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      Effect of Hirulog-Like Peptide on Balloon Catheter Injury-Induced Neointimal Formation in Femoral Arteries of Minipigs and Relationship with Inflammatory Mediators

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          Abstract

          Vascular intervention-induced neointimal formation is a major drawback for managing atherosclerotic cardiovascular diseases using invasive vascular procedures. Our previous studies demonstrated that hirulog-like peptide (HLP) reduced balloon catheter dilation-induced neointimal formation or restenosis in carotid arteries of rats or atherosclerotic rabbits with less interruption in coagulation or bleeding than heparin or hirulog-1. The present study examined the effect of HLP on balloon catheter injury-induced neointimal formation in femoral arteries of minipigs. Intravenous infusion of HLP (1.6 mg/kg/h for 4 h started 0.5 h before the intervention) or unfractured heparin (50 U/kg/h for 4 h) significantly reduced neointimal formation in femoral arteries 4 weeks after intervention compared with the vehicle. Heparin, but not HLP, significantly prolonged activated partial thromboplastin time. HLP or heparin significantly reduced vascular intervention-induced increases in C-reactive protein, P-selectin and interleukin-6 in serum. HLP, but not heparin, normalized vascular injury-induced increase in P-selectin in platelets. The results of the present study suggest that HLP is an effective agent for preventing balloon catheter injury-induced neointimal formation in femoral arteries of minipigs. The beneficial effects of HLP on vascular injury-induced neointimal formation may partially result from its inhibition on inflammatory mediators.

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          A comparison of recombinant hirudin with heparin for the treatment of acute coronary syndromes. The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) IIb investigators.

          EJ Topol (1996)
          Thrombin has a pivotal role in the pathogenesis of acute coronary thrombosis. We compared the clinical efficacy of a potent, direct thrombin inhibitor, recombinant hirudin, with that of heparin (an indirect antithrombin agent) in patients with unstable angina or acute myocardial infarction. At 373 hospitals in 13 countries, 12,142 patients with acute coronary syndromes were randomly assigned to 72 hours of therapy with either intravenous heparin or hirudin. Patients were stratified according to the presence of ST-segment elevation on the base-line electrocardiogram (4131 patients) or its absence (8011 patients), with the latter characteristic considered to indicate unstable angina or non-Q-wave myocardial infarction. At 24 hours, the risk of death or myocardial infarction was significantly lower in the group assigned to hirudin therapy than in the group assigned to heparin (1.3 percent vs. 2.1 percent, P = 0.001). The primary end point of death or nonfatal myocardial infarction or reinfarction at 30 days was reached in 9.8 percent of the heparin group as compared with 8.9 percent of the hirudin group (odds ratio for the risk of the end point in hirudin group,0.89; 95 percent confidence interval, 0.79 to 1.00; P = 0.06). The predominant effect of hirudin was on myocardial infarction or reinfarction and was not influenced by ST-segment status. There were no significant differences in the incidence of serious or life-threatening bleeding complications, but hirudin therapy was associated with a higher incidence of moderate bleeding (8.8 percent vs. 7.7 percent, P = 0.03). For acute coronary syndromes, recombinant hirudin provided a small advantage, as compared with heparin, principally related to a reduction in the risk of nonfatal myocardial infarction. The relative therapeutic effect was more pronounced early (at 24 hours) but dissipated over time. The small benefit was consistent across the spectrum of acute coronary syndromes and was not associated with a greater risk of major bleeding complications.
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            Restenosis After Percutaneous Angioplasty: The Role of Vascular Inflammation

            Martin Schillinger, Erich Minar (2005)
            Restenosis after endovascular treatment of atherosclerotic lesions in the peripheral, cerebrovascular, and coronary circulation is the major drawback of this minimally invasive technique. Although certain advances have been made during recent years to improve patency rates after percutaneous angioplasty, restenosis remains a challenging clinical problem. Understanding factors that contribute to the pathophysiology of late lumen loss is an effective strategy to improving patients' postangioplasty outcome. Vascular inflammation after balloon angioplasty or stent implantation has been identified as a cornerstone of the restenotic process, and several markers of inflammation have been referred to as potential predictors of outcome. This article reviews recent findings on the issue of inflammation and restenosis after percutaneous angioplasty with special attention given to the role of inflammatory parameters as markers for the restenosis risk in the peripheral vessel area.
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              Inflammatory cytokines and cardiovascular disease.

              Takayuki Ito, Uichi Ikeda (2003)
              The designation of atherosclerosis as a chronic inflammatory process represents an interesting paradigmatic shift for cardiologists. The plasma concentrations of interleukin-6 and its hepatic byproduct, C-reactive protein, may reflect the intensity of occult plaque inflammation and the vulnerability to rupture. Monocyte chemoattractant protein-1 and interleukin-8 play a crucial role in initiating atherosclerosis by recruiting monocytes/macrophages to the vessel wall, which promotes atherosclerotic lesions and plaque vulnerability. In addition, circulating levels of these proinflammatory cytokines increase in patients with acute myocardial infarction and unstable angina, but not in those with stable angina. Also, the plasma concentrations of these cytokines increase after percutaneous coronary intervention, causing late restenosis after the procedure. Angiotensin II and other atherogenic factors induce these cytokines in the cardiovascular tissues through the activation of transcription factors, such as nuclear factor-kappaB or peroxisome proliferator-activated receptors. Conversely, HMG-CoA reductase inhibitors (statins) can potently inhibit these proinflammatory factors in the vessels. A small GTP-binding protein, Rho, may be a key molecule to explain the anti-inflammatory effects of statins. Interleukin-10 also exerts anti-inflammatory effects on the cardiovascular tissues, possibly by deactivating proinflammatory cytokines and inducible nitric oxide synthase. Gene therapy using interleukin-10 may be a promising means for untreatable or complicated cases of cardiovascular diseases. Thus, therapeutic modulations of these inflammatory cytokines may be useful in the prevention of atherosclerosis and future cardiovascular events.
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                Author and article information

                Journal
                Journal ID (publisher-id): JVR
                Journal ID (nlm-ta): J Vasc Res
                Journal ID (doi): 10.1159/issn.1018-1172
                Title: Journal of Vascular Research
                Publisher: S. Karger AG
                ISSN (Print): 1018-1172
                ISSN (Electronic): 1423-0135
                Publication date Subscription-year: 2010
                Publication date (Print): April 2010
                Publication date (Electronic): 11 November 2009
                Volume: 47
                Issue: 3
                Pages: 262-269
                Affiliations
                aShanghai Key Laboratory of Vascular Biology, bDepartment of Radiology, and cRuijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiaotong University School of Medicine, Shanghai, China; dDepartments of Internal Medicine and Physiology, University of Manitoba, Winnipeg, Man., Canada
                Article
                Publisher ID: 257340 Other ID: J Vasc Res 2010;47:262–269
                DOI: 10.1159/000257340
                PubMed ID: 19907188
                SO-VID: 30726142-0588-4e44-899e-c8469083912c
                Copyright © © 2009 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 08 November 2008
                Date accepted : 03 July 2009
                Page count
                Figures: 4, Tables: 1, References: 27, Pages: 8
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Neointimal formation,Coagulation,Balloon catheter injury,Hirulog-like peptide
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Neointimal formation, Coagulation, Balloon catheter injury, Hirulog-like peptide

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