Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Vertebrobasilar Atherothrombotic Disease Medication

  • Author: Eddy S Lang, MDCM, CCFP(EM), CSPQ; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Sep 09, 2014
 

Medication Summary

Antiplatelet medications constitute first-line treatment for patients with vertebrobasilar atherothrombotic disease (VBATD). This approach is supported by a large body of clinical research in the secondary prevention of strokes, and although benefits are small, its application to posterior circulation events is well established.[8]

Important inferences can be drawn from the European Stroke Prevention Study, which examined the efficacy of a daily regimen of 225 mg of dipyridamole and 990 mg of aspirin in 2500 patients randomized to receive drug therapy or placebo.[9] The overall total incidence of stroke or death (the end points) during the 2-year follow-up in the placebo group was lower in the vertebrobasilar group compared to the carotid group (14% versus 24%, respectively). The combination therapy of dipyridamole and acetylsalicylic acid caused a marked reduction in the incidence of stroke or death in patients with vertebrobasilar (51%) and carotid (30%) events. When only stroke was considered as the end point, dipyridamole and acetylsalicylic acid seemed to be more effective in reducing the risk of transient ischemic attacks than stroke, and more effective in men than in women.

No randomized clinical trials have been conducted to determine antiplatelet therapy's efficacy in treating VBATD. Antiplatelet therapy's widely perceived benefits for cerebrovascular disease may prevent an ethically acceptable trial with a placebo arm.

Data from the International Stroke Trial (IST) revealed a small but real clinical benefit of antiplatelet therapy in patients who experienced a completed stroke.[10] The IST results suggest that only 1% of patients may benefit from aspirin therapy.

Arguments for anticoagulant therapy in VBATD are much more tenuous. A nonrandomized, concurrent, cohort study suggested that anticoagulation provided superior stroke protection for patients with vertebrobasilar TIAs than for patients with carotid TIAs.[11] No randomized clinical trials involving patients with vertebrobasilar TIAs have compared anticoagulants to antiplatelet therapy or to placebos.

A strong argument favoring use of anticoagulants in VBATD includes settings in which the embolic source of thrombi is known or suspected (eg, atrial fibrillation).

Use of low-molecular-weight heparins has shown no significant improvement in outcome over conventional treatments.

Very little evidence from well-powered RCTs supports using intravenous administered thrombolytics to patients with posterior circulation infarcts. A single study of 883 patients comparing anterior circulation strokes (ACS) and posterior circulation strokes (PCS) suggested that PCS had lower symptomatic intracranial hemorrhage frequency following intravenous thrombolysis. Although, favorable outcomes and mortality were both similar between the ACS and PCS patients.[32] All thrombolytics are plasminogen activators and act either directly (urokinase, alteplase) or indirectly (streptokinase).

Use of an intra-arterial thrombolytic is also supported by some experts for those patients within 6 hours of stroke onset who do not qualify for IV thrombolytics.

The incidence of intracerebral hemorrhage as a complication of treatment was apparently 10%, similar to rates seen in stroke trials using systemic thrombolysis.

Next

Anticoagulants

Class Summary

These agents prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation.

Heparin

 

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse yet is able to inhibit further thrombogenesis. Prevents reaccumulation of clots after spontaneous fibrinolysis.

Warfarin (Coumadin)

 

Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor dose to maintain INR in range of 2-3.

Previous
Next

Antiplatelet agents

Class Summary

These agents inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.

Aspirin (Anacin, Ascriptin, Bayer aspirin)

 

Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Studies report 300 mg/d dose as effective as larger dose and may be associated with fewer adverse effects.

Ticlopidine (Ticlid)

 

Second-line antiplatelet therapy for patients who cannot tolerate aspirin or in whom aspirin is ineffective.

Clopidogrel (Plavix)

 

Inhibits platelet aggregation by inhibiting binding of ADP to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex. Rapidly absorbed from GI tract. Used as second-line therapy for patients with TIA crescendo symptoms who are already taking aspirin.

Previous
Next

Thrombolytics

Class Summary

These agents restore perfusion in the infarct-related artery.

