Comparison of Two Platelet Glycoprotein IIb/IIIa Inhibitors, Tirofiban and Abciximab, for the Prevention of Ischemic Events with Percutaneous Coronary Revascularization

Topol, Eric J.; Moliterno, David J.; Herrmann, Howard C.; Powers, Eric R.; Grines, Cindy L.; Cohen, David J.; Cohen, Éric A.; Bertrand, M; Neumann, Franz‐Josef; Stone, Gregg W.; DiBattiste, Peter M.; Demopoulos, Laura A.; Tirofiban, Target Investigators. Do; Trial, ReoPro Give Similar Efficacy

doi:10.1056/nejm200106213442502

Cited by 630 publications

(372 citation statements)

References 26 publications

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“…indicated for use at the time of PCI as it has been demonstrated to be inferior to the benchmark therapy of abciximab [25]. As predicted by Schneider et al [32] from in vitro studies of highdose tirofiban dosing, the current study has demonstrated a consistently high level of platelet inhibition.…”

Section: Discussion Effect Of Hd-tirofibansupporting

confidence: 63%

“…UFH heparin was administered as a bolus of 70 U kg )1 [23] prior to PCI and additional heparin was given to maintain the activated clotting time (ACT) at 250 s. Enoxaparin was administered at a dose of 0AE75 mg kg )1 [24]. Tirofiban was administered once the wire had crossed the lesion during PCI with a bolus dose of 25 lg kg )1 of bodyweight, followed by an infusion of 0AE15 lg per kilogram per min for 18-24 h [12,25].…”

Section: Pci Proceduresmentioning

confidence: 99%

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High‐dose tirofiban with enoxaparin and inflammatory markers in high‐risk percutaneous intervention

Walters¹,

Ray²,

Wood³

et al. 2010

Eur J Clin Investigation

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Aim The study assessed the benefit of high bolus dose tirofiban (HD-tirofiban) with enoxaparin compared with HD-tirofiban with unfractionated heparin (UFH). The study examined markers of platelet activation, thrombin generation and inflammation. Materials and methodsThe study is a prospective single centre open-label trial of patients with high-risk acute coronary syndrome treated with percutaneous intervention (PCI) who were randomized to anticoagulation with UFH or enoxaparin with HD-tirofiban (25 lg kg )1 bolus). This study measured a panel of platelet activation markers, inflammatory biomarkers and thrombus generation between the two groups.Result Sixty patients undergoing high-risk PCI were enroled in the study. Platelet inhibition as assessed by whole blood aggregometry following HD-tirofiban infusion was similar in both the UFH and enoxaparin groups. CD40 ligand expression on platelets was significantly reduced following PCI with HD-tirofiban and either UFH or enoxaparin. Following PCI, there were significant reductions measured in other markers of platelet activation including PAC-1, P selectin, factor V ⁄ Va, platelet-monocyte aggregates and monocyte expression of Mac-1 as determined by analysis of venous blood samples using flow cytometry. Prothrombin fragment 1+2, D-dimer, von Willebrand factor and high sensitive C-reactive protein levels were significantly less post PCI in the enoxaparin group compared with those patients receiving UFH. ConclusionThe combination of HD tirofiban with enoxaparin resulted in an attenuated inflammatory response when compared with that of the combination of HD tirofiban with UFH.

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Section: Discussion Effect Of Hd-tirofibansupporting

confidence: 63%

Section: Pci Proceduresmentioning

confidence: 99%

High‐dose tirofiban with enoxaparin and inflammatory markers in high‐risk percutaneous intervention

Walters¹,

Ray²,

Wood³

et al. 2010

Eur J Clin Investigation

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“…18,19 In brief, patients of any age undergoing PCI were considered for enrollment if all lesions were amenable to stent implantation. Principle exclusion criteria included acute MI, cardiogenic shock or decompensated heart failure, renal insufficiency, thrombocytopenia, and bleeding diathesis.…”

Section: Methodsmentioning

confidence: 99%

“…Compared with tirofiban, abciximab was found to result in greater protection from periprocedural myonecrosis at 30 days. 18 Notably, a significant interaction effect was present between GP IIb/IIIa inhibitor assignment and presenting clinical syndrome. 18 The purpose of the present report is to explore the potential impact of clinical syndrome acuity on the differential response to abciximab versus tirofiban in patients undergoing coronary stent implantation.…”

mentioning

confidence: 94%

Impact of clinical syndrome acuity on the differential response to 2 glycoprotein IIb/IIIa inhibitors in patients undergoing coronary stenting. The TARGET trial

Stone¹,

Moliterno²,

Bertrand³

2002

ACC Current Journal Review

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Background-Although glycoprotein IIb/IIIa inhibitors have been shown to reduce periprocedural and late ischemic events in patients undergoing stent implantation, the relative safety and efficacy of different agents in this class is less established. Also unknown is whether the acuity of the presenting clinical syndrome, which may affect the degree of platelet inhibition required or achieved, influences the response to different antiplatelet agents. Methods and Results-A prospective, multicenter, double-blind, randomized trial was performed in which 4809 patients undergoing planned stenting were randomized to receive abciximab or tirofiban. In patients with acute coronary syndromes (ACS; nϭ3025), abciximab resulted in lower rates of myocardial infarction at 30 days (5.8% versus 8.5%; Pϭ0.004) and 6 months (7.2% versus 9.8%; Pϭ0.013), although 6-month mortality rates were identical (1.39% in both groups; Pϭ0.99). Conversely, in patients without ACS (nϭ1784), myocardial infarction rates were not significantly lower with tirofiban, survival was similar, and target vessel revascularization was reduced, which translated into a trend toward enhanced 6-month event-free survival with tirofiban (89.7% versus 86.6%; Pϭ0.056). Conclusions-In patients with ACS undergoing stent implantation, abciximab use compared with tirofiban results in greater suppression of periprocedural myonecrosis, although a survival benefit has not been demonstrated. Patients with stable coronary syndromes may have equivalent or better outcomes with tirofiban relative to abciximab, with fewer adverse hematologic and hemorrhagic events. These data raise important issues regarding the relative pharmacodynamic inhibition of platelet function required in varying clinical scenarios and have important implications for the cost-effective utilization of glycoprotein IIb/IIIa inhibitors.

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“…Intravenous antagonists of the GPIIb/IIIa integrin have significant clinical benefits in patients with acute coronary syndromes undergoing percutaneous coronary intervention (Bhatt and Topol, 2000;Topol et al, 2001). However, subtherapeutic doses of GPIIb/IIIa antagonists especially orally active compounds have been shown to have deleterious outcomes on patients Quinn et al, 2002).…”

Section: Gpiib/iiia Integrin Blockers: a Cautionary Notementioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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Comparison of Two Platelet Glycoprotein IIb/IIIa Inhibitors, Tirofiban and Abciximab, for the Prevention of Ischemic Events with Percutaneous Coronary Revascularization

Abstract: Although the trial was intended to assess the noninferiority of tirofiban as compared with abciximab, the findings demonstrated that tirofiban offered less protection from major ischemic events than did abciximab.

Cited by 630 publications

References 26 publications

High‐dose tirofiban with enoxaparin and inflammatory markers in high‐risk percutaneous intervention

High‐dose tirofiban with enoxaparin and inflammatory markers in high‐risk percutaneous intervention

Impact of clinical syndrome acuity on the differential response to 2 glycoprotein IIb/IIIa inhibitors in patients undergoing coronary stenting. The TARGET trial

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

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