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Medication Safety Issues
High alert medication: 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.
Pronunciation
(ab SIK si mab)
U.S. Brand Names
Index Terms
Generic Available
No
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention (PCI); prevention of cardiac ischemic complications in patients with unstable angina not responding to conventional therapy when PCI is scheduled within 24 hours
Note: Intended for use with aspirin and heparin, at a minimum.
Use: Unlabeled/Investigational
ST-elevation MI: Combination regimen of abciximab (full dose), tenecteplase (half dose), and heparin (unlabeled dose)
Pregnancy Risk Factor
C
Pregnancy Considerations
Animal reproduction studies have not been conducted. In vitro studies have shown only small amounts of abciximab to cross the placenta. It is not known whether abciximab can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity.
Lactation
Excretion in breast milk unknown/use caution
Contraindications
Hypersensitivity to abciximab, to murine proteins, or any component of the formulation; active internal hemorrhage or recent (within 6 weeks) clinically-significant GI or GU bleeding; history of cerebrovascular accident within 2 years or cerebrovascular accident with significant neurological deficit; clotting abnormalities or administration of oral anticoagulants within 7 days unless prothrombin time (PT) is ?1.2 times control PT value; thrombocytopenia (<100,000 cells/?L); recent (within 6 weeks) major surgery or trauma; intracranial tumor, arteriovenous malformation, or aneurysm; severe uncontrolled hypertension; history of vasculitis; use of dextran before PTCA or intent to use dextran during PTCA; concomitant use of another parenteral GP IIb/IIIa inhibitor
Warnings/Precautions
Concerns related to adverse effects:
• 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.
• 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.
Special populations:
• 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.
• Pediatrics: Safety and efficacy have not been established in children.
Other warnings/precautions:
• 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.
Adverse Reactions
As with all drugs which may affect hemostasis, bleeding is associated with abciximab. Hemorrhage may occur at virtually any site. Risk is dependent on multiple variables, including the concurrent use of multiple agents which alter hemostasis and patient susceptibility.
>10%:
Cardiovascular: Hypotension (14%), chest pain (11%)
Gastrointestinal: Nausea (14%)
Hematologic: Minor bleeding (4% to 17%)
Neuromuscular & skeletal: Back pain (18%)
1% to 10%:
Cardiovascular: Bradycardia (5%), peripheral edema (2%)
Central nervous system: Headache (7%)
Gastrointestinal: Vomiting (7%), abdominal pain (3%)
Hematologic: Major bleeding (1% to 14%), thrombocytopenia: <100,000 cells/mm3 (3% to 6%); <50,000 cells/mm3 (0.4% to 2%)
Local: Injection site pain (4%)
<1% (Limited to important or life-threatening): Abnormal thinking, abnormal vision, agitation, allergic reactions/anaphylaxis (possible), anemia, anxiety, arteriovenous fistula, bronchitis, bronchospasm, bullous eruption, cellulitis, coma, complete AV block, confusion, cystalgia, diabetes mellitus, diaphoresis increased, diarrhea, diplopia, dizziness, dyspepsia, dysuria, embolism, gastroesophageal reflux, hyperkalemia, hypertonia, hypoesthesia, ileus, incomplete AV block, inflammation, intracranial hemorrhage, leukocytosis, muscle contractions, myalgia, nodal arrhythmia, pain, palpitation, peripheral coldness, petechiae, pleural effusion, pneumonia, prostatitis, pruritus, pseudoaneurysm, pulmonary embolism, stroke, thrombophlebitis, urinary incontinence, urinary retention, ventricular tachycardia, weakness, xerostomia
Drug Interactions
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
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. Risk D: Consider therapy modification
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. Exceptions: Alefacept. 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
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
Storage
Vials should be stored at 2°C to 8°C. Do not freeze or shake. After admixture, the prepared solution is stable for 12 hours.
Compatibility
Abciximab should be administered in a separate intravenous line. No incompatibilities have been observed with glass bottles or PVC bags.
