Eptifibatide


Article Author:
Agam Bansal
Yasar Sattar


Article Editor:
Radia Jamil


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
8/4/2019 12:27:57 AM

Indications

Eptifibatide is an antiplatelet drug which reversibly binds and inhibits glycoprotein IIb/IIIa receptor of platelets. A protein found in the venom of a southeastern pygmy rattlesnake is used to make eptifibatide. The PURSUIT and IMPACT-II account for the indications of eptifibatide by Food and Drug Administration(FDA)as mentioned below:

  • Acute coronary syndrome: FDA approved eptifibatide for the medical management of unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI). In the PURSUIT trial, the eptifibatide showed favorable outcomes in reducing the composite end-point mortality and prevented nonfatal myocardial infarction in patients with non-ST elevation myocardial infarction and unstable angina.[1]
  • Percutaneous coronary intervention (PCI): FDA also approved eptifibatide for patients undergoing PCI, including intracoronary stenting. The IMPACT-II trial proved that eptifibatide use with heparin and aspirin reduces ischemic events following a percutaneous coronary intervention (PCI), especially in individuals with unstable angina.[2]

Non-FDA-labeled indications are:

  • Eptifibatide used to enhance myocardial perfusion in the ST-elevation myocardial infarction(STEMI) before PCI as supported by evidence by the "Time to Integrefilin Therapy in Acute Myocardial Infarction (TITAN)-TIMI 34 trial.[3]
  • Another possible use of eptifibatide is to enhance incidence and speed of reperfusion when used in large doses in combination with heparin, aspirin, tissue plasminogen activators in STEMI patients as evidenced by the small group the IMPACT-AMI trial. In the IMPACT-AMI trial, the use of eptifibatide showed complete reperfusion and an early ST-segment recovery on the electrocardiogram.[4]
  • Eptifibatide can be possibly used in combination of TPA in acute ischemic strokes to prevent progression to subacute intracerebral hemorrhage as supported by the "Combined Approach to Lysis Utilizing Eptifibatide and rt-PA in Acute Ischemic Stroke (CLEAR)" trial.[5]

Mechanism of Action

Rupture of atherosclerotic plaque or injury to vessel wall exposes the subendothelial matrix of the coronary blood vessel to circulating platelets. This event triggers a platelet signaling cascade that leads to the activation of the glycoprotein IIb/IIIa receptor (GpIIb/IIIa). The activation of Gp IIb/IIIa receptors leads to cross-linking of fibrinogen to attach multiple platelets to form a durable secondary platelet plug. The secondary platelet plug is essential for progression and stability of the clot. The glycoprotein IIb/IIIa receptor inhibitors, including abciximab, eptifibatide, sibrafiban, and tirofiban, which block the activation of Gp IIb/IIIa receptors, ultimately preventing clot formation/progression.[6] 

GP IIb/IIIa heterodimer contains a large extracellular region, a transmembrane domain, and a short intracellular cytoplasmic tail. The Gp IIb/IIIa receptor is a calcium and manganese-dependent heterodimer protein consisting of an alpha- and a beta-subunit. The alpha-subunit characterized by three or four divalent Ca- or Mn-binding domains that are crucial in the GP IIb/IIIa heterodimer. The beta-subunit comprises of disulfide bonds, binding sites including lysine-glycine-aspartic acid (KGD) bindings binding sites or arginine-glycine-aspartic acid (RGD) for attachment of fibrinogen, von Willebrand factor (vWF) and prothrombin. The binding sites of GP IIb/IIIa are hidden as latent and become active on the surface by undergoing a conformational change via inside-out signaling.[7]

The eptifibatide is a natural disintegrin from snake venom and have highly specific binding to the Gp IIb/IIIa receptor because of the structural resemblance of KGD (Lys-Gly-Asp) sequence. Eptifibatide binds to the KGD binding sites on Gp IIb/IIIa receptor and competitively fights against the binding of the receptor with fibrinogen, von Willebrand factor (vWF) and prothrombin. Higher plasma levels of eptifibatide are needed to competitively inhibit the target of over 80% block of KGD binding sites. Eptifibatide can competitively inhibit the KGD (Lys-Gly-Asp) sequence binding site in both active and inactive states. Eptifibatide has a half-life of 2 to 2.5 hrs and cleared by the kidney. The low affinity for direct binding with GP IIb/IIIa is responsible for rapid states. Furthermore, high doses of eptifibatide provide additional antithrombotic benefits by blocking vitronectin binding site, the ligand for alpha-beta in vascular cells, which may offer other antithrombotic benefits.[8][9][10][11]

