Carotid Artery Stenting Medication

Updated: Apr 08, 2016
  • Author: Faisal Aziz, MD; Chief Editor: Karlheinz Peter, MD, PhD  more...
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Medication

Medication Summary

Medications are routinely used before, during, and after CAS.

One day before the stenting procedure, all patients receive combined platelet inhibition with aspirin 81 mg and clopidogrel 300 mg. [14, 15] During the procedure, before guide wire passage, patients are anticoagulated with an 80 IU/kg heparin bolus. Heparin is not reversed at the end of the procedure.

After the stenting procedure, combined platelet inhibition with clopidogrel 75 mg/day and aspirin 81 mg/day is continued for at least 30 days and up to 12 months. [14, 15] Aspirin 81 mg/day and maximal-dose statins are continued indefinitely.

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Anticoagulants, Cardiovascular

Class Summary

Anticoagulants 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 but is able to inhibit further thrombogenesis. Prevents recurrence of a clot after spontaneous fibrinolysis.

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Antiplatelet Agents, Cardiovascular

Class Summary

Antiplatelets inhibit the activation of factors involved in platelet aggregation. This class of drugs has been shown to reduce mortality by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of TIAs.

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

Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.

Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for life of cell (approximately 10 d). May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. Reduces likelihood of myocardial infarction. Also very effective in reducing risk of stroke. Early administration of aspirin in patients with AMI may reduce cardiac mortality in first mo.

Clopidogrel (Plavix)

Thienopyridine antiplatelet agent. Used off-label to maintain carotid artery stent patency. Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

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