Mechanism of Action
Fab antibody fragment of the chimeric human-murine monoclonal antibody 7E3; this agent binds to platelet IIb/IIIa receptors, resulting in steric hindrance, thus inhibiting platelet aggregation
Pharmacodynamics/Kinetics
Half-life elimination: ~30 minutes
Dosage
Percutaneous coronary intervention (PCI): I.V.: 0.25 mg/kg bolus administered 10-60 minutes prior to start of PCI followed by an infusion of 0.125 mcg/kg/minute (maximum: 10 mcg/minute) for 12 hours
Patients with unstable angina not responding to conventional medical therapy with planned PCI within 24 hours: 0.25 mg/kg bolus followed by an 18- to 24-hour infusion of 10 mcg/minute, concluding 1 hour after PCI.
ST-elevation MI combination regimen (unlabeled): Half-dose tenecteplase (15-25 mg based on weight), abciximab 0.25 mg/kg bolus then 0.125 mcg/kg/minute (maximum: 10 mcg/minute) for 12 hours and heparin dosing as follows: Concurrent bolus of 40 units/kg (maximum: 3000 units), then 7 units/kg/hour (maximum: 800 units/hour) as continuous infusion. Adjust to aPTT target of 50-70 seconds.
Administration: I.V.
Abciximab is intended for coadministration with aspirin postangioplasty and heparin infused and weight adjusted to maintain a therapeutic bleeding time (eg, ACT 300-500 seconds). Solution must be filtered prior to administration. Do not shake the vial.
Administration: I.V. Detail
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.
Monitoring Parameters
Prothrombin time, activated partial thromboplastin time (aPTT), hemoglobin, hematocrit, platelet count, fibrinogen, fibrin split products, transfusion requirements, signs of hypersensitivity reactions, guaiac stools, Hemastix® urine. Platelet count should be monitored at baseline, 2-4 hours following bolus infusion, and at 24 hours (or prior to discharge, if before 24 hours). To minimize risk of bleeding:
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.
Patient Education
This medication can only be administered I.V. You will have a tendency to bleed easily following this medication; use caution to prevent injury (use electric razor, soft toothbrush, and use caution with knives, needles, or anything sharp). If bleeding occurs, apply pressure to bleeding spot until bleeding stops completely. Report unusual bruising or bleeding; blood in urine, stool, or vomitus; bleeding gums; or vision changes. Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend to become pregnant. Consult prescriber if breast-feeding.
Anesthesia and Critical Care Concerns/Other Considerations
Clinical Pearls/Comments: Platelet Effects: As an irreversible inhibitor of the platelet glycoprotein IIb/IIIa receptor, abciximab has a long duration of action and platelet effects reverse slowly. It can take 24-48 hours for platelet function to return to normal after discontinuation of infusion making it difficult to use in patients likely to need CABG. Antiplatelet effects can be reversed with platelet transfusions.
Platelet count monitoring is recommended 2-4 hours after initiation, and at 24 hours or prior to discharge, whichever is first. Profound thrombocytopenia occurs shortly after the initiation of abciximab therapy, generally between 2 and 31 hours (Jubelirer, 1999). Specific management guidelines for GP IIb/IIIa induced thrombocytopenia have been published (Berkovitz, 1997; Huxtable, 2006; Llevadot, 2000). Platelet counts should recover rapidly after discontinuation. Platelet transfusion may be necessary. The presence of active bleeding at any time, emergent invasive procedure, or a platelet level of <20,000 cells/microL should prompt the consideration of platelet transfusion.
Cardiovascular Considerations
Percutaneous Coronary Intervention (PCI): A glycoprotein llb/llla inhibitor is recommended for patients who will undergo PCI, especially those with unstable angina or other high risks for postprocedure ischemic complications. In the TARGET trial, abciximab (FDA-approved dose) and tirofiban (10 mcg/kg bolus; infusion of 0.15 mcg/kg/minute for 18-24 hours) were compared to each other in patients undergoing coronary stenting. The primary endpoint was death, nonfatal MI, or urgent target vessel revascularization at 30 days. Abciximab improved outcome to a greater extent than tirofiban did primarily by reducing nonfatal MI. Follow-up at 6 months revealed no significant difference in primary outcomes between treatments, but a trend existed in favor of abciximab reducing the occurrence of MIs.
