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Stroke. 2003;34:2560-2567
Published online before print October 16, 2003, doi: 10.1161/01.STR.0000094425.06242.64
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(Stroke. 2003;34:2560.)
© 2003 American Heart Association, Inc.


Original Contributions

Abciximab Reduces Monocyte Tissue Factor in Carotid Angioplasty and Stenting

Christoph W. Kopp, MD; Sabine Steiner, MD; Christian Nasel, MD; Daniela Seidinger, MTA; Irene Mlekusch, MSc; Wilfried Lang, MD; Andrea Bartok, MD; Ramazanali Ahmadi, MD Erich Minar, MD

From the Second Department of Medicine, Division of Angiology (C.W.K., S.S., D.S., I.M., A.B., R.A., E.M.), Department of Radiology (C.N.), and Department of Neurology (W.L.), University of Vienna Medical School, Vienna, Austria.

Correspondence to Christoph W. Kopp, MD, Second Department of Medicine, Division of Angiology, University of Vienna Medical School, General Hospital, AKH, Waehringer Guertel 18-20, 1090 Vienna, Austria. E-mail christoph.kopp{at}univie.ac.at

Background and Purpose— Abciximab, a nonselective glycoprotein IIb/IIIa inhibitor, was shown to reduce peri-interventional stroke rate in carotid stenting. We evaluated the effect of adjunct abciximab therapy on monocyte-platelet cross talk and neurological deficit in unprotected carotid stenting and compared its efficacy with distal filter protection.

Methods— Fifty patients were randomized to either standard antithrombotic therapy (n=30) consisting of aspirin, clopidogrel, and heparin or adjunct bolus (0.25 mg/kg) and 12-hour infusion (0.125 µg · kg-1 · min-1) of abciximab (n=20). A third cohort of patients was stented with filter protection (n=30). Monocyte-platelet aggregate formation and monocyte tissue factor expression were determined by whole blood flow cytometry, and F1.2 generation and soluble CD40 ligand (sCD40L) were determined by immunoassay.

Results— The incidence of peri-interventional ischemic episodes (23% versus 10%; P=0.2) and the number of de novo ischemic lesions detected by diffusion-weighted MRI (47% versus 30%; P=0.17) were not significantly different between standard antithrombotic therapy and adjunct abciximab but were reduced with filter protection (P=0.023). However, the number of transient ischemic attacks was lower (P=0.05) and the National Institutes of Health Stroke Score rapidly decreased in patients with adjunct abciximab. This clinical improvement was paralleled by a reduction in the postinterventional percentage of activated monocyte-platelet aggregates (CD62P+/CD14+; P=0.018) and the number of tissue factor–positive monocytes (TF+/CD14+; P=0.005). Both abciximab and filter protection suppressed F1.2 generation and significantly reduced sCD40L.

Conclusions— Abciximab limits thrombus propagation and thrombus stabilization after carotid stenting by reducing monocyte-platelet cross talk and sCD40L. Although abciximab seems inferior to filter devices in peri-interventional cerebral protection, it may be considered in patients who do not allow placement of protection devices.


Key Words: antibodies, monoclonal • carotid stenosis • procoagulant • stents




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