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Tirofiban. A review of its use in acute coronary syndromes
1Adis International Limited, Auckland, New Zealand. demail@adis.co.nz
Insights
Tirofiban, an antiplatelet medication, effectively lowers the risk of ischemic events in patients with acute coronary syndromes when combined with aspirin and heparin. It demonstrates an acceptable safety profile, making it a valuable addition to treatment regimens.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Tirofiban is an intravenous glycoprotein IIb/IIIa receptor antagonist.
- It inhibits platelet aggregation and prolongs bleeding times in acute coronary syndromes.
- Its short half-life allows for rapid recovery of platelet function.
Purpose of the Study:
- To evaluate the efficacy and safety of tirofiban in patients with acute coronary syndromes.
- To assess tirofiban's role in reducing ischaemic complications in unstable angina/non-Q-wave myocardial infarction (MI) and during percutaneous revascularisation.
Main Methods:
- Analysis of data from large clinical trials, including PRISM-PLUS and RESTORE.
- Intravenous administration of tirofiban with standard heparin and aspirin regimens.
- Comparison of outcomes between tirofiban-treated groups and control groups receiving heparin alone.
Main Results:
- Tirofiban significantly reduced the 7-day risk of MI, death, and refractory ischaemia by 32% in PRISM-PLUS.
- In RESTORE, tirofiban reduced ischaemic complications by 38% on day 2 and 27% on day 7 during percutaneous revascularisation.
- Bleeding complications were the most common adverse events, but major bleeding rates were similar to heparin alone.
Conclusions:
- Tirofiban, as an adjunct to heparin and aspirin, reduces ischaemic complications in acute coronary syndromes and high-risk revascularisation patients.
- The drug exhibits an acceptable tolerability profile.
- Intravenous tirofiban is a recommended treatment for specific patient groups with acute coronary syndromes.
Unlabelled:
Tirofiban is an intravenously administered nonpeptide glycoprotein IIb/IIIa receptor antagonist which specifically inhibits fibrinogen-dependent platelet aggregation and prolongs bleeding times in patients with acute coronary syndromes. Adenosine diphosphate (ADP)-induced platelet aggregation returns to near-baseline levels within 4 to 8 hours after cessation of a tirofiban infusion, a finding consistent with the drug's elimination half-life of approximately 2 hours. Three large clinical trials have shown that, when administered with a standard heparin and aspirin regimen, tirofiban reduces the risk of ischaemic complications in patients with unstable angina/non-Q-wave myocardial infarction (MI) and in patients undergoing percutaneous revascularisation. In PRISM-PLUS, a study involving 1915 patients with unstable angina/non-Q-wave MI, administration of intravenous tirofiban (0.4 microgram/kg/min loading dose for 30 minutes followed by a 0.10 microgram/kg/min infusion) with heparin for at least 48 (mean 71.3) hours reduced the 7-day risk of the composite end-point of MI, death and refractory ischaemia by 32% compared with heparin alone. The between-group risk reduction remained significant at 30 days (22%) and 6 months (19%). Similarly, in high-risk patients undergoing coronary angioplasty in RESTORE, the addition of tirofiban (10 micrograms/kg bolus in the 3 minutes prior to intervention followed by 0.15 microgram/kg/min for 36 hours) to a standard heparin regimen significantly reduced the risk of ischaemic complications by 38% on day 2 and 27% on day 7 compared with heparin alone. Although interim analysis in PRISM-PLUS showed that the use of tirofiban without heparin increased the 7-day risk of death compared with heparin alone, this finding was inconsistent with the effects of tirofiban on the risk of death in PRISM, a study involving 3232 patients with unstable angina/non-Q-wave MI. Tirofiban is generally well tolerated. Bleeding complications were the most commonly reported events associated with tirofiban in clinical trials, but the rate of major bleeding in tirofiban recipients was not significantly different from that reported with heparin. Thrombocytopenia (platelet count < 90,000 cells/microliter) occurred slightly more frequently with tirofiban (with or without heparin) than with heparin alone.
Conclusions:
Tirofiban reduces the risk of ischaemic complications in patients with unstable angina/non-Q-wave MI and high-risk patients undergoing revascularisation when used against a background of heparin and aspirin. Furthermore, the drug has an acceptable tolerability profile. Therefore, intravenous tirofiban is likely to be used as an adjunct to heparin and aspirin in patients with acute coronary syndromes including high-risk patients undergoing revascularisation.