ST-Segment Elevation Myocardial Infarction (STEMI):
Adjunct to Thrombolysis: In the GUSTO V trial, patients with acute MI were randomized to standard-dose reteplase or half-dose reteplase (two boluses of 5 units each, 30 minutes apart) and full-dose abciximab. Mortality at 30 days (primary endpoint) was similar in both groups. The combination treatment group had significantly fewer reinfarctions or recurrent episodes of ischemia. Combination treatment was also associated with less need for urgent revascularization. More bleeding occurred in the combination treatment group, but the incidence of nonfatal disabling stroke and stroke of any type were similar in both groups. Overall, no difference in intracranial hemorrhages was observed between the two treatments, but a trend towards an increased incidence occurred in patients >75 years of age who received combination treatment. Patients with acute MI were randomized in an open-label study to full-dose tenecteplase and enoxaparin, half-dose tenecteplase with low-dose, weight-based heparin and a 12-hour infusion of abciximab or full-dose tenecteplase with weight-based heparin (ASSENT-3 Investigators, 2001). The primary endpoint (30 days) was mortality, in-house reinfarction, and in-house refractory ischemia. The abciximab arm and the enoxaparin arm had significantly less mortality, reinfarction, and refractory ischemia than in the unfractionated heparin/full-dose tenecteplase. One year mortality (secondary endpoint) was similar in all three treatment arms (Sinnaeve PR, 2004). However, the 1-year outcome tended to be worse with abciximab in patients with diabetes. The 2004 ACC/AHA guidelines for STEMI recommend that pharmacologic reperfusion with abciximab and half-dose reteplase or tenecteplase may be considered in patients <75 years of age with anterior wall infarctions and no risk factors for bleeding.
Facilitated Percutaneous Coronary Intervention (PCI): Facilitated PCI describes administration of a thrombolytic, a glycoprotein (GP) IIb/IIIa inhibitor, or a combination of the two in addition to standard treatment prior to planned PCI for STEMI. The concept is based on the premise that the patient will have a higher likelihood of entering the procedure with an open-artery which has been shown to improve outcomes at least in patients who have spontaneous reperfusion. Although a number of facilitated PCI clinical trials have shown that a higher rate of patients enter the catheterization laboratory with an open coronary artery, clinical outcomes are not improved, safety is compromised (eg, increased rates of bleeding complications), and mortality may be increased (Keeley, 2006). More recently, the FINESSE trial (Ellis, 2008), a prospective, international, multicenter trial, enrolled 2452 high-risk patients with STEMI and randomized them to either facilitated PCI with half-dose reteplase and abciximab, facilitated PCI with abciximab alone, or primary PCI with abciximab administered at the time of PCI. The primary endpoint of the trial was a composite of all-cause mortality and post-MI complications (ventricular fibrillation occurring >48 hours after randomization, cardiogenic shock, and CHF requiring hospitalization or emergency department visit within 90 days). Although patients who received a facilitated strategy with reteplase/abciximab had higher rates of ST-segment resolution at 60-90 minutes and TIMI 3 flow prior to PCI compared to facilitated PCI with abciximab or primary PCI with abciximab, there was no difference in the primary endpoint or 90-day mortality among the groups. Facilitated PCI significantly increased the incidence of nonintracranial TIMI major and minor bleeding. Of note, 5 patients in the reteplase/abciximab group developed an intracranial hemorrhage. The authors concluded that there is no clinical benefit in facilitating PCI with abciximab or half-dose reteplase/abciximab. If PCI is the chosen strategy for reperfusion, patients should be given a GPIIb/IIIa inhibitor at the time of PCI. Currently, the ACC/AHA/SCAI 2007 Update for PCI and the ACC/AHA 2007 Update for STEMI recommend facilitated PCI with agents other than full-dose thrombolytics in patients who are high-risk (eg, large MI, hemodynamic or electrical instability), low risk of bleeding, and when PCI is not immediately available within 90 minutes. The 2008 Chest guidelines do not recommend facilitated PCI with a thrombolytic (with or without GP IIb/IIIa inhibition) in any patient with STEMI.
