Carotid Endarterectomy Medication

Updated: Jul 22, 2022
  • Author: Omar Haqqani, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
  • Print

Medication Summary

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


Antidysrhythmics, Ib

Class Summary

Antidysrhythmic Ib agents increase the electrical stimulation threshold of the ventricle by suppressing automaticity of conduction.

Lidocaine hydrochloride (Xylocaine)

Lidocaine hydrochloride is a class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue.

If sinus bradycardia develops, 1-2 mL of 1% lidocaine is injected into the tissues of the carotid bifurcation to correct reflex sympathetic bradycardia.


Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are required to reduce the risk of coronary or cerebrovascular thrombotic events.


Heparin (5000-7000 U) is administered intravenously (IV). Heparin augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. It prevents recurrence of a clot after spontaneous fibrinolysis.


Antiplatelet Agents

Class Summary

These agents can be considered to help prevent future ischemic strokes. As with anticoagulation, aspirin is of unproven benefit in moyamoya disease; its use is considered empirical.

All patients resume their antiplatelet drugs, primarily aspirin, immediately after surgery; clopidogrel is given if aspirin is contraindicated. Maximal medical therapy, including statins and beta blockers, should be given.

Aspirin (Ecotrin, Ascriptin Maximum Strength, Ascriptin, Bayer Aspirin)

Aspirin's efficacy in preventing stroke relies on the inhibitory effect of aspirin on platelet function. This presumably helps to prevent thrombus formation and propagation.

Clopidogrel (Plavix)

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

Clopidogrel may have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis, not only through inhibition of platelet function but also through changes in the hemorrhagic profile.