Fibromuscular Dysplasia Medication

Updated: Apr 03, 2017
  • Author: James A Wilson, MD, MSc, FRCPC; Chief Editor: Helmi L Lutsep, MD  more...
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Medication

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.

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.

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.

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).

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.

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.

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.

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.

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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