eMedicine Specialties > Neurology > Neuro-vascular Diseases

Cardioembolic Stroke: Treatment & Medication

Author: Michael J Schneck, MD, Associate Professor, Departments of Neurology and Neurosurgery, Stritch School of Medicine, Loyola University; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center
Coauthor(s): Lei Xu, MD, PhD, Resident Physician, Department of Neurology, Loyola University Chicago, Stritch School of Medicine; Santiago Palacio, MD, Neurology Fellow, Department of Medicine (Division of Neurology)
Contributor Information and Disclosures

Updated: Feb 13, 2008

Treatment

Medical Care

  • Antiplatelet and anticoagulant therapies are mainstays in the prevention of cardioembolic stroke. Consider the absolute rate of stroke associated with each source, the risk-benefit relationship of each therapy, and each patient's preferences. Warfarin is first-line anticoagulant treatment of most causes of cardioembolic stoke. Among antiplatelet agents, aspirin has been proved in clinical trials to reduce risk of cardioembolic stroke. Clopidogrel plus aspirin did not show efficacy compared to warfarin in patients with atrial fibrillation (ACTIVE W trial).
  • A meta-analysis of several randomized trials indicates that in patients with acute cardioembolic stroke, early anticoagulation is associated with a nonsignificant reduction in recurrence of ischemic stroke, no substantial reduction in death and disability, and increased intracranial bleeding. Early aspirin followed by vitamin K antagonists for long-term secondary prevention is reasonable.12
  • Randomized trials have demonstrated that the efficacy of warfarin anticoagulation is related directly to how carefully it is used. Inadequate anticoagulation produces minimal or no protection, while supratherapeutic anticoagulation may increase the risk of serious hemorrhagic complications. To optimize the level of anticoagulation, interactions with concomitant medications known to potentiate or inhibit the anticoagulant effect should be considered.
  • Monitor INRs weekly initially, then at least monthly.
  • Ximelagatran, a new oral thrombin inhibitor, has been tested in large clinical trials and appears to be an attractive alternative to adjusted-dose warfarin, but it was not approved by the US FDA because of potential hepatic toxicity.

Consultations

  • Cardiologist - To evaluate the management of arrhythmias and structural abnormalities of the heart
  • Hematologist - When the possibility of a prothrombotic state is suspected, typically in patients with PFO who have a history of venous thromboembolism or family history of thrombosis
  • Anticoagulation clinic personnel - Management of anticoagulation at a specialized clinic (if available) recommended in several studies

Diet

  • Provide patients treated with warfarin with a list of vitamin K–containing foods (eg, broccoli, avocado, other green vegetables) that inhibit its anticoagulant effects.
  • Most clinicians severely limit or proscribe consumption of alcoholic beverages in patients taking warfarin.

Activity

Review limitations on physical activities (eg, contact sports, skiing) in patients on warfarin.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

At present, warfarin and related coumarins remain the mainstay of oral anticoagulation. Several new oral anticoagulant medications are being tested in clinical trials for use in the prophylaxis of ischemic thromboembolic stroke. Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Anticoagulants

These agents prevent initial and recurrent cardiogenic embolism to the brain for many major-risk cardioembolic sources (eg, atrial fibrillation, left ventricular thrombi).


Warfarin (Coumadin)

Inhibits synthesis of 6 vitamin K–dependent proteins involved in coagulation system (factors II, VII, IX, X; proteins C, S). Many other coumarin derivatives are used worldwide.

Adult

Initial dose: 5 mg/d PO for 2-4 d (lower in very elderly patients)
Subsequent doses determined by INR achieved and source of embolism (INR 2-3 for most cardiac sources)

Pediatric

Not established

Extensive literature documents interactions with other drugs, with variable levels of evidence; drugs that increase anticoagulant effects include co-trimoxazole, erythromycin, fluconazole, isoniazid, amiodarone, aspirin, simvastatin, sulfinpyrazone, phenylbutazone, alcohol, cimetidine, and omeprazole; drugs that inhibit anticoagulant effect include rifampin, nafcillin, cholestyramine, barbiturates, carbamazepine, sucralfate, and azathioprine; OTC NSAIDs (eg, Naprosyn, ibuprofen) and aspirin are associated with increased risk of upper GI bleeding when used with warfarin; high doses of acetaminophen can prolong INR

Documented hypersensitivity; active bleeding; heparin-induced thrombocytopenia; severe renal or hepatic disease; open wounds; gastric ulcer

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Antiplatelet agents

Aspirin inhibits the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.


Aspirin (Bayer Aspirin, Anacin, Ascriptin)

Inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate).

Adult

1-2 mg/kg/d PO; dosages of 50-325 mg/d are FDA-approved for stroke prevention; typically, 81 mg/d (baby aspirin) or 325 mg/d (adult aspirin) are used, with no compelling evidence favoring either dosage

Pediatric

Not established

Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding time; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; administration in children (<16 y) with flu because of association with Reye syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Chronic renal disease; severe anemia; blood dyscrasias

More on Cardioembolic Stroke

Overview: Cardioembolic Stroke
Differential Diagnoses & Workup: Cardioembolic Stroke
Treatment & Medication: Cardioembolic Stroke
Follow-up: Cardioembolic Stroke
Multimedia: Cardioembolic Stroke
References
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References

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Further Reading

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Keywords

cardiogenic embolism, cardiac embolism, cardioembolic stroke, atrial fibrillation, atrial flutter, heart attack, transient ischemic attack, TIA, coronary artery disease, CAD, congestive heart failure, CHF, myocardial infarction, MI

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Contributor Information and Disclosures

Author

Michael J Schneck, MD, Associate Professor, Departments of Neurology and Neurosurgery, Stritch School of Medicine, Loyola University; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center
Michael J Schneck, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, Neurocritical Care Society, and Stroke Council of the American Heart Association
Disclosure: boehringer-ingelheim Honoraria Speaking and teaching; sanofi/bms Honoraria Speaking and teaching; pfizer Honoraria Speaking and teaching; genentech Honoraria Speaking and teaching; ucb pharma Honoraria Speaking and teaching; talecris Consulting fee Other; nmt medical  Independent contractor; NIH Grant/research funds Independent contractor; vernalis Grant/research funds Independent contractor; sanofi Grant/research funds Independent contractor

Coauthor(s)

Lei Xu, MD, PhD, Resident Physician, Department of Neurology, Loyola University Chicago, Stritch School of Medicine
Lei Xu, MD, PhD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Santiago Palacio, MD, Neurology Fellow, Department of Medicine (Division of Neurology)
Santiago Palacio, MD is a member of the following medical societies: American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Neurological Association, American Society for Biochemistry and Molecular Biology, Phi Beta Kappa, Sigma Xi, Society for Neuroscience, and Southern Clinical Neurological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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