Administration

Eptifibatide is intravenously administered and is available in strengths of 0.75 mg/ml and 2 mg/ml. The dose of eptifibatide is different in patients diagnosed with acute coronary syndrome (ACS) and in patients undergoing percutaneous coronary intervention (PCI). In patients with ACS, it is given immediately after the diagnosis at a loading dose of 180 mcg/kg IV followed by a continuous i.v. infusion of 2 mcg/kg/min. The infusion is continued up to 72 hours. Pre-PCI, eptifibatide is used as a loading dose of 180 mcg/kg IV followed by a continuous infusion of 2 mcg/kg/min with another 180 mcg/kg IV bolus (double bolus regimen) given 10 minutes after the first one. Status post-PCI eptifibatide infusion continued up to 18 hours.  Kidney clears eptifibatide; a maintenance dose is cut down to 50% in patients with serum creatinine greater than 2 mg/dL and keeping loading dose same as that of a normal kidney function. Contraindications to eptifibatide in patients with serum creatinine greater than 4 mg/dL or patients requiring hemodialysis.[12] 

In ACS, eptifibatide is a therapeutic option along with other medications, including alteplase, heparin, metoprolol, nitroglycerin, morphine, or furosemide. Eptifibatide is chemically incompatible with furosemide, and thus they should not be administered in the same intravenous line.[13][14]

Adverse Effects

The significant side effect of eptifibatide described in the PURSUIT trial was bleeding. In most cases, bleeding was mild and occurred at femoral access sites. There were more red cell transfusions required in the Eptifibatide group compared to placebo to counteract anemia.[1] However, there is increased bleeding following abciximab administration compared to eptifibatide or tirofiban because of rapid reversibility of latter agents.

Thrombocytopenia is another side effect of eptifibatide reported in several case reports.[15][16] Thrombocytopenia infrequently occurs with Gp IIb/IIIa inhibitors but sometimes may be profound. The risk of thrombocytopenia associated with eptifibatide (0.1 to 0.2%) and tirofiban (0.1 to 0.3%) is lesser compared to abciximab (0.4 to 1.1%). Tirofiban induced thrombocytopenia (secondary to eptifibatide) occurs because of the naturally occurring drug-dependent antibodies specific for eptifibatide occupied Gp IIb/IIIa receptor site. It is also clinically relevant to distinguish eptifibatide-induced thrombocytopenia from other etiologies. Pseudothrombocytopenia can be seen using complete blood cell analysis when blood samples are collected in EDTA- containing tubes. The absence of platelet clumping on peripheral smear rules out pseudo-thrombocytopenia. Amongst the Gp IIb/IIIa inhibitors, only abciximab has been reported to have an association with pseudo-thrombocytopenia.[17] Heparin and eptifibatide are administered simultaneously during PCI and in treatment of ACS. In comparison to heparin-induced thrombocytopenia (HIT), eptifibatide usually causes a steep decline in platelet count (less than 30000 cells/ uL). HIT-1 occurs within one and five days, whereas HIT-2 occurs within 4 to 20 days following heparin administration.[18] Thus thrombocytopenia developing within the first day or severe thrombocytopenia favor thrombocytopenia secondary to eptifibatide. Also, the detection of platelet factor-4 (PF-4) assay in HIT can help differentiate it from eptifibatide-induced thrombocytopenia. Eptifibatide can inhibit to new platelets in both active and inactive state. Thrombocytopenia due to eptifibatide responds better after discontinuation of medication, and addition of platelet bag is not helpful if the patient has a high concentration of eptifibatide in plasma. Other side effects reported include hypotension, heart failure, arrhythmias (ventricular fibrillation, atrial fibrillation), hypersensitivity reactions, gastrointestinal, genitourinary or pulmonary alveolar hemorrhage.[15]

Contraindications

The contraindications to using eptifibatide mentioned below[19]:

  • Thrombocytopenia: eptifibatide is contraindicated in patients with a platelet count of less than 100000/microliter
  • Renal failure: eptifibatide is contraindicated in patients with serum creatinine higher than 4 mg/dL or patients requiring hemodialysis because of its renal elimination. In such patients, abciximab is an alternative
  • Hypersensitivity to eptifibatide
  • Severe, uncontrolled hypertension
  • History of bleeding diathesis within 30 days
  • Major surgery or trauma within the prior 6 weeks
  • Active internal bleeding or recent significant gastrointestinal or genitourinary bleed within the past 6 months
  • History of stroke within 30 days or hemorrhagic stroke at any time
  • Intracranial neoplasm, arteriovenous malformations, aneurysms or aortic dissection
  • Use of another parenteral glycoprotein IIb/IIIa inhibitor

Eptifibatide is a pregnancy category B drug. It should only be used cautiously in lactating mothers. Also, the drug is not recommended for use in the pediatric population.

