Back To Search Results


Editor: Radia T. Jamil Updated: 2/28/2024 4:07:21 AM


FDA-Approved Indications

Eptifibatide is an antiplatelet drug that reversibly binds and inhibits platelets' glycoprotein IIb/IIIa receptors. A protein found in the venom of the pygmy rattlesnake is used to make eptifibatide. The PURSUIT and IMPACT-II clinical trials account for the indications of eptifibatide by the Food and Drug Administration (FDA) 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, eptifibatide showed favorable outcomes in reducing the composite end-point mortality and preventing nonfatal myocardial infarction (MI) in patients with NSTEMI 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 PCI, especially in individuals with unstable angina.[2]

Non-FDA-Labeled Indications

Eptifibatide is used to enhance myocardial perfusion in the ST-elevation myocardial infarction (STEMI) before PCI, as supported by the Time to Integrefilin Therapy in Acute Myocardial Infarction (TITAN)-TIMI 34 trial.[3] Another possible use of eptifibatide is to enhance the incidence and speed of reperfusion when used in large doses in combination with heparin, aspirin, and tissue plasminogen activators in STEMI patients, as evidenced by the small group in the IMPACT-AMI trial. In the IMPACT-AMI trial, using eptifibatide showed complete reperfusion and an early ST-segment recovery on the electrocardiogram.[4] Eptifibatide can be used in combination with 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] A recent meta-analysis demonstrated eptifibatide's potential safety and efficacy as a bridging strategy for patients undergoing surgery following coronary stent implantation. Additional randomized controlled trials are warranted to strengthen the scientific evidence and validate these findings.[6]

Mechanism of Action

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Mechanism of Action

The rupture of atherosclerotic plaque or injury to the vessel wall exposes the subendothelial matrix of the coronary blood vessel to circulating platelets. This event triggers a platelet signaling cascade that activates the glycoprotein IIb/IIIa receptor (Gp IIb/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 the progression and stability of the clot. The glycoprotein IIb/IIIa receptor inhibitors, including abciximab, eptifibatide, sibrafiban, and tirofiban, block the activation of Gp IIb/IIIa receptors, preventing clot formation/progression.[7][8]

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 with an α- and a β-subunit. The α-subunit is characterized by 3 or 4 divalent Ca- or Mn-binding domains crucial in the Gp IIb/IIIa heterodimer. The β-subunit comprises 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 latent and become active on the surface by undergoing a conformational change via inside-out signaling.[9]

The eptifibatide is a natural disintegrin from snake venom. The drug exhibits particular binding to the Gp IIb/IIIa receptor because of the structural resemblance of the KGD (Lys-Gly-Asp) sequence. Eptifibatide binds to the KGD binding sites on Gp IIb/IIIa receptor and competitively fights against the receptor's binding 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 active and inactive states. 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 the vitronectin binding site, the ligand for alpha-beta in vascular cells, which may offer other benefits.[10] Glanzmann thrombasthenia is an autosomal recessive disease with platelet receptor deficiency similar to the site of action of eptifibatide.


Absorption: Intravenous (IV) administration of therapeutic peptides avoids pre-systemic metabolism, resulting in total systemic availability. Eptifibatide has linear pharmacokinetics, proportional to the bolus drug for doses ranging from 90 to 250 mcg/kg with an infusion rate from 0.5 to 3 mcg/kg/min. Therefore, administering a 180-mcg/kg bolus dose combined with an infusion produces an early peak, followed by a slight decline before attaining a steady state (within 4 to 6 hours). Clinicians can prevent this by administering a second 180-mcg/kg bolus dose 10 minutes after the first dose.

Distribution: The onset of action is rapid (inhibition of platelet aggregation 15 min after bolus 84%). Platelet function returns to normal levels approximately 4 to 8 hours following discontinuation.[11] The plasma elimination half-life is 2.5 hours. The plasma protein binding is about 25%.

Metabolism: Eptifibatide is not known to be metabolized by cytochrome P450 but is deaminated by metabolic enzymes. The short half-life is due to the cleavage of eptifibatide by the proteases and peptidases.[12]

Elimination: In healthy patients, renal clearance is approximately 50% of total body clearances because most of the drug is excreted in the urine as eptifibatide, deaminated eptifibatide, and other, more polar metabolites.


