Basilar Artery Thrombosis Medication

Updated: Jan 11, 2019
  • Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA; Chief Editor: Helmi L Lutsep, MD  more...
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Medication Summary

The medications used in the treatment of patients with basilar artery thrombosis include thrombolytic agents, anticoagulants, antihypertensive agents, and antiplatelet agents. Some patients, particularly those with severe and active comorbid conditions, such as an acute myocardial infarction, require inotropic agents and vasopressors.

Several new oral anticoagulant medications are in the final stages of 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.


Antihypertensive agents

Class Summary

These agents control severe hypertension. They are recommended for patients considered candidates for thrombolytic therapy who have a systolic blood pressure of greater than 185mm Hg and/or a diastolic blood pressure of greater than 110mm Hg.

Nicardipine (Cardene)

Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.


Labetalol blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Nitroprusside sodium (Nitropress)

Nitroprusside sodium produces vasodilation and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate.

Enalapril (Vasotec, Epaned)

Enalapril is a competitive inhibitor of angiotensin-converting enzyme (ACE). It reduces angiotensin II levels, decreasing aldosterone secretion.



Class Summary

The potential benefits of thrombolytic therapy for the treatment of thrombosis include fast dissolution of physiologically compromising pulmonary emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.

Alteplase (Activase)

Alteplase is a tPA. Its safety and efficacy with concomitant heparin or aspirin during the first 24 hours after symptom onset have not been investigated. It is the only drug approved for use in patients within 3 hours of onset of acute ischemic stroke.


Anticoagulant Agents

Class Summary

The rationale for the use of these agents is to prevent recurrent embolism or extension of the thrombosis.


Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of a clot after spontaneous fibrinolysis.

Enoxaparin (Lovenox)

Enoxaparin is a low–molecular-weight heparin (LMWH) produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). It binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from UFH by having a higher ratio of anti–factor Xa to anti–factor IIa.

Enoxaparin does not actively lyse thrombi but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Its advantages include intermittent dosing and a decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. There is no point in checking the aPTT; the drug has a wide therapeutic window, and aPTT does not correlate with anticoagulant effect.

Desirudin (Iprivask)

Desirudin is a highly selective thrombin inhibitor. It inhibits fibrin formation, activation of coagulation factors, and thrombin-induced platelet aggregation. This results in prolongation of activated partial thromboplastin time.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with the hepatic synthesis of vitamin K–dependent coagulation factors. It is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain the INR in the range of 2-3. Warfarin is used for long-term stroke prophylaxis.

Dabigatran (Pradaxa)

Dabigatran etexilate is a selective thrombin inhibitor that inhibits thrombin formation by binding to the active thrombin site of free and fibrin-bound thrombin. It inhibits thrombin-induced platelet aggregation.

Rivaroxaban (Xarelto)

Rivaroxaban is a selective and reversible inhibition factor of Xa (FXa) in the intrinsic and extrinsic coagulation pathways. This interrupts the blood coagulation cascade, which in turn inhibits thrombin formation and thrombus development.

Apixaban (Eliquis)

Inhibits platelet activation and fibrin clot formation via direct, selective, and reversible inhibition of free and clot-bound factor Xa. Factor Xa, as part of the prothrombinase complex, catalyzes the conversion of prothrombin to thrombin. Thrombin activates platelets and catalyzes the conversion of fibrinogen to fibrin.


Antiplatelet Agents, Cardiovascular

Class Summary

Antiplatelet agents inhibit the cyclo-oxygenase system, decreasing the level of thromboxane A2, a potent platelet activator.

Aspirin (Bayer Aspirin, Ascriptin, Bufferin, Ecotrin)

Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It may be used in low doses to inhibit platelet aggregation and improve complications of venous stasis and thrombosis. Aspirin is used for long-term stroke prophylaxis.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to the platelet receptor and subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Aspirin 25 mg/dipyridamole 200 mg (Aggrenox)

This drug combination has antithrombotic action. Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It may be used in low doses to inhibit platelet aggregation and to improve the complications of venous stasis and thrombosis.

Dipyridamole is a platelet adhesion inhibitor that possibly inhibits red blood cell uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, dipyridamole may inhibit phosphodiesterase activity, leading to increased cyclic adenosine monophosphate (cAMP) within platelets and the formation of thromboxane A2.


Ticlopidine is second-line antiplatelet therapy for patients in whom aspirin is not tolerated or is ineffective.



Class Summary

These agents augment coronary and cerebral blood flow during the low-flow state associated with hypotension. If the MAP continues to be low despite fluid management, vasopressors such as dopamine, dobutamine, norepinephrine or phenylephrine should be used.


Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.


Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It produces systemic vasodilation and increases the inotropic state. Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia. Dobutamine is the pressor of choice in patients with congestive heart failure.

Norepinephrine (Levophed)

Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.

Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic blood pressure <70mm Hg) or hypotension unresponsive to other medication.

Phenylephrine (Vazculep)

Produces systemic arterial vasoconstriction, which in turn results in dose dependent increases in systolic and diastolic blood pressure and reductions in heart rate and cardiac output, especially in patients with heart failure. As a second-line treatment, phenylephrine (Neo-Synephrine) may be added to or substituted for dopamine.