Monitoring

Monitor complete blood count (CBC), serum creatinine, and PT/aPTT. In patients undergoing PCI, measure activated clotting time (ACT).[19]

  • CBC: look for thrombocytopenia and anemia due to bleeding. It is strongly recommended to measure platelet count within 2 to 6 hours of administering eptifibatide to detect thrombocytopenia if any.
  • Serum creatinine: Since eptifibatide gets cleared renally, it is essential to monitor renal function tests.
  • PT/aPTT: to monitor the risk of bleeding
  • ACT: eptifibatide is known to have an additive effect on activated clotting time (ACT) when used together with heparin. Therefore, aPTT and ACT should be monitored closely when administering these agents concurrently.

Toxicity

Bleeding at intravenous sites is the most common adverse effect. Simultaneous use of NSAIDs or other antiplatelet drugs and renal insufficiency would increase the risk of bleeding.

There is no specific antidote for eptifibatide toxicity. Eptifibatide should be discontinued when platelet counts are under 50000 cells/microliter, and a platelet transfusion ordered when platelet counts are less than 20000 cells/microliter, or there is significant bleeding.[15]

Enhancing Healthcare Team Outcomes

Eptifibatide is useful in the treatment of acute coronary syndrome (ACS) and following percutaneous coronary intervention (PCI). Healthcare workers, including nurses, pharmacists, and clinicians, should be aware that bleeding and thrombocytopenia are major complications following eptifibatide administration, and they should work together as a team to identify these complications. Nursing should be first in line for monitoring for adverse events, especially bleeding, and pharmacists should conduct thorough medication reconciliation and verify dosing since medication errors in either of these areas can lead either to therapeutic failure or severe bleeding. Any concerns in these areas require immediate communication to the physician in charge as well as the rest of the team involved in care. Only through this type of interprofessional collaboration can patients achieve optimal therapeutic outcomes with eptifibatide. [Level V]

Also, since heparin is used in conjunction with eptifibatide in the treatment of ACS and during PCI, it is imperative to learn how to differentiate heparin-induced thrombocytopenia from eptifibatide-induced thrombocytopenia.


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Eptifibatide - Questions

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A 57-year old male presents to the emergency department with a 2-hour history of substernal chest pain and diaphoresis. His past medical history is significant for diabetes mellitus diagnosed 20 years ago and is on metformin. He also has a 20 pack-year smoking history. He was diagnosed with chronic kidney disease 5 years ago. His baseline serum creatinine is 2.5 mg/dl. In the emergency department, his ECG shows ST-segment depression. Cardiac markers return positive. His physical examination reveals bilateral pedal edema. His blood pressure is 147/79 mm Hg, pulse is 82/min, and oxygen saturation is 98% on room air. In the emergency department, he is given sublingual nitroglycerin, aspirin, clopidogrel, metoprolol. The treating physician discusses with the patient and family members and plans for percutaneous coronary intervention. Eptifibatide is planned to be given following percutanous coronary intervention. What is the correct method and dose of administration?



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A 56-year-old male comes to the emergency department with a 2-hour history of chest pain. He was watching television when he had substernal chest pain followed by profuse diaphoresis. He has a 20 pack-year smoking history. His mother had a history of a heart attack. His blood pressure is 138/82 mmHg, pulse is 82/min, and oxygen saturation is 97% on room air. ECG is performed, and it shows ST segment depression. Cardiac enzymes return negative. The patient is started on medications for his condition. Which of the following describes the mechanism of action of eptifibatide in the above described condition?



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A 49-year-old male with a past medical history significant for diabetes mellitus and hypertension presents to the emergency department with a 2-hour history of chest pain and profuse diaphoresis. He has a 20 pack-year smoking history. His blood pressure is 140/80 mm Hg, pulse is 83/min, and oxygen saturation is 98% on room air. In the emergency department, his ECG shows ST-segment depression and cardiac markers return positive. He is started on medications for his condition. However, 8 hours after his admission, his complete blood count (CBC) reveals a platelet count of 18000 cells/microliter with no significant bleeding. Which of the following medications is responsible for his thrombocytopenia, and what is the appropriate course of management?



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A 65-year-old female presents to the emergency department with a 3-hour history of chest pain radiating to the left arm, nausea, and diaphoresis. An EKG is performed, which shows ST-segment depression. Troponins and CK-MB are elevated in the first blood draw. Her blood pressure is 140/90 mm Hg, pulse is 86/min, and oxygen saturation is 96% on room air. She is given sublingual nitroglycerin, aspirin, metoprolol, and clopidogrel. Her past medical history is notable for acute cholecystitis for which she underwent surgery one month back and a history of chronic kidney disease with a baseline creatinine 2.7 mg/dL. She recalls having upper gastrointestinal bleeding one year ago, which she believes could have been because of her excess ibuprofen use secondary to her back pain. Which of the following conditions in the patient's history would limit the use of eptifibatide?



