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Effects of glycoprotein IIb/IIIa receptor blocker (tirofiban) in acute coronary syndromes angiographic, scintigraphic and molecular biology studies


Platelet activation and aggregation are central mechanisms in the pathogenesis of coronary thrombus formation in acute coronary syndromes ACS. One final obligatory step for platelet aggregation is binding to GP IIb/IIIa receptor. In this study an attempt has been made to assess the effects of the glycoprotein IIb/IIIa receptors antagonist (tirofiban) on angiographic patency, scintigraphic perfusion and GP IIb/IIIa receptors activity in ACS.


A total of 20 pts comprising 11 M and 9 F (mean age 43.8 ± 14.3 years) were included in this study. Sixteen pts had unstable angina and 4 pts had non Q MI. All pts were randomly assigned in a blind manner to receive either heparin and aspirin only (Gp1) or heparin and aspirin combined with tirofiban (Gp2) (in a dose of 0.4 μg/kg/min for 30 min then 0.1 μg/kg/min for 48 hours). Following clinical evaluation, all pts were subjected to acute perfusion imaging both on admission as well as prior to discharge — by injecting 10 mCi Tc-sesta MIBI I.V. — with coronary angiography within 1 week following admission. Four blood samples were collected from all pts to measure Gp II ± b/IIIa receptor activity: On admission, after 30 min, 48 hours and before discharge respectively.


Compared to Gp1, Gp2 exhibited significantly greater decline in GP IIb/IIIa receptor activity (91.4% vs 71.8%, P < 0.002 for IIb & 87.1% vs 65.2%, P < 0.002 for IIIa in the second sample and 88.6% vs 60.7%, P < 0.0007 for IIb & 84.4% vs 54%, P < 0.001 for IIIa in the 3rd sample). Subsequent return to baseline values were significantly higher in both groups compared to control group (89.6%, 89.3% vs 74.3, P < 0.001 for IIb & 86.6%, 84.8% vs 68.4%, P < 0.0006 for IIIa). This dramatic effect on platelet function was not paralleled by coronary angiographic patency (TIMI flow ≥ 2 is 70% in both groups, P > 0.05) but was expressed in significantly better myocardial perfusion as evidenced by regression of myocardium at risk from a mean of 20.3 ± 5.7% to a mean of 8.1 ± 4.9% in Gp2 vs a mean of 20.4 ± 8.59% to a mean of 14.4 ± 7.05% in Gp1, P < 0.03 and improved perfusion scoring from a mean of 12.3 ± 3.5 to a mean of 4.6 ± 3 in Gp2 vs a mean of 12.4+5.1 to a mean of 8.7 ± 4.2 in Gp1, P < 0.03 with salvage index exceeding 30% in 80% of pts in Gp2 vs 50% in Gp1, P < 0.05.


In acute coronary syndromes, the use of platelet glycoprotein IIb/IIIa blocker tirofiban could effectively reduce GP IIb/IIIa receptor activity, enhance myocardial perfusion, improve salvage of myocardium, reduce residual ischemia and improve short term outcome.


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Rizk, A., El-Fattah, A., Tayeh, O. et al. Effects of glycoprotein IIb/IIIa receptor blocker (tirofiban) in acute coronary syndromes angiographic, scintigraphic and molecular biology studies. Crit Care 5, P162 (2001).

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  • Aspirin
  • Heparin
  • Acute Coronary Syndrome
  • Myocardial Perfusion
  • Receptor Activity