Increased concentrations of tirofiban in blood and their correlation with inhibition of platelet aggregation after greater bolus doses of tirofiban

Schneider, David J.; Herrmann, Howard C.; Lakkis, Nasser; Aguirre, Frank V.; Lo, Man Wai; Yin, Kuo Chang; Aggarwal, Atul; Kabbani, Samer; DiBattiste, Peter M.

doi:10.1016/s0002-9149(02)03163-6

Cited by 68 publications

(47 citation statements)

References 11 publications

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“…Schneider et al [7,13] found that the extent of platelet aggregation inhibition 15-60 min after GP IIb/IIIa administration was greater with the use of abciximab than with the TARGET study dose of tirofiban (10 g/kg bolus followed by an infusion of 0.15 g/kg/min), and this subtherapeutic inhibition of GP IIb/IIIa binding activity was held responsible for the reduced efficacy of tirofiban.…”

Section: Discussionmentioning

confidence: 99%

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Safety of a high bolus dose of tirofiban in patients undergoing coronary stent placement

Danzi

Capuano

Sesana

et al. 2004

Cathet Cardio Intervent

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To overcome the suboptimal platelet inhibition induced by tirofiban in the first hour after a percutaneous coronary intervention, a new regimen of 25 microg/kg bolus followed by an 18-hr infusion of 0.15 microg/kg/min has been proposed. The aim of this study was to compare the effects of this high bolus dose of tirofiban with those of abciximab on bleeding risk and 30-day clinical outcome in patients undergoing coronary stenting. We compared two cohorts of patients who underwent coronary stent placement between January 2000 and December 2002. In the first cohort, the only available IIb/IIIa receptor inhibitor was abciximab, which was given to 280 (34.9%) out of 802 stented patients; in the second cohort, tirofiban was administered to 274 (38.3%) out of 716 treated patients. The primary endpoints were the proportion of patients with major bleeding and the rate of site access complications; the 30-day incidence of major adverse cardiac events (MACE) was also assessed. After the procedure, the patients were given ticlopidine for 4 weeks and aspirin indefinitely. Major bleeding episodes were observed in four patients receiving abciximab and in none receiving tirofiban (1.4% vs. 0%; P = 0.12); the rates of site access complications were similar (3.6% vs. 3.3%; P = 0.96). The 30-day incidence of MACE was 7.1% in the abciximab group and 5.8% in the tirofiban group (P = 0.65). In patients undergoing coronary stenting, the high bolus dose of tirofiban is safe and not associated with an increased risk of major bleeding or site access complications in comparison with abciximab.

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Section: Discussionmentioning

confidence: 99%

“…With the use of flow cytometry, it has been recently demonstrated that a higher tirofiban bolus dose of 25 g/kg can increase average platelet inhibition to 92-95% during the first hour of treatment [7,13]; the utility and the risks of this dosage were compared with those obtained by using abciximab in this study of stented patients.…”

Section: Discussionmentioning

confidence: 99%

Safety of a high bolus dose of tirofiban in patients undergoing coronary stent placement

Danzi

Capuano

Sesana

et al. 2004

Cathet Cardio Intervent

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“…Patients with ACS may have a decreased response to antiplatelet agents, 21 and tirofiban may be less effective than abciximab within 60 min after administration. 22 Recently, Schneider et al 23 have identified a tirofiban bolus of 25 mg/kg (followed by a maintenance infusion of 0.15 mg/kg per min) that achieves inhibition of platelet aggregation .85% for 60 min. However, the role of this regimen in high-risk patients with NSTE-ACS remains to be established.…”

Section: How To Mitigate Post-pci Myocardial Damagementioning

confidence: 99%

Myocardial damage during percutaneous interventions for non-ST-elevation acute coronary syndromes

Bolognese

Falsini

Liïstro

et al. 2005

European Heart Journal Supplements

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The prognostic significance and pathophysiological mechanisms underlying elevations in cardiac enzymes in patients with non-ST-segment elevation acute coronary syndromes (ACS) post-percutaneous coronary intervention (PCI) is a matter of debate. The few available data, derived mainly from sub-analyses of large randomized trials and from small prospective observational studies, suggest that patients with ACS who undergo PCI have an increased risk for procedural myocardial damage which, in turn, is associated with an adverse clinical outcome. Although the pathophysiology of post-PCI myocardial damage is multifactorial, the embolization of debris or calcified plaque material, or exposure of thrombogenic material at intravascular sites seems to play a key role, as shown by mechanistic studies that demonstrate a close relationship between post-procedural enzyme release and abnormal tissue perfusion. Several pre-procedural treatment strategies using antithrombotic therapies have evolved in an attempt to lower the rate of myocardial damage related to the performance of PCI in ACS patients. Major trials that evaluated the use of glycoprotein (GP) IIb/IIIa inhibitors during PCI in patients with ACS have suggested that maximum benefit is obtained in patients with increased troponin levels and in patients undergoing PCI, reducing the incidence of cardiac enzyme release after the procedure. However, a number of lingering unsolved issues concerning which agent should be used and the most appropriate timing and dosage remain to be explored. Mechanistic and clinical findings suggest that an early invasive strategy with upstream GP IIb/IIIa inhibitors may yield more favourable outcomes than downstream strategies.

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“…We assessed platelet function with the use of flow cytometry in response to diverse agonists. We have used this assay previously to assess effects of antiplatelet agents [10] and the influence of platelet function on the risk of subsequent cardiac events after coronary intervention [11].…”

mentioning

confidence: 99%

Lack of early augmentation of platelet reactivity after coronary intervention in patients treated with bivalirudin

Schneider

Sobel

2008

J Thromb Thrombolysis

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To determine whether a regimen of aspirin pretreatment, bivalirudin during the procedure and clopidogrel (600 mg) immediately after percutaneous coronary intervention (PCI) was associated with platelet activation during and shortly after (1 and 2 h) PCI, we characterized platelet function in 10 patients with the use of flow cytometry in the absence of agonist and in response to thrombin (10 nM), ADP (1 microM), the collagen-mimetic convulxin (5 ng/ml), and platelet activating factor (10 nM). Activation of platelets in peripheral blood was rare (<0.5% of platelets) before, during and after PCI. Platelet reactivity in response to each of the agonists was lower after the PCI compared with that in blood taken before the PCI. Accordingly, platelet activation and platelet reactivity were not increased after elective PCI when patients were treated during the procedure with aspirin and bivalirudin and immediately after the procedure with a 600 mg loading dose of clopidogrel.

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Increased concentrations of tirofiban in blood and their correlation with inhibition of platelet aggregation after greater bolus doses of tirofiban

Cited by 68 publications

References 11 publications

Safety of a high bolus dose of tirofiban in patients undergoing coronary stent placement

Safety of a high bolus dose of tirofiban in patients undergoing coronary stent placement

Myocardial damage during percutaneous interventions for non-ST-elevation acute coronary syndromes

Lack of early augmentation of platelet reactivity after coronary intervention in patients treated with bivalirudin

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