ABSTRACT
Tirofiban is a nonpeptide GP IIb=IIIa antagonist that binds reversibly to IIb=IIIa receptors. Its efficacy has been evaluated in many clinical scenarios, including acute coronary syndromes with
and without ST elevation, PCl, and as treatment prior to early revascularization. In the PRISM-
Plus study, which enrolled patients with acute coronary syndromes without persistent ST-
segment elevation who were treated with intravenous heparin, those randomized to receive
tirofiban had a lower incidence of death or nonfatal myocardial infarction (MI) at 30 d than those
randomized to receive a placebo (8.7 vs. 11.9%, p ¼ 0.03). In the PRISM study, which also enrolled patients with non-ST-elevation acute coronary syndromes, the 30-day incidence of death
or MI was 5.8% in patients randomized to tirofiban, compared with 7.1% in those randomized to
heparin (p ¼ 0.12), but in patients who had elevated troponin T levels (0:1 mg=L) 6-8 h after presentation, the comparative rates were 13.7 and 3.5%, respectively (p < 0.01). In the
RESTORE trial in high-risk patients who underwent angioplasty, tirofiban reduced the combined
30-day incidence of death, MI, or urgent revascularization from 10.5 to 8.0% (p ¼ 0.052). In the TACTICS-TIMI-18 trial, 4-48 h of tirofiban treatment followed by early revascular-
ization was compared with an early conservative strategy in patients with non-ST-elevation acute
coronary syndromes and reduced the 6-month incidence of death, MI, or severe angina requiring
hospitalisation from 26.3 to 16.4% (p ¼ 0.006) in patients with 0.5mm of ST-segment depression and from 24.2 to 14.3% (p < 0.001) in patients with elevated troponin levels.
