B, Ander BP et al. Prediction of cardioembolic, arterial, and lacunar causes of cryptogenic stroke by gene expression and infarct location. Stroke. 2012; 43(8):2036-41
  • Kanji S, Corman C, Douen AG. Blood Pressure Management in Acute Stroke: Comparison of Current Guidelines with Prescribing Patterns
  • Koositamongkol S, Sindhu S, Pinyopasakul W et al. Factors influencing functional recovery in patients with acute ischemic stroke. Collegian: The Australian Journal of Nursing Practice, Scholarship and Research (2012). Published online
  • DOI: 10.1016/j.colegn.2012.09.002
  • Kral M, Skoloudik D, Sanak D et al. Assessment of relationship between acute ischemic stroke and heart disease- protocol of a prospective observational trial. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2012 Sep; 156(3):284-289
  • Mohr JP, Albers GW, Amarenco P et al. Etiology of stroke. Stroke journal of AHA. 1997; 28: 1501-1506
  • Patel MR, Mahaffey KW, Garg J, et al, for the ROCKET AF Steering Committee for the ROCKET AF Investigators. Rivaroxaban versus Warfarin in Nonvalvular Atrial Fibrillation N Engl J Med 2011; 365:883-891
  • Sacco RL, Diener HC, Yusuf S, Cotton D et al; the PRoFESS Study Group. Aspirin and extended- release dipyridamole versus clopidogrel for recurrent stroke. N Engl J Med. 2008;359:1238-1251
  • Saposnik G, Barinagarrementeria F, Brown RD et al. Statement for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2011;42:1158-1192
  • Tekle WG, Chaudhry SA, Fatima Z et al. Intravenous Thrombolysis in Expanded Time Window (3-4.5 hours) in General Practice with Concurrent Availability of Endovascular Treatment. Journal of Vascular and Interventional Neurology 2012
  • The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE W). The Lancet, 2006 367, Pages 1903-1912
  • Weir, N.U. An update on cardioembolic stroke ( Review ) Postgraduate Medical Journal. 2008; 84(989):133-142
  • Wolf PA, Abbott RD and Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991;22:983-988. doi: 10.1161/01.STR.22.8.983


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Andre G. Douen, MD, PhD, FRCPC, FAHA, Staff Physician, Division of Neurology, Trillium Health Partners, Mississauga, ON Canada

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