- Antiplatelet Agent, Glycoprotein IIb/IIIa Inhibitor
Patients with unstable angina not responding to conventional medical therapy with planned PCI within 24 hours: I.V.: 0.25 mg/kg bolus followed by an 18- to 24-hour infusion of 10 mcg/minute, concluding 1 hour after PCI.
ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) (unlabeled use; Kushner, 2009): I.V.:
Loading dose: 0.25 mg/kg bolus administered at the time of PCI
Maintenance infusion: 0.125 mcg/kg/minute (maximum: 10 mcg/minute) continued for up to 12 hours
Injection, solution [preservative free]:
Reopro®: 2 mg/mL (5 mL) [contains polysorbate 80]
Bolus dose: Aseptically withdraw the necessary amount of abciximab for the bolus dose into a syringe using a 0.2 or 5 micron low protein-binding syringe filter (or equivalent); the bolus should be administered 10-60 minutes before the procedure.
Continuous infusion: Aseptically withdraw amount required of abciximab for the infusion through a 0.2 or 5 micron low protein-binding syringe filter into a syringe; inject this into 250 mL of NS or D5W to make solution. If a syringe filter was not used when preparing the infusion, administer using an in-line 0.2 or 0.22 micron low protein-binding filter. Note: Alternatively, a standard concentration of 7.2 mg in 250 mL of NS or D5W may also be prepared for all patients and administered at the standard dose (0.125 mcg/kg/minute; maximum: 10 mcg/minute) with a variable rate in mL/hour. Infuse for 12-24 hours via pump after bolus dose; length of therapy dependent on indication.
Y-site administration: Compatible: Adenosine, argatroban, atropine, bivalirudin, diphenhydramine, fentanyl, metoprolol, midazolam. Variable (consult detailed reference): Tenecteplase.
Note: Intended for use with aspirin and heparin, at a minimum.
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs which have a heightened risk of causing significant patient harm when used in error.
Cardiovascular: Hypotension (14.4%), chest pain (11.4%)
Gastrointestinal: Nausea (13.6%)
Hematologic: Minor bleeding (4.0% to 16.8%)
Neuromuscular & skeletal: Back pain (17.6%)
1% to 10%:
Cardiovascular: Bradycardia (4.5%), peripheral edema (1.6%)
Central nervous system: Headache (6.45)
Gastrointestinal: Vomiting (7.3%), abdominal pain (3.1%)
Hematologic: Major bleeding (1.1% to 14%), thrombocytopenia: <100,000 cells/mm3 (2.5% to 5.6%); <50,000 cells/mm3 (0.4% to 1.7%)
Local: Injection site pain (3.6%)
<1% (Limited to important or life-threatening): Abnormal thinking, allergic reactions/anaphylaxis (possible), AV block, bronchospasm, bullous eruption, coma, confusion, diabetes mellitus, embolism, hyperkalemia, ileus, inflammation, intracranial hemorrhage, myalgia, nodal arrhythmia, pleural effusion, pulmonary embolism, prostatitis, pruritus, stroke, urinary retention, ventricular tachycardia, xerostomia
• Anaphylaxis/hypersensitivity reactions: Administration may result in human antichimeric antibody formation that can cause hypersensitivity reactions (including anaphylaxis).
• Bleeding: The most common complication is bleeding, including retroperitoneal, pulmonary, and spontaneous GI and/or GU bleeding; watch closely for bleeding, especially the arterial access site for the cardiac catheterization. Use with extreme caution in patients with platelet counts <150,000/mm3, patients with hemorrhagic retinopathy, previous history of GI disease, recent thrombolytic therapy and in chronic dialysis patients. Use caution with administration of other drugs affecting hemostasis. Minimize other procedures including arterial and venous punctures, I.M. injections, nasogastric tubes, etc. Increased risk of hemorrhage during or following angioplasty is associated with unsuccessful PTCA, PTCA procedure >70 minutes duration, or PTCA performed within 12 hours of symptom onset for acute myocardial infarction. When attempting I.V. access, avoid noncompressible sites (eg, subclavian or jugular veins).
• Thrombocytopenia: Administration may result in human antichimeric antibody formation that can cause thrombocytopenia; readministration within 30 days or in patients with human antichimeric antibodies (HACA) increases the incidence and severity of thrombocytopenia.
• Elderly: Use with caution in patients >65 years of age; increased risk of bleeding.
• Low weight patients: Use with caution in patients weighing <75 kg; increased risk of bleeding.
• Diminished efficacy: Administration may result in human antichimeric antibody formation that can cause diminished efficacy.
• Sheath removal: Prior to pulling the sheath, heparin should be discontinued for 3-4 hours and ACT ≤175 seconds or aPTT ≤50 seconds. Use standard compression techniques after sheath removal. Watch the site closely afterwards for further bleeding.
