The Egyptian Heart Journal (Sep 2014)

Platelet aggregation inhibition by Eptifibatide versus high dose Tirofiban during primary percutaneous interventions

  • Yasser Sadek Nassar,
  • Mohamed Laimud,
  • Mohamed Afify,
  • Mohamed Ashraf Shawky

DOI
https://doi.org/10.1016/j.ehj.2013.04.002
Journal volume & issue
Vol. 66, no. 3
pp. 241 – 250

Abstract

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Background: Platelet aggregation occurs as a central role in acute coronary syndrome (ACS), and glycoprotein GP IIb/IIIa inhibitors may enhance the benefits expected from early recanalisation. Aim: To compare the degree of platelet aggregation inhibition achieved by Eptifibatide versus high dose Tirofiban, and its clinical effects regarding myocardial reperfusion parameters: myocardial blush grade (MBG) and ST-segment resolution (STR) >70%, and regarding peri procedural complications, bleeding and major adverse cardiac events (MACE). Methods: Between the period of June 2010–January 2012, 46 patients with acute myocardial infarction whose symptom onset is within 12 h of presentation and ECG showing ST-segment elevation 1 mm in two contiguous limb leads or 2 mm in two contiguous precordial leads or acute left bundle branch block were included. Exclusion criteria were active bleeding, thrombocytopenia, bleeding diathesis, anticoagulation or thrombolitics, recent major surgery or stroke, cardiogenic shock, and pregnancy. Patients were randomized alternatively (1:1) into two groups before primary percutaneous cardiac intervention (PCI) to receive the specific glycoprotin IIb/IIIa inhibitor as follows: (I) Tirofiban group: intravenous high bolus dose of 25 mcg/kg over 3 min followed by maintenance infusion of 0.15 mcg/kg/min. (II) Eptifibatide group: intravenous two boluses 10 min apart (each one is 180 mcg/kg) followed by maintenance of 2 mcg/kg/min. Platelet aggregation inhibition was measured by light transmission aggregometer, angiographic assessment was done before and after final interventions for TIMI flow and myocardial blush grade before and after the procedure. Electrocardiographic assessment standard 12-lead ECG on admission, immediately after PCI. Resolution of ST segment elevation was expressed as a percentage of the initial ST segment elevation. Resolution of ⩾70% was defined as complete resolution. Clinical safety assessment was done in terms of the incidence of: bleeding complications and major adverse cardiac events (MACE): death, non-fatal myocardial infarction (MI), and target vessel revascularization (TVR). Results: The total patients in our study included 46 patients, 40 males (87%) and six females (13%) with a mean age of 55 ± 10, Tirofiban group: included 23 patients, 19 males (82.5%) and four females (17.4%) with a mean age of 57 ± 9.65. Eptifibatide group: included 23 patients, 21 males (87%) and two females (8.7%) with a mean age of 53.48 ± 8.6. Platelet aggregation inhibition during PCI was significantly correlated with STR (p 0.013, r 0.71). The cut-off point for platelet aggregation inhibition as a predictor of STR >70% was 89.5% (sensitivity 92.3%, specificity 69.2%, PPV 75% and NPV 10%, AUC 0.87). Platelet aggregation inhibition during PCI was positively correlated with MBG (p 0.045, r 0.453). The cut-off point for platelet aggregation inhibition as a predictor of MBG 2–3 was 87.5% (sensitivity 73.6%, specificity 66.7%, PPV 93.9% and NPV 76.9%, AUC 0.81). Platelet aggregation inhibition 60 min after bolus was (93.57 ± 2.07% versus 87.62 ± 3.2%, p 70% (56.22% versus 39.13%, p 0.005) in Eptifibatide versus Tirofiban group, respectively. There was no significant statistical difference regarding thrombocytopenia (46.73 ± 41.48 versus 39.04 ± 34.41, p 0.37), minor bleeding (17.4% versus 21.7%, p 0.5), major bleeding (0% versus 4.3%, p 0.5), post procedural infarction (0% versus 17.4%, p 0.12), TVR (0% versus 8.7%, p 0.24), MACE and 30 days mortality (4.3% versus 13%, p 0.34) in Eptifibatide versus Tirofiban group, respectively. Conclusions: • Platelet aggregation inhibition during PCI was significantly correlated with STR and MBG. Platelet aggregation inhibition cut-off point as a predictor of STR >70% was 89.5%, and as a predictor of MBG 2–3 was 87.5%. • Eptifibatide achieves better platelet aggregation inhibition 60 min after bolus and 6 h after PCI than high dose Tirofiban. • Eptifibatide is associated with better myocardial perfusion as indicated by post procedural mean MBG and STR >70% than high dose Tirofiban. • There was no significant differences between Eptifibatide and high dose Tirofiban regarding thrombocytopenia, major or minor bleeding, MACE and 30 days mortality.

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