Available Dosage Forms and Strengths

In patients diagnosed with acute coronary syndrome undergoing PCI and presenting with a substantial thrombus load, administering an IV Gp IIb/IIIa inhibitor, such as eptifibatide, is recommended. Eptifibatide is administered IV and is available in strengths of 0.75 and 2 mg/ml. The dose of eptifibatide differs in patients diagnosed with ACS and patients undergoing PCI.

In patients with ACS, eptifibatide is given after diagnosis at a loading dose of 180 mcg/kg IV, followed by a continuous IV infusion of 2 mcg/kg/min. The infusion continues for up to 72 hours. Pre-PCI, eptifibatide is given 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. According to the 2021 guidelines by ACC, AHA, and SCAI (American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography & Interventions), eptifibatide infusion is continued for up to 18 hours.[13]

Eptifibatide injection is a sterile solution in 10-mL single-dose vials containing 20 mg of eptifibatide and 100-mL single-dose vials containing 75 mg of eptifibatide. Eptifibatide vials should be refrigerated at 2 °C to 8 °C (36 °F to 46 °F). Upon transfer, the hospital pharmacist must mark the vial with a "DISCARD BY" time (Two months from the transfer date or the expiration date, whichever comes first). In addition, eptifibatide should be protected from light until administration.

In ACS, eptifibatide is a therapeutic option, and other medications include alteplase, heparin, metoprolol, nitroglycerin, morphine, or furosemide. However, eptifibatide is chemically incompatible with furosemide; it should not be administered in the same IV line. Eptifibatide may be injected in the same IV line with 0.9% NaCl or 0.9% NaCl/5% dextrose.[14]

Specific Patient Populations

Patients with renal impairment: Total drug clearance is reduced by almost 50%, and the steady-state plasma eptifibatide concentrations are doubled in patients with an estimated CrCl of less than 50 mL/min. Consequently, clinicians should reduce the infusion dose to 1 mcg/kg/min in such patients and keep the loading dose similar to that of a normal kidney function. Eptifibatide is contraindicated in patients with serum creatinine greater than 4 mg/dL or requiring hemodialysis.[15] 

Patients with hepatic impairment: Information regarding hepatic impairment is not provided in the manufacturer's labeling (no clinical studies have been conducted on patients with hepatic impairment).

Pregnancy considerations: Published literature and the pharmacovigilance database are insufficient to establish an eptifibatide associated with significant congenital disability or adverse maternal or fetal outcomes. No adverse developmental effects are apparent in animal reproduction studies when eptifibatide was administered IV to pregnant rats and rabbits at approximately 4 times the recommended maximum daily human dose. However, if left untreated, MI is a medical emergency that can be fatal to the pregnant woman and fetus. Hence, the clinician should not withhold therapy for the pregnant woman because of potential concerns regarding the effects of eptifibatide on the fetus.

Breastfeeding considerations: No published information is available on using eptifibatide during breastfeeding. Eptifibatide is a small cyclic peptide; absorption by the infant is unlikely because it is likely destroyed in the infant's gastrointestinal tract.[16]

Older patients: Adjust the dosage of eptifibatide based on renal function.

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. More red cell transfusions were required to counteract anemia in the eptifibatide group than in the placebo group.[1] However, increased bleeding is typical following abciximab administration compared to eptifibatide or tirofiban because of the rapid reversibility of these latter 2 agents.

Thrombocytopenia is another side effect of eptifibatide reported in several case reports.[17][18] 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 the naturally occurring drug-dependent antibodies specific for eptifibatide occupy Gp IIb/IIIa receptor site. This is also clinically relevant to distinguish eptifibatide-induced thrombocytopenia from other etiologies.

Pseudothrombocytopenia is detectable 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. Among the Gp IIb/IIIa inhibitors, only abciximab has reportedly shown an association with pseudo-thrombocytopenia.[19]  Heparin and eptifibatide are administered simultaneously during PCI and ACS treatment. Compared to heparin-induced thrombocytopenia (HIT), eptifibatide usually causes a steep decline in platelet count (less than 30000 cells/uL). HIT-1 occurs within 1 and 5 days, whereas HIT-2 occurs within 4 to 20 days following heparin administration.[20] Thus, thrombocytopenia develops within the first day, or severe thrombocytopenia favors thrombocytopenia secondary to eptifibatide. Also, detecting platelet factor-4 (PF-4) assay in HIT can help differentiate it from eptifibatide-induced thrombocytopenia.

