Platelet activation and aggregation has been shown to be heightened in the setting of acute coronary syndromes and to be an independent predictor of adverse events. Blocking platelet aggregation with medicai therapy (aspirin. clopidogrel, glycoprotein (GP)lIb/llla antagonists) has been demonstrated to be of unequivocal benefit. GPllb/llla is a plateletspecific adhesion receptor that mediates the formation of platelet aggregates. Tirofiban is a srnoll, synthetic. nonpeptide. competitive GPllb/llla antagonist with high specificity and affinity for the GPllb/llia receptor. The Platelet Receptor Inhibition for ischemic Syndrome Management (PRISM)and Platelet Receptor Inhibition for ischemic Syndrome Management in Patients limited by Unstable signs and Symptoms (PRISM-PLUS)studies found that tirofiban, administered in the upstream setting - based on an infusion of a 30-min bolus - reduced the incidence of major adverse cardiovascular events in patients with non-STsegment elevation acute coronary syndromes. compared with heparin alone. Accordlnqtv, the use of tirofiban in this setting has become a class I indication in the USand European guidelines. A 3-min bolus was also developed to allow the use of tirofiban directly in the catheterization laboratory. However. the do Tirofiban And ReoPro™ Give Similar Efficacy Trial (TARGET)study has demonstrated clinica I inferiority of tirofiban versus abciximab due to suboptimal platelet inhibition soon after administration of 10 ).lg/kg bolus. To achieve an inhibition of platelet aggregation of more than 90% in the first hour after treatment. a new bolus of tirofiban was identified (10-25 ).lg/kg). The first case-control and randomized studies based on this new regimen have shown that this dosage was safe and effective in reducing the incidence 01 adverse events in patients treated with percutaneous coronary intervention. Several Phase Il and 111studies are ongoing to extend these preliminary lindings.
Tirofiban: a critical reappraisal of the clinical use, recent developpements and future perspectives.
CAMPO, Gianluca Calogero;FERRARI, Roberto
2006
Abstract
Platelet activation and aggregation has been shown to be heightened in the setting of acute coronary syndromes and to be an independent predictor of adverse events. Blocking platelet aggregation with medicai therapy (aspirin. clopidogrel, glycoprotein (GP)lIb/llla antagonists) has been demonstrated to be of unequivocal benefit. GPllb/llla is a plateletspecific adhesion receptor that mediates the formation of platelet aggregates. Tirofiban is a srnoll, synthetic. nonpeptide. competitive GPllb/llla antagonist with high specificity and affinity for the GPllb/llia receptor. The Platelet Receptor Inhibition for ischemic Syndrome Management (PRISM)and Platelet Receptor Inhibition for ischemic Syndrome Management in Patients limited by Unstable signs and Symptoms (PRISM-PLUS)studies found that tirofiban, administered in the upstream setting - based on an infusion of a 30-min bolus - reduced the incidence of major adverse cardiovascular events in patients with non-STsegment elevation acute coronary syndromes. compared with heparin alone. Accordlnqtv, the use of tirofiban in this setting has become a class I indication in the USand European guidelines. A 3-min bolus was also developed to allow the use of tirofiban directly in the catheterization laboratory. However. the do Tirofiban And ReoPro™ Give Similar Efficacy Trial (TARGET)study has demonstrated clinica I inferiority of tirofiban versus abciximab due to suboptimal platelet inhibition soon after administration of 10 ).lg/kg bolus. To achieve an inhibition of platelet aggregation of more than 90% in the first hour after treatment. a new bolus of tirofiban was identified (10-25 ).lg/kg). The first case-control and randomized studies based on this new regimen have shown that this dosage was safe and effective in reducing the incidence 01 adverse events in patients treated with percutaneous coronary intervention. Several Phase Il and 111studies are ongoing to extend these preliminary lindings.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
