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Undergoing Elective Angioplasty in Patients with Stable Coronary Artery

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Undergoing Elective Angioplasty in Patients with Stable Coronary Artery Downloaded from heart.bmjjournals.com on 17 October 2006 Pharmacodynamics and safety of lefradafiban, an oral platelet glycoprotein IIb/IIIa receptor antagonist, in patients with stable coronary artery disease undergoing elective angioplasty K M Akkerhuis, M J B M van den Brand, C van der Zwaan, H O J Peels, H Suryapranata, L R van der Wieken, J Stibbe, J Hoffmann, T Baardman, J W Deckers and M L Simoons Heart 2001;85;444-450 doi:10.1136/heart.85.4.444 Updated information and services can be found at: http://heart.bmjjournals.com/cgi/content/full/85/4/444 These include: References This article cites 27 articles, 17 of which can be accessed free at: http://heart.bmjjournals.com/cgi/content/full/85/4/444#BIBL 1 online articles that cite this article can be accessed at: http://heart.bmjjournals.com/cgi/content/full/85/4/444#otherarticles Rapid responses You can respond to this article at: http://heart.bmjjournals.com/cgi/eletter-submit/85/4/444 Email alerting Receive free email alerts when new articles cite this article - sign up in the box at the service top right corner of the article Topic collections Articles on similar topics can be found in the following collections Drugs: cardiovascular system (857 articles) Ischemic heart disease (2078 articles) Notes To order reprints of this article go to: http://www.bmjjournals.com/cgi/reprintform To subscribe to Heart go to: http://www.bmjjournals.com/subscriptions/ Downloaded from heart.bmjjournals.com on 17 October 2006 444 Heart 2001;85:444–450 Pharmacodynamics and safety of lefradafiban, an oral platelet glycoprotein IIb/IIIa receptor antagonist, in patients with stable coronary artery disease undergoing elective angioplasty K M Akkerhuis, MJBMvandenBrand, C van der Zwaan, HOJPeels, H Suryapranata, L R van der Wieken, J Stibbe, J HoVmann, T Baardman, J W Deckers, M L Simoons Abstract Objective—Lefradafiban is the orally active prodrug of fradafiban, a glycoprotein IIb/IIIa receptor antagonist. The present phase II study aimed to determine the dose of lefradafiban that provides 80% blockade of the glycoprotein IIb/IIIa receptors by fradafiban, and to study the pharmacodynamics and safety of diVerent doses in patients with stable angina undergoing angioplasty. Design—A double blind, placebo controlled, dose finding study. Setting—Four academic and community hospitals in the Netherlands. Patients—64 patients with stable coronary artery disease undergoing elective percutaneous Thoraxcenter, transluminal coronary angioplasty. Erasmus University and University Interventions—30 mg, 45 mg, and 60 mg of lefradafiban three times daily or placebo was given Hospital Rotterdam, for 48 hours. Netherlands Main outcome measures—The primary safety end point was the occurrence of bleeding, clas- K M Akkerhuis sified as major, minor, or insignificant according to the thrombolysis in myocardial infarction MJBMvandenBrand (TIMI) criteria. EYcacy indices included per cent fibrinogen receptor occupancy (FRO), ex vivo C van der Zwaan platelet aggregation, and plasma concentrations of fradafiban. M L Simoons Results—Administration of lefradafiban 30, 45, and 60 mg three times daily resulted in a dose Department of dependent increase in median FRO levels of 71%, 85%, and 88%, respectively. Inhibition of Cardiology, University platelet aggregation was closely related to FRO. There were no major bleeding events. The 60 mg Hospital Groningen, lefradafiban group had a high (71%) incidence of minor and insignificant bleeding. The Netherlands incidence of bleeding was 44% in the 30 mg and 45 mg groups, compared with 9% in placebo HOJPeels patients. Puncture site bleeding was the most common event. The odds of bleeding increased by Department of 3% for every 1% increase in FRO. Cardiology, Hospital Conclusions—Lefradafiban is an eVective oral glycoprotein IIb/IIIa receptor blocker. The clini- De Weezenlanden, cal eVectiveness of doses up to 45 mg three times daily should be investigated. Zwolle, Netherlands (Heart 2001;85:444–450) H Suryapranata Keywords: platelet aggregation inhibitors; glycoprotein IIb/IIIa blockers; lefradafiban; angioplasty Department of Cardiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, Platelet adhesion, activation, and aggregation ischaemia in patients with unstable angina or Netherlands are pivotal events in the process leading to cor- non-ST-segment elevation myocardial L R van der Wieken onary thrombosis in patients with unstable infarction.11–13 coronary artery disease.1 This process is also The clinical use of monoclonal antibodies Department of activated during percutaneous transluminal Haematology, and small molecules as GP IIb/IIIa receptor University Hospital coronary angioplasty (PTCA) by local vascular blockers is limited to the treatment of acute Rotterdam, injury, which exposes circulating platelets to episodes of unstable angina, or treatment dur- Netherlands various prothrombotic stimuli within the sub- ing coronary procedures, as oral administration 23 J Stibbe endothelium. The final common pathway to is not feasible. Lefradafiban (Boehringer Ingel- coronary thrombus formation involves aggre- Boehringer Ingelheim, heim, Germany) is an orally active prodrug Germany gation of platelets through cross linkage of their which is metabolised in two steps to fradafiban, JHoVmann glycoprotein (GP) IIb/IIIa receptors by the an intravenously active, non-peptide GP IIb/ primary binding ligand fibrinogen.4 T Baardman IIIa receptor inhibitor.14 In studies with healthy Several inhibitors of the GP IIb/IIIa receptor volunteers, both fradafiban and lefradafiban Cardialysis BV, have been developed. The monoclonal anti- led to a reversible and dose dependent Clinical Research body c7E3 (abciximab) has been shown to Management and Core 14 reduce the incidence of death and myocardial inhibition of platelet aggregation. Laboratories, Our aim in this first phase II study was to Rotterdam infarction in patients undergoing PTCA, with J W Deckers or without stent deployment.5–8 Small mol- determine the dose regimen of lefradafiban ecules (eptifibatide, tirofiban) given intrave- that provides 80% blockade of the platelet GP Correspondence to: nously also reduce complications associated IIb/IIIa receptors by fradafiban, as well as to Dr Akkerhuis, Cardialysis BV, PO Box 2125, 3000 CC with PTCA, although their eVects were of bor- study the pharmacodynamics and safety of dif- Rotterdam, The Netherlands derline significance.910 These intravenous GP ferent doses in patients with stable coronary [email protected] IIb/IIIa receptor blockers have also recently artery disease undergoing elective PTCA, in Accepted 12 September been shown to reduce the incidence of death, order to select the appropriate range of dose 2000 recurrent myocardial infarction, and recurrent regimens for subsequent larger studies. www.heartjnl.com Downloaded from heart.bmjjournals.com on 17 October 2006 Oral platelet glycoprotein IIb/IIIa receptor antagonist 445 Methods CONCOMITANT TREATMENT STUDY POPULATION Before the start of the PTCA, all patients Patients aged between 18 and 80 years with received an intravenous bolus of heparin of stable coronary artery disease were eligible for 5000 IU, as well as an intravenous bolus of enrolment if they were scheduled for elective 250 mg aspirin. During the procedure, heparin PTCA. Patients were excluded if they suVered was repeated in boluses of 5000 IU after 30, 60 from unstable angina or if there was a total and, if necessary, 120 minutes. Aspirin was occlusion of the vessel to be treated. Other cri- continued in a dose of 100 mg daily. The use of teria for exclusion included myocardial infarc- ticlopidine together with lefradafiban was tion within the preceding 14 days; planned excluded by the protocol because no interac- stent implantation; major surgery or trauma tion data were available at that time. Therefore, within the preceding six weeks; any history of if stenting was performed, the study drug was discontinued and ticlopidine (250 mg once or cerebrovascular haemorrhage or haemorrhagic twice a day) was initiated. Other drugs were diathesis, cardiopulmonary resuscitation, or continued as before randomisation and ad- complicated puncture of a major vein or artery justed as required by the clinical status of the within the preceding six weeks; retinopathy patient. grade 3 or greater; gastrointestinal or genito- urinary bleeding within the preceding six CLINICAL AND LABORATORY MONITORING weeks; peptic ulcer disease; platelet count A coronary angiogram was performed immedi- 9 < 100 × 10 /l; uncontrolled hypertension ately before and after PTCA. Coronary flow (systolic blood pressure > 200 mm Hg and/or was classified according to the thrombolysis in diastolic blood pressure > 100 mm Hg); cur- myocardial infarction (TIMI) study classifi- rent treatment with oral anticoagulants or any cation by a central angiographic core labora- antiplatelet agent other than acetylsalicylic tory (Cardialysis BV).15 Sheaths were removed acid, including any non-steroidal anti- 4–6 hours after discontinuation of the heparin inflammatory agent; pregnant or nursing infusion and as close as possible to the next women or women not using medically ap- intake of study drug, assuming that the platelet proved means of contraception; known hepatic inhibitory activity of fradafiban would be at its or renal insuYciency; or any other concomitant nadir. Patients underwent daily clinical assess- serious illness which would limit life expect- ment for the occurrence of bleeding complica- ancy or interfere with the study end points. tions
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