Eptifibatide can inhibit new platelets in both active and inactive states. Thrombocytopenia due to eptifibatide responds better after discontinuation of the medication. Adding a 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, and gastrointestinal, genitourinary, or pulmonary alveolar hemorrhage.[17]

Drug-Drug Interactions

Caution is necessary due to the potential interactions when administering eptifibatide with drugs inhibiting platelet aggregation. These drugs include clopidogrel, ticlopidine, thrombolytics, oral anticoagulants, adenosine, NSAIDs, dipyridamole, and dextran solution. Therefore, regular monitoring and appropriate dose adjustment may be required to optimize treatment and minimize the risk of bleeding.[12]


Warnings and Precautions

Several contraindications to using eptifibatide include the following[21]:

  • Thrombocytopenia: in patients with a platelet count of less than 100,000/μL
  • Renal failure: in patients with serum creatinine higher than 4 mg/dL or requiring hemodialysis because of its renal elimination, 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 bleeding 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. However, therapy for acute coronary syndrome should not be delayed due to maternal risk-benefit considerations. Clinicians should only use the drug cautiously in lactating mothers. Also, the drug is not recommended for use in the pediatric population.
  • According to the 2021 guidelines by ACC/AHA/SCAI Guidelines for Coronary Artery Revascularization recommendations, in patients undergoing CABG, discontinuation of glycoprotein IIb/IIIa inhibitors such as eptifibatide for 4 hours before surgery is recommended to decrease the risk of bleeding and transfusion.[13]


Monitoring parameters include the following:

  • Monitor complete blood count (CBC), serum creatinine, and PT/aPTT. In patients undergoing PCI, measure activated clotting time (ACT).[21]
  • Attach cardiac monitoring to detect dynamic EKG changes.
  • Monitor for reperfusion arrhythmias during and after the percutaneous coronary intervention (PCI).[22]
  • Check the arterial line insertion site for evidence of bleeding manifestations.
  • Troponin I rises after 4 hours (peaks at 24 hr) and is elevated for 7 to 10 days, more specific than other protein markers.
  • CBC: look for thrombocytopenia and anemia due to bleeding. Measuring the platelet count within 2 to 6 hours of administering eptifibatide to detect thrombocytopenia is strongly recommended.
  • Serum creatinine: Since eptifibatide gets cleared renally, it is essential to monitor renal function tests.
  • PT/aPTT: to monitor the risk of bleeding
  • ACT: additive effect on activated clotting time (ACT) when used with heparin, aPTT, and ACT requires close monitoring when administering these agents concurrently.[23]


Limited knowledge of the overdosage of eptifibatide in literature is evident. In preclinical studies, eptifibatide was not lethal to experimental animals in a dosage of 2 to 5 times the recommended MRHD (maximum daily human dose). However, symptoms of acute toxicity were evident, such as loss of righting reflex, dyspnea, ptosis, decreased muscle tone in rabbits, and petechial hemorrhages in monkeys' femoral and abdominal areas. From in vitro studies, eptifibatide has limited protein binding; consequently, it may be removed from the plasma by dialysis (according to the manufacturer's labeling). 

Bleeding at IV sites is the most common adverse effect. Simultaneous use of NSAIDs or other antiplatelet drugs and renal insufficiency would increase the risk of bleeding. No specific antidote for eptifibatide toxicity exists. Clinicians should discontinue eptifibatide when platelet counts are under 50000 cells/µL. A platelet transfusion should be ordered when platelet counts are less than 20000 cells/µL or if significant bleeding occurs.[17] According to the American Association of Poison Control Center (National Poison Data System), rare case fatalities have been reported due to eptifibatide. Administer with caution due to the hazard of therapeutic error.[24][25]

Enhancing Healthcare Team Outcomes

Eptifibatide is useful in treating ACS and following PCI. The interprofessional healthcare team, including cardiologists and other specialists, mid-level practitioners, nurses, and pharmacists, should know that bleeding and thrombocytopenia are significant complications following the administration of eptifibatide. They should coordinate to identify these complications. Nurses should be first in line to monitor for adverse events, especially bleeding. Pharmacists should conduct thorough medication reconciliation and verify dosing since medication errors in either area can lead to therapeutic failure or severe bleeding. Any concerns in these areas require immediate communication with the team involved in care. A hematology consult should be obtained for severe thrombocytopenia.