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A 66-year old male presents to the emergency department with a 2-hour history of substernal chest pain radiating to the jaw and both the arms. He also has had dyspnea at rest for 1 month which has worsened over the past week. The dyspnea is worse with exertion and on lying down. He is a known diabetic for 20 years and has a 30 pack-year smoking history. In the emergency department, an ECG is obtained, which showed ST-segment depression, and cardiac markers returned positive. On physical examination, there is bilateral pedal edema and raised jugular venous pressure. His cardiovascular examination is significant for an S3 heart sound, but there are no murmurs. On chest auscultation, rales are present bilaterally. His blood pressure is 148/82 mm Hg, pulse is 82/min, and oxygen saturation is 87% on room air. In the emergency department, he receives morphine, aspirin, sublingual nitroglycerin, furosemide, metoprolol, and heparin. The treating provider decides to add on eptifibatide. Which of the following medications cannot be given in the same intravenous line as eptifibatide?



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A 23-year-old female presents to the emergency department with multiple episodes of epistaxis. The patient denies any history of nose pricking or taking any medication or illicit drugs. Past medical history is significant for menorrhagia of unknown cause. Family history is significant for frequent epistaxis in maternal aunt. Vitals include blood pressure of 80/40 mmHg, heart rate of 110/min, and oxygen saturation is 98% on ambient air. Laboratory findings are remarkable for hemoglobin of 10 mg/dL with low MCV, high red cell distribution width. Coagulation studies show prolonged bleeding time, prolonged platelet function analyzer test, normal platelet count, normal PT, normal aPTT, normal ristocetin cofactor assay, and normal von-Willebrand factor and clotting factor levels. Genetic testing, and flow cytometry analysis is sent for diagnosis of hereditary bleeding disorders. In the emergency department, she hemodynamically stabilized by giving 2-liter normal saline and by putting rhino rocket to stop the epistaxis. Which of the following diseases has platelet receptor deficiency similar to the site of action of eptifibatide?



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Eptifibatide - References

References

Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention: IMPACT-II. Integrilin to Minimise Platelet Aggregation and Coronary Thrombosis-II. Lancet (London, England). 1997 May 17;     [PubMed]
Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes. The New England journal of medicine. 1998 Aug 13;     [PubMed]
Lefkovits J,Plow EF,Topol EJ, Platelet glycoprotein IIb/IIIa receptors in cardiovascular medicine. The New England journal of medicine. 1995 Jun 8;     [PubMed]
Sane DC,Damaraju LV,Topol EJ,Cabot CF,Mascelli MA,Harrington RA,Simoons ML,Califf RM, Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy. Journal of the American College of Cardiology. 2000 Jul;     [PubMed]
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Ohman EM,Kleiman NS,Gacioch G,Worley SJ,Navetta FI,Talley JD,Anderson HV,Ellis SG,Cohen MD,Spriggs D,Miller M,Kereiakes D,Yakubov S,Kitt MM,Sigmon KN,Califf RM,Krucoff MW,Topol EJ, Combined accelerated tissue-plasminogen activator and platelet glycoprotein IIb/IIIa integrin receptor blockade with Integrilin in acute myocardial infarction. Results of a randomized, placebo-controlled, dose-ranging trial. IMPACT-AMI Investigators. Circulation. 1997 Feb 18     [PubMed]
Adeoye O,Sucharew H,Khoury J,Vagal A,Schmit PA,Ewing I,Levine SR,Demel S,Eckerle B,Katz B,Kleindorfer D,Stettler B,Woo D,Khatri P,Broderick JP,Pancioli AM, Combined Approach to Lysis Utilizing Eptifibatide and Recombinant Tissue-Type Plasminogen Activator in Acute Ischemic Stroke-Full Dose Regimen Stroke Trial. Stroke. 2015 Sep     [PubMed]
Schrör K,Weber AA, Comparative pharmacology of GP IIb/IIIa antagonists. Journal of thrombosis and thrombolysis. 2003 Apr     [PubMed]
Coller BS, Blockade of platelet GPIIb/IIIa receptors as an antithrombotic strategy. Circulation. 1995 Nov 1     [PubMed]
Chong PH, Glycoprotein IIb/IIIa receptor antagonists in the management of cardiovascular diseases. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 1998 Nov 15     [PubMed]
Madan M,Berkowitz SD,Tcheng JE, Glycoprotein IIb/IIIa integrin blockade. Circulation. 1998 Dec 8     [PubMed]
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Schneider DJ, Anti-platelet therapy: glycoprotein IIb-IIIa antagonists. British journal of clinical pharmacology. 2011 Oct     [PubMed]

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