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      News & Perspective Drugs & Diseases CME & Education Academy Video Decision Point
      Drugs & Diseases > Clinical Procedures

      Percutaneous Coronary Intervention (PCI) Medication

      Updated: Nov 27, 2019
      • Author: George A Stouffer, III, MD; Chief Editor: Karlheinz Peter, MD, PhD  more...
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      Medication

      Medication Summary

      The goals of pharmacotherapy in percutaneous coronary intervention (PCI) are to reduce morbidity and prevent complications.

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      Anticoagulants, Hematologic

      Class Summary

      Anticoagulants prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation.

      Heparin

      Heparin has been a traditional adjunctive medical therapy for patients undergoing coronary angioplasty and has been shown to decrease complications after the procedure. It augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents the recurrence of a clot after spontaneous fibrinolysis.

      Argatroban

      Argatroban 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.

      Bivalirudin (Angiomax)

      Bivalirudin inhibits coagulant effects by preventing thrombin-mediated cleavage of fibrinogen to fibrin.

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      Antiplatelet Agents, Cardiovascular

      Class Summary

      Agents in this class inhibit the activation of factors responsible for platelet aggregation.

      Cangrelor (Kengreal)

      Cangrelor is a fast-acting and rapidly reversible intravenous (IV) P2Y12 platelet inhibitor. It is indicated as an adjunct to PCI to reduce the risk of periprocedural myocardial infarction (MI), repeat coronary revascularization, and stent thrombosis in patients who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein (GP) IIb/IIIa inhibitor. Once the cangrelor IV infusion is discontinued following PCI, patients are transitioned to an oral P2Y12 platelet inhibitor (eg, clopidogrel, prasugrel, or ticagrelor).

      Clopidogrel (Plavix)

      Clopidogrel selectively inhibits the P2Y12 receptor on platelets and prevents adenosine diphosphate (ADP)-mediated activation of GPIIb/IIIa complex, thereby inhibiting platelet aggregation. It is a prodrug that must undergo activation to an active form.

      Prasugrel (Effient)

      Prasugrel is an oral P2Y12 platelet inhibitor. It is indicated for reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome (ACS) managed by means of PCI who have either (a) unstable angina or non-ST-elevation MI (NSTEMI) or (b) ST-elevation MI (STEMI) when managed with primary or delayed PCI. Prasugrel is a prodrug that must be converted to an active form. No cases of resistance have been reported.

      Ticagrelor (Brilinta)

      Ticagrelor is an oral P2Y12 platelet inhibitor. It is indicated to reduce the rate of thrombotic cardiovascular events in patients with ACS. In patients treated with PCI, it also reduces the rate of stent thrombosis.

      Aspirin (Ascriptin Maximum Strength, Bayer Aspirin Extra Strength, Bufferin, Ecotrin, Tri-Buffered Aspirin)

      Aspirin has been a traditional adjunctive medical therapy for patients undergoing coronary angioplasty and has been shown to decrease complications after the procedure. It is used as part of the regimen with P2Y12 platelet inhibitors. Aspirin is an odorless, white, powdery substance available at 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.

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

      It 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 the life of the cell (~10 days). It may be used in low doses to inhibit platelet aggregation and improve complications of venous stases and thromboses. It reduces the likelihood of myocardial infarction and is very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute myocardial infarction may reduce cardiac mortality in the first month.

      Abciximab (ReoPro)

      Abciximab is a chimeric human-murine monoclonal antibody that has been approved for use in elective/urgent/emergent PCI. It binds to the receptor with high affinity and reduces platelet aggregation by 80% for up to 48 hours following infusion.

      Eptifibatide (Integrilin)

      Eptifibatide is a reversible antagonist of the GPIIb/IIIa receptor that inhibits platelet aggregation. Its effects persist over the duration of the maintenance infusion and are eliminated within a few hourswhen the infusion ends.

      Tirofiban (Aggrastat)

      Tirofiban is a nonpeptide antagonist of the GPIIb/IIIa receptor. It is a reversible antagonist of fibrinogen binding. When tirofiban is administered IV, more than 90% of platelet aggregation is inhibited.

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