Eptibitaide is a high-risk medication, according to the Institute for Safe Medication Practices. Also, since heparin is used in conjunction with eptifibatide in ACS treatment and during PCI, it is imperative to learn how to differentiate heparin-induced thrombocytopenia (HIT) from eptifibatide-induced thrombocytopenia. Consequently, interprofessional communication and coordination between ordering clinicians (MD, DO, NP, PA), specialists, pharmacists, and nurses can help patients achieve optimal therapeutic outcomes with eptifibatide. 



Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) Trial Investigators. Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes. The New England journal of medicine. 1998 Aug 13:339(7):436-43     [PubMed PMID: 9705684]

Level 1 (high-level) evidence


. 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 17:349(9063):1422-8     [PubMed PMID: 9164315]

Level 1 (high-level) evidence


Gibson CM, Kirtane AJ, Murphy SA, Rohrbeck S, Menon V, Lins J, Kazziha S, Rokos I, Shammas NW, Palabrica TM, Fish P, McCabe CH, Braunwald E, TIMI Study Group. Early initiation of eptifibatide in the emergency department before primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: results of the Time to Integrilin Therapy in Acute Myocardial Infarction (TITAN)-TIMI 34 trial. American heart journal. 2006 Oct:152(4):668-75     [PubMed PMID: 16996831]

Level 1 (high-level) evidence


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 18:95(4):846-54     [PubMed PMID: 9054741]

Level 1 (high-level) evidence


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:46(9):2529-33. doi: 10.1161/STROKEAHA.115.010260. Epub 2015 Aug 4     [PubMed PMID: 26243231]


Wu F,Ma K,Xiang R,Han B,Chang J,Zuo Z,Luo Y,Mao M, Efficacy and safety of a bridging strategy that uses intravenous platelet glycoprotein receptor inhibitors for patients undergoing surgery after coronary stent implantation: a meta-analysis. BMC cardiovascular disorders. 2022 Mar 24;     [PubMed PMID: 35331138]

Level 1 (high-level) evidence


Sangkuhl K, Shuldiner AR, Klein TE, Altman RB. Platelet aggregation pathway. Pharmacogenetics and genomics. 2011 Aug:21(8):516-21. doi: 10.1097/FPC.0b013e3283406323. Epub     [PubMed PMID: 20938371]


Scharf RE. Drugs that affect platelet function. Seminars in thrombosis and hemostasis. 2012 Nov:38(8):865-83. doi: 10.1055/s-0032-1328881. Epub 2012 Oct 30     [PubMed PMID: 23111864]


Schrör K, Weber AA. Comparative pharmacology of GP IIb/IIIa antagonists. Journal of thrombosis and thrombolysis. 2003 Apr:15(2):71-80     [PubMed PMID: 14618072]

Level 2 (mid-level) evidence


Leclerc JR. Platelet glycoprotein IIb/IIIa antagonists: lessons learned from clinical trials and future directions. Critical care medicine. 2002 May:30(5 Suppl):S332-40     [PubMed PMID: 12004256]

Level 3 (low-level) evidence


Tardiff BE, Jennings LK, Harrington RA, Gretler D, Potthoff RF, Vorchheimer DA, Eisenberg PR, Lincoff AM, Labinaz M, Joseph DM, McDougal MF, Kleiman NS, PERIGEE Investigators. Pharmacodynamics and pharmacokinetics of eptifibatide in patients with acute coronary syndromes: prospective analysis from PURSUIT. Circulation. 2001 Jul 24:104(4):399-405     [PubMed PMID: 11468200]

Level 1 (high-level) evidence


Tonin G, Klen J. Eptifibatide, an Older Therapeutic Peptide with New Indications: From Clinical Pharmacology to Everyday Clinical Practice. International journal of molecular sciences. 2023 Mar 13:24(6):. doi: 10.3390/ijms24065446. Epub 2023 Mar 13     [PubMed PMID: 36982519]


