Fibromuscular Dysplasia Medication

  • Author: James A Wilson, MD, MSc, FRCPC; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Apr 4, 2012
 

Medication Summary

As discussed above, acute treatment of any ischemic stroke may involve tPA, regardless of the presence or absence of FMD.

Secondary prevention of stroke generally involves the use of antiplatelet agents, and failure of a first agent results in either the switch to another agent or the addition of a second antiplatelet agent. Selection of a particular antiplatelet agent is variable, depending on physician preference. The complication of arterial dissection is generally treated with anticoagulation, first intravenously then orally. Finally, subarachnoid hemorrhage due to aneurysm rupture precludes anticoagulation and indicates a need for antivasospastic medications.

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Fibrinolytic agents

Class Summary

tPA exerts an effect on fibrinolytic system to convert plasminogen to plasmin. They are used for dissolving blood clots and have a role in the acute management of ischemic strokes.

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Alteplase (Activase)

 

Used in management of acute ischemic stroke, acute MI, and PE. Safety and efficacy with concomitant heparin or aspirin during first 24 h after symptom onset not investigated.

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Antiplatelet agents

Class Summary

These agents are used for secondary stroke prophylaxis after previous stroke or transient ischemic attack.

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Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

 

Treats mild to moderate pain and headache. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Generally considered first-line therapy in the secondary prophylaxis of cerebrovascular disease.

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Clopidogrel (Plavix)

 

Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, inhibiting platelet aggregation.

May have positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis (inhibition of platelet function and changes in hemorrhagic profile).

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Ticlopidine (Ticlid)

 

Second-line antiplatelet therapy for patients who cannot tolerate acetylsalicylic acid therapy or for whom such therapy is unsuccessful. Rarely used because of serious adverse effects and replacement by newer agents.

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Aspirin 25 mg/Dipyridamole 200 mg (Aggrenox)

 

Drug combination with antithrombotic action. Aspirin inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stasis and thrombosis. Dipyridamole is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. May also inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-adenosine monophosphate levels in platelets and formation of the potent platelet activator thromboxane A2.

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Anticoagulants

Class Summary

The use of anticoagulation in the acute management of stroke has been under hot debate for many years. However, many neurologists advocate the use of heparin acutely in stroke in the setting of an arterial dissection. Heparin is used acutely in this case, followed by several months of warfarin.

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Heparin

 

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

Most centers have protocols to titrate heparin rate to achieve specific anticoagulation levels on blood work.

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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.

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Calcium channel blockers

Class Summary

These agents are used in cases of subarachnoid hemorrhage.

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Nimodipine (Nimotop)

 

To improve neurologic impairments resulting from vasospasm after subarachnoid hemorrhage caused by a ruptured congenital intracranial aneurysm in patients who are in good neurologic condition postictus.

Studies show benefit on the severity of neurologic deficits caused by cerebral vasospasm after subarachnoid hemorrhage, but no evidence indicates that the drug either prevents or relieves spasm of the cerebral arteries. Actual mechanism of action unknown, and a neuroprotective effect is suggested.

Therapy should start within 96 h of the subarachnoid hemorrhage. If capsule cannot be swallowed because patient is undergoing surgery or unconscious, a hole can be made at both ends of the capsule with an 18-gauge needle and the contents extracted into a syringe and emptied into the patient's in situ nasogastric tube and flush with 30-mL isotonic saline.

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Contributor Information and Disclosures
Author

James A Wilson, MD, MSc, FRCPC  Neurologist and Clinical Neurophysiologist, Oconee Neurology Services

James A Wilson, MD, MSc, FRCPC, is a member of the following medical societies: American Academy of Neurology and Ontario Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Richard L Hughes, MD  Professor of Neurology, University of Colorado at Denver School of Medicine; Chief, Division of Neurology, Denver Health Medical Center

Richard L Hughes, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey L Saver, MD, FAHA, FAAN  Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine

Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, and National Stroke Association

Disclosure: University of California The University of California Regents receive funds for consulting services on clinical trial design provided to Telecris, Ev3, and CoAxia. Consulting

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

Disclosure: Medscape Salary Employment

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: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; 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; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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Digital subtraction angiogram of the right internal carotid artery demonstrates an irregular extracranial portion that is consistent with FMD.
Conventional angiogram of the left carotid artery demonstrates a 1.5-cm, long, smooth, severe stenosis of the extracranial internal carotid artery. Note that the artery is not completely occluded and a thin continuous string of contrast is present along the length of the stenosis. This smooth tubular stenosis is suggestive of the intimal fibroplasia form of FMD but can be observed with any of the subtypes.
Cerebral angiogram of the left carotid artery territory demonstrates a long, irregular stenosis with a string-of-beads appearance along the entire extracranial length of the internal carotid artery (ICA). This is consistent with the most common medial dysplasia form of fibromuscular dysplasia. Also note similar involvement of the first 3 cm of the external carotid artery (ECA). Such extensive ICA involvement, as well as ECA involvement, is atypical. Note sparing of the carotid bulb.
Lateral view of a right carotid angiogram demonstrates multiple stenoses of FMD of the internal carotid artery. The string of beads appearance is suggestive of the medial dysplasia form of FMD.
Anteroposterior view of a right carotid angiogram demonstrates FMD of the extracranial portion of the right internal carotid artery.
Angiogram of the descending aorta demonstrates the stenoses of FMD in the renal arteries bilaterally.
Angiogram of the right vertebral artery demonstrating irregular stenoses of fibromuscular dysplasia at the level of C2-3.
Illustration of the operative approach of graduated dilatation of the internal carotid artery (ICA). The common carotid and external carotid arteries are cross-clamped, and the superior thyroid artery is clipped while the ICA is isolated, opened, and dilated with progressively larger dilators. This technique has been shown to be successful in the management of medically refractive FMD stenoses.
Illustration depicts the intraluminal appearance of graduated dilatation of the stenoses of FMD. The dilator is passed into the vessel and opens the bandlike narrowings.
Illustration depicts the locations of FMD lesions, which differentiate regions with typical and atypical angiographic appearances of this disease.
Digital subtraction angiography of the left internal carotid artery distribution demonstrates a large 1.5-cm-diameter aneurysm of the right anterior communicating artery. Aneurysms may be associated with systemic vasculopathies such as FMD.
Small infarct in woman with fibromuscular dysplasia from dissected vertebral artery. An incidental aneurysm, or ovoid diverticula, is noted in the supraclinoid left internal carotid artery.
Small infarct in woman with fibromuscular dysplasia from dissected vertebral artery. An incidental aneurysm, or ovoid diverticula, is noted in the supraclinoid left internal carotid artery. Dissected vertebral artery.
Small infarct in woman with fibromuscular dysplasia from dissected vertebral artery. An incidental aneurysm, or ovoid diverticula, is noted in the supraclinoid left internal carotid artery. Internal carotid angiogram.
 
 
 
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