Platelet Effects: Abciximab has a long duration of action and platelet effects reverse slowly. It can take 24-48 hours for platelet function to return to normal after discontinuation of infusion making it difficult to use in patients likely to need CABG. Antiplatelet effects can be reversed with platelet transfusions.
Platelet count monitoring is recommended 2-4 hours after initiation, and at 24 hours or prior to discharge, whichever is first. Acute profound thrombocytopenia with abciximab occurs generally between 2 and 31 hours of administration. If this occurs, discontinuation of the infusion is recommended. The presence of active bleeding at any time, emergent invasive procedure, or a platelet level of <20,000 cells/microL should prompt the consideration of platelet transfusion, but there is evidence that a threshold level of 10,000 cells/microL in patients without clinical signs of bleeding may be safe (Giugliano, 1998; Wandt, 1998). Patients who develop severe thrombocytopenia (<20,000 cells/microL) should be monitored closely for signs of intracerebral hemorrhage (Trivedi, 2002; Vahdat, 2000). Platelet count recovery may take up to 2 weeks. Readministration of a GP IIb/IIIa inhibitor is not recommended after an episode of thrombocytopenia, since there may be a risk for more severe thrombocytopenia after rechallenge (Tcheng, 2001).
Unstable Angina/Non-ST-Elevation Myocardial Infarction (UA/NSTEMI): The 2007 ACC/AHA guidelines for UA/NSTEMI recommend, in addition to aspirin and either heparin or enoxaparin, administration of an intravenous glycoprotein llb/llla inhibitor or clopidogrel (uncertainty exists about optimum dose) in patients with non-ST-segment elevation ACS who are expected to undergo diagnostic angiography and PCI (invasive strategy); abciximab is recommended only if there is no appreciable delay to angiography. In such patients in which PCI is not expected (conservative strategy), eptifibatide or tirofiban should be administered (along with aspirin, clopidogrel and anticoagulant therapy) if high-risk features (eg, positive biochemical markers of infarction, ST-segment depression, sustained VT, >75 years of age, or signs of LV dysfunction) or refractory ischemia are present.
Dental Health: Effects on Dental Treatment
Key adverse event(s) related to dental treatment: Bleeding is a potential adverse effect of abciximab during dental surgery. See Effects on Bleeding.
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
None reported
Mental Health: Effects on Psychiatric Treatment
None reported
Nursing: Physical Assessment/Monitoring
Monitor vital signs and laboratory results prior to, during, and after therapy. Assess infusion insertion site and peripheral pulses during and after therapy. Observe and teach patient bleeding precautions (avoid invasive procedures and activities that could result in injury). Monitor closely for signs of excessive bleeding. Pregnancy risk factor C. Note breast-feeding caution.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Injection, solution:
ReoPro®: 2 mg/mL (5 mL)
References
Anderson JL, Adams CD, Antman EM, et al, “ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) Developed in Collaboration With the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine,” J Am Coll Cardiol, 2007, 50(7):e1-e157.
Antman EM, Anbe SC, Alpert JS, et al, “ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction - Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction),” Circulation, 2004, 110(5):588-636. Available at: http://www.circulationaha.org/cgi/content/full/110/5/588. Last accessed October 26, 2004.
Antman EM, Hand M, Armstrong PW, et al, “2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines,” J Am Coll Cardiol, 2008, 51(2):210-49.
Aguirre FV, Topol EJ, and Ferguson JJ, “Bleeding Complications With the Chimeric Antibody to Platelet Glycoprotein IIb/IIIa Intergrin in Patients Undergoing Percutaneous Coronary Intervention. EPIC Investigators,” Circulation, 1995, 91(12):2882-90.
Antman EM, Giugliano RP, Gibson CM, et al, “Abciximab Facilitates the Rate and Extent of Thrombolysis: Results of the Thrombolysis in Myocardial Infarction (TIMI) 14 Trial. The TIMI 14 Investigators,” Circulation, 1999, 99(21):2720-32.
“ASSENT-3 Investigators. Efficacy and Safety of Tenecteplase in Combination With Enoxaparin, Abciximab, or Unfractionated Heparin: The ASSENT-3 Randomised Trial in Acute Myocardial Infarction,” Lancet, 2001, 358 (9282):605-13.
