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European Heart Journal 1995 16(Supplement L):36-42; doi:10.1093/eurheartj/16.suppl_L.36
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Scociety of Cardiology

Antiplatelet therapy in therapy-resistant unstable angina

A pilot study with REO PRO (c7E3)

M. J. B. M. van den Brand*,, M. L. Simoons*, M. J. De Boer{dagger}, A. van Miltenburg*, L. R. van der Wieken{ddagger}, P. J. De Feyter* and The European Cooperative Study Group

* Thoraxcenter, Erasmus University and University Hospital Dijkzigt Rotterdam NL
{dagger} Department of Cardiology, de Weezenlanden Ziekenhuis, Zwolle NL
{ddagger} Department of Cardiology, Onze Lieve Vrouwen Gasthuis, Amsterdam NL

Correspondence: M.van den Brand, Thoraxcenter, Erasmus University and University Hospital Dijkzigt, P.O. Box 1738, 3000 DR Rotterdam, NL

Patients with unstable angina, refractory to intensive medical therapy, are at high risk of developing thrombotic complications, such as myocardial infarction and coronary occlusion during coronary angioplasty. As platelet aggregation and thrombus formation play an important role in this ongoing ischaemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) has been designed to modify the clinical course and underlying coronary lesion morphology.

To evaluate whether c7E3 could influence the incidence of complications, we randomized 60 patients to c7E3 or placebo after initial angiography had demonstrated a culprit lesion amenable for angioplasty. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite intensive medical therapy. After study drug bolus and infusion, angiography was repeated and angioplasty performed.

Recurrent ischaemia during study drug infusion occurred in nine and 16 patients from the c7E3 and placebo groups, respectively (P=0.06). Major events defined as death, myocardial infarction or urgent intervention occurred in one and seven patients respectively (P=0.03). One patient from the placebo group died as a result of recurrent infarction. Resolution of clots was only observed in the c7E3 group, combined with improvement in TIMI flow grade in 20% of patients. Quantitative angiography showed an improvement in percentage diameter stenosis in the c7E3 group, which was not observed in the placebo group, although the difference between the two treatment groups was not significant. No excess bleeding was observed in the treatment group. Thus, c7E3 bolus and infusion, combined with heparin and aspirin improved the clinical course, the coronary lesion morphology and rheology in patients with unstable angina, refractory to medical treatment.

Key Words: Unstable angina • platelet aggregation inhibition • quantitative coronary angiography • monoclonal antibodies


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