Alteplase (Activase)

 

Tissue plasminogen activator exerts effect on fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. Serum half-life is 4-6 min but half-life lengthened when bound to fibrin in clot. Used in management of acute myocardial infarction (MI), acute ischemic stroke, and pulmonary embolism (PE). Heparin and aspirin are not given for 24 h after tPA. Must be given within 3 h of stroke onset. Exclude hemorrhage by CT scan. If hypertensive, lower BP with labetalol, 10 mg IV. Safety and efficacy of concomitant administration with aspirin and heparin during first 24 h after onset of symptoms have not been investigated.

Previous
 
 
Contributor Information and Disclosures
Author

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Marc Afilalo, MD, FACEP, FRCPC MCFP (EM), CSPQ, Director, Emergency Department, Associate Professor, Faculty of Medicine, Section of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital

Marc Afilalo, MD, FACEP, FRCPC is a member of the following medical societies: American College of Emergency Physicians, Royal College of Physicians and Surgeons of Canada, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan Wilkie University of Calgary Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

J Stephen Huff, MD, FACEP Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD, FACEP is a member of the following medical societies: American Academy of Neurology, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Flossmann E, Rothwell PM. Prognosis of vertebrobasilar transient ischaemic attack and minor stroke. Brain. 2003 Sep. 126(Pt 9):1940-54. [Medline].

  2. Goldmakher GV, Camargo EC, Furie KL, Singhal AB, Roccatagliata L, Halpern EF, et al. Hyperdense basilar artery sign on unenhanced CT predicts thrombus and outcome in acute posterior circulation stroke. Stroke. 2009 Jan. 40(1):134-9. [Medline].

  3. Pade O, Eggers J, Schreiber SJ, Valdueza J. Complete basilar artery assessment by transcranial color-coded duplex sonography using the combined transforaminal and transtemporal approach. Ultraschall Med. 2011 Dec. 32 Suppl 2:E63-8. [Medline].

  4. [Guideline] Adams HP Jr, del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007 May. 38(5):1655-711. [Medline].

  5. Coull BM, Williams LB, Goldstein LS. Anticoagulants and antiplatelet agents in acute ischemic stroke. Report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a Division of the American Heart Association). Neurology. 2002. 59 (1):13-22. [Medline].

  6. Brandt T, von Kummer R, Muller-Kuppers M. Thrombolytic therapy of acute basilar artery occlusion. Variables affecting recanalization and outcome. Stroke. 1996 May. 27(5):875-81. [Medline].

  7. Webb S, Yashar P, Kan P, Siddiqui AH, Hopkins LN, Levy EI. Treatment and outcomes of acute intracranial vertebrobasilar artery occlusion: one institution's experience. J Neurosurg. 2012 Feb 3. [Medline].

  8. Fintel DJ. Oral antiplatelet therapy for atherothrombotic disease: overview of current and emerging treatment options. Vasc Health Risk Manag. 2012. 8:77-89. [Medline]. [Full Text].

  9. Sivenius J, Riekkinen PJ, Smets P. The European Stroke Prevention Study (ESPS): results by arterial distribution. Ann Neurol. 1991 Jun. 29(6):596-600. [Medline].

  10. International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet. 1997 May 31. 349(9065):1569-81. [Medline].

  11. Whisnant JP, Cartlidge NE, Elveback LR. Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. Ann Neurol. 1978 Feb. 3(2):107-15. [Medline].

  12. Macleod MR, Davis SM, Mitchell PJ. Results of a multicentre, randomised controlled trial of intra-arterial urokinase in the treatment of acute posterior circulation ischaemic stroke. Cerebrovasc Dis. 2005. 20(1):12-7. [Medline].

  13. Becker KJ, Purcell LL, Hacke W. Vertebrobasilar thrombosis: diagnosis, management, and the use of intra- arterial thrombolytics. Crit Care Med. 1996 Oct. 24(10):1729-42. [Medline].

  14. Caplan LR. Vertebrobasilar occlusive disease. Stroke: Pathophysiology, Diagnosis and Management. 1992. Vol 1: 549-619.

  15. [Guideline] Culebras A, Kase CS, Masdeu JC. Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke. A report of the Stroke Council, American Heart Association. Stroke. 1997 Jul. 28(7):1480-97. [Medline].

  16. Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med. 2003 Dec. 10(12):1388-95. [Medline].

  17. [Guideline] Feinberg WM, Albers GW, Barnett HJ. Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. Circulation. 1994 Jun. 89(6):2950-65. [Medline].