Writing Committee Members, Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM, Bischoff JM, Bittl JA, Cohen MG, DiMaio JM, Don CW, Fremes SE, Gaudino MF, Goldberger ZD, Grant MC, Jaswal JB, Kurlansky PA, Mehran R, Metkus TS Jr, Nnacheta LC, Rao SV, Sellke FW, Sharma G, Yong CM, Zwischenberger BA. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Journal of the American College of Cardiology. 2022 Jan 18:79(2):e21-e129. doi: 10.1016/j.jacc.2021.09.006. Epub 2021 Dec 9     [PubMed PMID: 34895950]

Level 1 (high-level) evidence


Oak MS, Rege NN. Eptifibatide: in the treatment of acute coronary syndromes. Journal of postgraduate medicine. 2000 Apr-Jun:46(2):155-6     [PubMed PMID: 11013490]


O'Shea JC, Hafley GE, Greenberg S, Hasselblad V, Lorenz TJ, Kitt MM, Strony J, Tcheng JE, ESPRIT Investigators (Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy trial). Platelet glycoprotein IIb/IIIa integrin blockade with eptifibatide in coronary stent intervention: the ESPRIT trial: a randomized controlled trial. JAMA. 2001 May 16:285(19):2468-73     [PubMed PMID: 11368699]

Level 1 (high-level) evidence


. Eptifibatide. Drugs and Lactation Database (LactMed®). 2006:():     [PubMed PMID: 31260228]


Hongo RH, Brent BN. Association of eptifibatide and acute profound thrombocytopenia. The American journal of cardiology. 2001 Aug 15:88(4):428-31     [PubMed PMID: 11545770]


Tempelhof MW, Benzuly KH, Fintel D, Krichavsky MZ. Eptifibatide-induced thrombocytopenia: with thrombosis and disseminated intravascular coagulation immediately after left main coronary artery percutaneous coronary angioplasty. Texas Heart Institute journal. 2012:39(1):86-91     [PubMed PMID: 22412237]

Level 3 (low-level) evidence


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:36(1):75-83     [PubMed PMID: 10898416]

Level 1 (high-level) evidence


Dager WE, Dougherty JA, Nguyen PH, Militello MA, Smythe MA. Heparin-induced thrombocytopenia: treatment options and special considerations. Pharmacotherapy. 2007 Apr:27(4):564-87     [PubMed PMID: 17381384]


Schneider DJ. Anti-platelet therapy: glycoprotein IIb-IIIa antagonists. British journal of clinical pharmacology. 2011 Oct:72(4):672-82. doi: 10.1111/j.1365-2125.2010.03879.x. Epub     [PubMed PMID: 21906121]


Taha HSED, Shaker MM. Percutaneous management of reperfusion arrhythmias during primary percutaneous coronary intervention: a case report. The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology. 2021 Mar 25:73(1):30. doi: 10.1186/s43044-021-00158-5. Epub 2021 Mar 25     [PubMed PMID: 33765245]

Level 3 (low-level) evidence


Dillinger JG, Ducrocq G, Elbez Y, Cohen M, Bode C, Pollack C Jr, Nicolau JC, Henry P, Kedev S, Wiviott SD, Sabatine MS, Mehta SR, Steg PG. Activated Clotting Time to Guide Heparin Dosing in Non-ST-Segment-Elevation Acute Coronary Syndrome Patients Undergoing Percutaneous Coronary Intervention and Treated With IIb/IIIa Inhibitors: Impact on Ischemic and Bleeding Outcomes: Insights From the TAO Trial. Circulation. Cardiovascular interventions. 2018 Jun:11(6):e006084. doi: 10.1161/CIRCINTERVENTIONS.118.006084. Epub     [PubMed PMID: 29895599]


Gummin DD, Mowry JB, Beuhler MC, Spyker DA, Brooks DE, Dibert KW, Rivers LJ, Pham NPT, Ryan ML. 2019 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 37th Annual Report. Clinical toxicology (Philadelphia, Pa.). 2020 Dec:58(12):1360-1541. doi: 10.1080/15563650.2020.1834219. Epub     [PubMed PMID: 33305966]


Lai MW, Klein-Schwartz W, Rodgers GC, Abrams JY, Haber DA, Bronstein AC, Wruk KM. 2005 Annual Report of the American Association of Poison Control Centers' national poisoning and exposure database. Clinical toxicology (Philadelphia, Pa.). 2006:44(6-7):803-932     [PubMed PMID: 17015284]