Anticoagulants: Antiplatelet Agents may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy
Antiplatelet Agents: May enhance the anticoagulant effect of other Antiplatelet Agents. Risk C: Monitor therapy
Belimumab: Monoclonal Antibodies may enhance the adverse/toxic effect of Belimumab. Risk X: Avoid combination
Collagenase (Systemic): Antiplatelet Agents may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and/or bleeding may be increased. Risk C: Monitor therapy
Dasatinib: May enhance the anticoagulant effect of Antiplatelet Agents. Risk C: Monitor therapy
Dextran: May enhance the anticoagulant effect of Abciximab. Risk X: Avoid combination
Drotrecogin Alfa: Antiplatelet Agents may enhance the adverse/toxic effect of Drotrecogin Alfa. Bleeding may occur. Management: When possible, avoid use of drotrecogin within 7 days of use of any IIb/IIIa antagonists, higher dose aspirin (more than 650 mg/day), or use of other antiplatelet agents. Risk D: Consider therapy modification
Glucosamine: May enhance the antiplatelet effect of Antiplatelet Agents. Risk C: Monitor therapy
Herbs (Anticoagulant/Antiplatelet Properties) (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Antiplatelet Agents. Bleeding may occur. Risk D: Consider therapy modification
Ibritumomab: Antiplatelet Agents may enhance the adverse/toxic effect of Ibritumomab. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy
Monoclonal Antibodies: Abciximab may enhance the potential for allergic or hypersensitivity reactions to Monoclonal Antibodies. Also may cause thrombocytopenia or diminished therapeutic effects. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of Antiplatelet Agents. An increased risk of bleeding may occur. Nonsteroidal Anti-Inflammatory Agents may diminish the cardioprotective effect of Antiplatelet Agents. This interaction is likely specific to aspirin, and not to other antiplatelet agents. Risk C: Monitor therapy
Omega-3-Acid Ethyl Esters: May enhance the antiplatelet effect of Antiplatelet Agents. Risk C: Monitor therapy
Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Antiplatelet Agents. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the antiplatelet effect of Antiplatelet Agents. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the antiplatelet effect of Antiplatelet Agents. Risk C: Monitor therapy
Rivaroxaban: Antiplatelet Agents may enhance the anticoagulant effect of Rivaroxaban. Management: Avoid concurrent use of clopidogrel with rivaroxaban unless the anticipated benefits outweigh the risks of bleeding. Avoid concurrent use of rivaroxaban with other antiplatelet agents whenever possible. Risk D: Consider therapy modification
Salicylates: Antiplatelet Agents may enhance the adverse/toxic effect of Salicylates. Increased risk of bleeding may result. Risk C: Monitor therapy
Thrombolytic Agents: Antiplatelet Agents may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy
Tositumomab and Iodine I 131 Tositumomab: Antiplatelet Agents may enhance the adverse/toxic effect of Tositumomab and Iodine I 131 Tositumomab. Specifically, the risk of bleeding-related adverse events may be increased. Risk C: Monitor therapy
Vitamin E: May enhance the antiplatelet effect of Antiplatelet Agents. Risk C: Monitor therapy
Abciximab initiated 18-24 hours prior to PCI: Maintain aPTT between 60-85 seconds during the heparin/abciximab infusion period
During PCI: Maintain ACT between 200-300 seconds
Following PCI (if anticoagulation is maintained): Maintain aPTT between 50-75 seconds
Sheath removal should not occur until aPTT is ≤50 seconds or ACT ≤175 seconds.
Maintain bleeding precautions, avoid unnecessary arterial and venous punctures, use saline or heparin lock for blood drawing, assess sheath insertion site and distal pulses of affected leg every 15 minutes for the first hour and then every 1 hour for the next 6 hours. Arterial access site care is important to prevent bleeding. Care should be taken when attempting vascular access that only the anterior wall of the femoral artery is punctured, avoiding a Seldinger (through and through) technique for obtaining sheath access. Femoral vein sheath placement should be avoided unless needed. While the vascular sheath is in place, patients should be maintained on complete bedrest with the head of the bed at a 30° angle and the affected limb restrained in a straight position.
Observe patient for mental status changes, hemorrhage; assess nose and mouth mucous membranes, puncture sites for oozing, ecchymosis, and hematoma formation; and examine urine, stool, and emesis for presence of occult or frank blood; gentle care should be provided when removing dressings.
- ReoPro (AR, AT, AU, BE, BG, BR, CH, CN, CO, CZ, DE, DK, ES, FI, FR, GB, GR, HK, IE, IN, IT, KP, LU, MX, MY, NL, NO, NZ, PE, PK, PL, PT, RU, SE, SG, TH, TW, ZA)
Duration: Up to 72 hours for restoration of normal hemostasis (Schror, 2003)
Distribution: Vd: 0.07 L/kg (Schror, 2003)
Protein binding: Mostly bound to GP IIb/IIIa receptors on platelet surface
Metabolism: Unbound abciximab metabolized via proteolytic cleavage (Schror, 2003)
Half-life elimination: Plasma: ~30 minutes; dissociation half-life from GP IIb/IIIa receptors: up to 4 hours (Schror, 2003). Note: 29% and 13% of abciximab estimated to remain on GP IIb/IIIa receptors at 8 and 15 days, respectively (Mascelli, 1998). Platelet function may remain abnormal for up to 7 days post infusion (Osende, 2001).
Time to peak: Platelet inhibition: ~30 minutes (Mascelli, 1998)