  18. Froehling DA, Silverstein MD, Mohr DN. The rational clinical examination. Does this dizzy patient have a serious form of vertigo?. JAMA. 1994 Feb 2. 271(5):385-8. [Medline].

  19. Libman RB, Kwiatkowski TG, Hansen MD. Differences between anterior and posterior circulation stroke in TOAST. Cerebrovasc Dis. 2001. 11(4):311-6. [Medline].

  20. Lipinski CA, Swanson ER. Vertebrobasilar distribution stroke mimicking transtentorial herniation. Ann Emerg Med. 1998 May. 31(5):640-2. [Medline].

  21. Ois A, Gomis M, Rodriguez-Campello A, et al. Factors associated with a high risk of recurrence in patients with transient ischemic attack or minor stroke. Stroke. 2008 Jun. 39(6):1717-21. [Medline]. [Full Text].

  22. Phan TG, Wijdicks EF. Intra-arterial thrombolysis for vertebrobasilar circulation ischemia. Crit Care Clin. 1999 Oct. 15(4):719-42, vi. [Medline].

  23. Piechowski-Jozwiak B, Bogousslavsky J. Basilar occlusive disease: the descent of the feared foe?. Arch Neurol. 2004 Apr. 61(4):471-2. [Medline].

  24. Sauvaget E, Kici S, Petelle B. Vertebrobasilar occlusive disorders presenting as sudden sensorineural hearing loss. Laryngoscope. 2004 Feb. 114(2):327-32. [Medline].

  25. Terada T, Higashida RT, Halbach VV. Transluminal angioplasty for arteriosclerotic disease of the distal vertebral and basilar arteries. J Neurol Neurosurg Psychiatry. 1996 Apr. 60(4):377-81. [Medline].

  26. Voetsch B, DeWitt LD, Pessin MS. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 2004 Apr. 61(4):496-504. [Medline].

  27. Markus HS, Bart van der Worp H, Rothwell PM. Posterior circulation ischaemic stroke and transient ischaemic attack: diagnosis, investigation, and secondary prevention. Lancet Neurology. 2013. 12:990. [Medline].

  28. Kim JS, Cho KH, Lee H. Isolated labyrinthine infarction as a harbinger of anterior inferior cerebellar artery territory infarction with normal diffusion-weighted brain MRI. Journal of the Neurological Sciences. 2009. 278(1-2):82-4. [Medline].

  29. Schneider JI, Olshaker JS. Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke. Emerg Med Clin North Am. 2012 Aug. 30(3):681-93. [Medline].

  30. Morasch MD. Vertebral Artery Disease. Cronenwett JL and Johnston KW. Rutherford's Vascular Surgery. 8th. Toronto: Saunders; 2014. Chapter 107. [Full Text].

  31. Khan S, Rich P, Clifton A and Markus HS. Noninvasive Detection of Vertebral Artery Stenosis: A Comparison of Contrast-Enhanced MR Angiography, CT Angiography, and Ultrasound. Stroke. 2009. 40(11):3499-3503. [Medline]. [Full Text].

  32. Sarikaya H, Arnold M, Engelter ST, Lyrer PA, Mattle HP, Georgiadis D, et al. Outcomes of intravenous thrombolysis in posterior versus anterior circulation stroke. Stroke. 2011. 42(9):2498-502. [Medline].

  33. Suri MF, Johnston SC. Epidemiology of intracranial stenosis. J Neuroimaging. 2009 Oct. 19 (suppl 1):11S-6S. [Medline].

  34. Markus HS, Khan U, Birns J, Evans A, Kalra L, Rudd AG, et al. Differences in stroke subtypes between black and white patients with stroke: the South London Ethnicity and Stroke Study. Circulation. 2007 Nov 6. 116(19):2157-64. [Medline].

 
Previous
Next
 
Vascular territories of the brain.
Diffusion-weighted MRI images showing a right cerebellar infarct.
Magnetic resonance angiography demonstrating the absence of flow in the vertebrobasilar system.
Right vertebral artery angiography showing an occlusion with no flow in the basilar artery.
Angiography performed after intra-arterial thrombolysis and angioplasty showing recanalization and perfusion of the basilar artery and its branches.
Hyperdense basilar artery (arrow).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.