Berkowitz SD, Harrington RA, Rund MM, et al, “Acute Profound Thrombocytopenia After C7E3 Fab (Abciximab) Therapy,” Circulation, 1997, 95(4):809-13.
Brener SJ, Barr LA, Burchenal JE, et al, “Randomized, Placebo-Controlled Trial of Platelet Glycoprotein IIb/IIIa Blockade With Primary Angioplasty for Acute Myocardial Infarction,” ReoPro and Primary PTCA Organization and Randomized Trial (RAPPORT) Investigators, Circulation, 1998, 98(8):734-41.
Ellis SG, Tendera M, de Belder MA, et al, “Facilitated PCI in Patients With ST-Elevation Myocardial Infarction,” N Engl J Med, 2008, 358(21):2205-17.
Giugliano RP, “Drug-Induced Thrombocytopenia: Is It a Serious Concern for Glycoprotein IIb/IIIa Receptor Inhibitors?” J Thromb Thrombolysis, 1998, 5(3):191-202.
Hamm CW, Heeschen C, Goldmann B, et al, “Benefit of Abciximab in Patients With Refractory Unstable Angina in Relation to Serum Troponin T Levels. c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) Study Investigators,” N Engl J Med, 1999, 340(21):1623-9.
Huxtable LM, Tafreshi MJ, and Rakkar AN, “Frequency and Management of Thrombocytopenia With the Glycoprotein IIb/IIIa Receptor Antagonists,” Am J Cardiol, 2006, 97(3):426-9.
Jubelirer SJ, Koenig BA, and Bates MC, “Acute Profound Thrombocytopenia Following C7E3 Fab (Abciximab) Therapy: Case Reports, Review of the Literature and Implications for Therapy,” Am J Hematol, 1999, 61(3):205-8.
Keeley EC, Boura JA, and Grines CL, “Comparison of Primary and Facilitated Percutaneous Coronary Interventions for ST-elevation Myocardial Infarction: Quantitative Review of Randomised Trials,” Lancet, 2006, 367(9510):579-88.
King SB 3rd, Smith SC Jr, Hirshfeld JW Jr, et al, “2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines,” J Am Coll Cardiol, 2008, 51(2):172-209.
Lincoff AM, Califf RM, Anderson KM, et al, “Evidence for Prevention of Death and Myocardial Infarction With Platelet Membrane Glycoprotein IIb/IIIa Receptor Blockade by Abciximab (c7E3 Fab) Among Patients With Unstable Angina Undergoing Percutaneous Coronary Revascularization. EPIC Investigators. Evaluation of 7E3 in Preventing Ischemic Complications,” J Am Coll Cardiol, 1997, 30(1):149-56.
Lincoff AM, Califf RM, Moliterno DJ, et al, “Complementary Clinical Benefits of Coronary-Artery Stenting and Blockade of Platelet Glycoprotein IIb/IIIa Receptors. Evaluation of Platelet IIb/IIIa Inhibition in Stenting Investigators,” N Engl J Med, 1999, 341(5):319-27.
Lincoff AM, Califf RM, Van de Werf F, et al, “Mortality at 1 Year With Combination Platelet Glycoprotein IIb/IIIa Inhibition and Reduced-Dose Fibrinolytic Therapy vs Conventional Fibrinolytic Therapy for Acute Myocardial Infarction: GUSTO V Randomized Trial,” JAMA, 2002, 288(17):2130-5.
Lincoff AM, Tcheng JE, Califf RM, et al, “Sustained Suppression of Ischemic Complications of Coronary Intervention by Platelet GP IIb/IIIa Blockade With Abciximab: One-Year Outcome in the EPILOG Trial. Evaluation in PTCA to Improve Long-Term Outcome With Abciximab GP IIb/IIIa Blockade,” Circulation, 1999, 99(15):1951-8.
Llevadot J, Coulter SA, and Giugliano RP, “A Practical Approach to the Diagnosis and Management of Thrombocytopenia Associated With Glycoprotein IIb/IIIa Receptor Inhibitors,” J Thromb Thrombolysis, 2000, 9(2):175-80.
Moliterno DJ, Yakubov SJ, DiBattiste PM, et al, “Outcomes at 6 months for the Direct Comparison of Tirofiban and Abciximab During Percutaneous Coronary Revascularization With Stent Placement: The TARGET Follow-up Study.” Lancet, 2002, 360(9330):355-60.
“Platelet Glycoprotein IIb/IIIa Receptor Blockade and Low-Dose Heparin During Percutaneous Coronary Revascularization. The EPILOG Investigators,” N Engl J Med, 1997, 336(24):1689-96.
“Randomised Placebo-Controlled Trial of Abciximab Before and During Coronary Intervention in Refractory Unstable Angina: The CAPTURE Study,” Lancet, 1997, 349(9063):1429-35.
Sinnaeve PR, Alexander JH, Bogaerts K, et al, "Efficacy of Tenecteplase in Combination With Enoxaparin, Abciximab, or Unfractionated Heparin: One-Year Follow-Up Results of the Assessment of the Safety of a New Thrombolytic-3 (ASSENT-3) Randomized Trial in Acute Myocardial Infarction," Am Heart J, 2004, 147:993-8.
Smith SC Jr, Dove JT, Jacobs AK, et al, “ACC/AHA Guidelines of Percutaneous Coronary Interventions (Revision of the 1993 PTCA Guidelines) - Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1993 Guidelines for Percutaneous Transluminal Coronary Angioplasty),” J Am Coll Cardiol, 2001, 37(8):2215-39.
Tcheng JE, Kereiakes DJ, Lincoff AM, et al, “Abciximab Readministration: Results of the ReoPro® Readministration Registry,” Circulation, 2001, 104(8):870-5.
Topol EJ, Ferguson JJ, Weisman HF, et al, “Long-Term Protection From Myocardial Ischemic Events in a Randomized Trial of Brief Integrin Beta3 Blockade With Percutaneous Coronary Intervention. EPIC Investigator Group. Evaluation of Platelet IIb/IIIa Inhibition for Prevention of Ischemic Complication,” JAMA, 1997, 278(6):479-84.
Topol EJ, GUSTO V Investigators, “Reperfusion Therapy for Acute Myocardial Infarction With Fibrinolytic Therapy or Combination Reduced Fibrinolytic Therapy and Platelet Glycoprotein IIb/IIIa Inhibition: The GUSTO V Randomized Trial,” Lancet, 2001, 357:1905-14.
Topol E, Moliterno DJ, Herrmann HC, et al, “Comparison of Two Platelet Glycoprotein IIb/IIIa Inhibitors, Tirofiban and Abciximab, for the Prevention of Ischemic Events With Percutaneous Coronary Revascularization,” N Engl J Med, 2001, 244:1888-94.
Trivedi SM, Shani J, and Hollander G, “Bleeding Complications of Platelet Glycoprotein IIb/IIIa Inhibitor Abciximab (ReoPro®),” J Invasive Cardiol, 2002, 14(7):423-5.
“Use of a Monoclonal Antibody Directed Against the Platelet Glycoprotein IIb/IIIa Receptor in High-Risk Coronary Angioplasty. The EPIC Investigation,” N Engl J Med, 1994, 330(14):956-61.
Vahdat B, Canavy I, Fourcade L, et al, “Fatal Cerebral Hemorrhage and Severe Thrombocytopenia During Abciximab Treatment,” Catheter Cardiovasc Interv, 2000, 49(2):177-80.
van den Merkhof LF, Zijlstra F, Olsson H, et al, “Abciximab in the Treatment of Acute Myocardial Infarction Eligible for Primary Percutaneous Transluminal Coronary Angioplasty. Results of the Glycoprotein Receptor Antagonist Patency Evaluation (GRAPE) Pilot Study,” J Am Coll Cardiol, 1999, 33(6):1528-32.
Wandt H, Frank M, Ehninger G, et al, “Safety and Cost Effectiveness of a 10 X 109/L Trigger for Prophylactic Platelet Transfusions Compared With the Traditional 20 X 109/L Trigger: A Prospective Comparative Trial in 105 Patients With Acute Myeloid Leukemia,” Blood, 1998, 91(10):3601-6.
International Brand Names
Lexi-Comp.com
Last full review/revision August 2009
Content last modified August 2009
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