Angioplasty Research Progress [1 ed.] 9781608767151, 9781604564228

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Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

ANGIOPLASTY RESEARCH PROGRESS

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

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Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

ANGIOPLASTY RESEARCH PROGRESS

KEVIN G. LAYTON AND

RAYMOND A. PERCELLE

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

EDITORS

Nova Biomedical Books New York

Copyright © 2009 by Nova Science Publishers, Inc. All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS.

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

Library of Congress Cataloging-in-Publication Data Angioplasty research progress / Kevin G. Layton and Raymond A. Percelle (editors). p. ; cm. Includes bibliographical references and index. ISBN 978-1-60876-715-1 (E-Book) 1. Angioplasty. 2. Cardiovascular system--Diseases--Treatment. I. Layton, Kevin G. II. Percelle, Raymond A. [DNLM: 1. Angioplasty--methods. 2. Cardiovascular Diseases--therapy. 3. Stents. WG 166.5.A3 A588 2008] RD598.35.A53A853 2008 617.4'13--dc22 2008004104

Published by Nova Science Publishers, Inc.  New York

Contents Preface

vii

Expert Commentary Regional Coronary Sampling and Angioplasty Research Mahmoud Ramadan

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Research and Review Articles

1 3 7

Chapter 1

Preclinical Testing of Percutaneous Cardiovascular Intervention Technologies: The Role, Development, and Evaluation of Animal Models Yoriyasu Suzuki and Fumiaki Ikeno

Chapter 2

Current Status of Carotid Artery Stenting Kamaldeep S. Heyer and Mark K. Eskandari

Chapter 3

Filter Assisted Carotid Artery Stenting: Is the Embolic Protection Improvable? Vlad-Adrian Alexandrescu, Christian Ngongang and Joseph Proumen

113

Chapter 4

Inflammatory Response to Percutaneous Coronary Intervention Mahmoud M. Ramadan and Makoto Kodama

149

Chapter 5

Coronary Pressure Measurement for the Decision Making of Percutaneous Coronary Intervention Kohichiro Iwasaki and Shozo Kusachi

303

Chapter 6

Percutaneous Coronary Intervention for Coronary Artery Stenosis Caused by Kawasaki Disease: Experience and Indications in Children Etsuko Tsuda

351

9

81

vi Chapter 7

Percutaneous Transluminal Coronary Angioplasty with DrugEluting Stent Implantation for Unprotected Left Main Coronary Disease: A Critical Appraisal and Meta-regression Imad Sheiban, Claudio Moretti, Dario Sillano and Giuseppe G.L. Biondi-Zoccai

365

Chapter 8

Self-Expandable Wire Stent Design Matthieu De Beule

387

Chapter 9

Advances in Antiplatelet Therapy to Prevent Stent Thrombosis A. Schäfer, J. Bauersachs and M. Eigenthaler

431

Chapter 10

A Comprehensive Analysis of the Risk of Thrombosis after Drug Eluting Stent Implantation Alexandre S. Quadros and Cristiano Cardoso

447

Chapter 11

Exercise versus PCI for Coronary Artery Disease: A Progenitor Cell Perspective Michel R. Hoenig and Frank W. Sellke

459

Chapter 12

Relevance of Antiplatelet Drug Resistance in the Contemporary Era of Percutaneous Coronary Interventions M. Singh, S. Singh, R. Walia, R. Arora and S. Khosla

473

Index

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Contents

493

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

Preface Angioplasty is the mechanical widening of a narrowed or totally obstructed blood vessel. These obstructions are often caused by atherosclerosis. The term angioplasty is a portmanteau of the words angio (from the Latin/Greek word meaning "vessel") and plasticos (Greek: "fit for moulding"). Angioplasty has come to include all manner of vascular interventions typically performed in a minimally invasive or percutaneous method. This new book presents recent advances in this fast moving field. As explained in the Expert Commentary, an important limitation of many clinical studies is the collection of blood samples for inflammatory response markers from peripheral veins. In particular, studies of the inflammatory response to PCI are hampered by the lack of specificity regarding the source of inflammatory markers, as the measurement of inflammatory indices from the peripheral circulation may not reflect intracoronary levels but, instead, can be indicative of a more generalized systemic process. If the blood could be sampled from a location close to the target site, inflammatory responses initiated by peripheral arterial and venous cannulation could be nullified, and just local PCI-dependent inflammatory response could be evaluated. Therefore, methods to reflect the coronary (or intracardiac) micro-environment are therefore needed. The treatment of cardiovascular disease has changed dramatically over the past 2 decades, allowing patients to live longer and better-quality lives. The introduction of new therapies (both drugs and devices) has contributed much to this success. Nowhere has this been more evident than in interventional cardiology, where percutaneous cardiovascular intervention has evolved from a quirky experimental procedure to a therapeutic cornerstone for patients with cardiovascular disease. Inherent in the development of these technologies is the role of preclinical testing using animal models. Once these technologies enter the clinical arena, a further understanding of their therapeutic mechanisms can be realized through comparative analysis of animal model research findings with those of clinical pathological specimens. Chapter 1 will provide an overview of the clinical application status and limitations of current percutaneous cardiovascular intervention technologies, future technologies under development, and results of preclinical studies including animal models. Treatment of cervical carotid stenosis remains the most common vascular surgery operation performed today; however over the past 10 years carotid angioplasty and stenting (CAS) has rapidly become an acceptable alternative to carotid endarterectomy (CEA), particularly in patients deemed high risk for surgery. In less than a decade, pharmacological

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viii

Kevin G. Layton and Raymond A. Percelle

as well as technologic advancements have blossomed dramatically, yet the true clinical efficacy of CAS remains a matter of controversy. This contemporary review of the literature provides some perspective on available carotid stent systems, embolic protection devices (EPDs), and the associated neurologic and target lesion outcome with consideration of both early and late events. In regards to mechanical embolic protection devices (EPDs), some data demonstrates a slight superiority of those which employ proximal balloon occlusion in reducing the procedural incidence of stroke. Theoretically this is due to the ability to obtain complete embolic capture prior to crossing the target lesion, however as with all EPDs there remains a significant and universal stroke risk merely from the maneuvers required to adequately position the guiding catheter or sheath into the common carotid artery. Not surprisingly stent materials, configurations, and designs have varied clinical implications. Nitinol stents tend to have a slightly lower rate of major stroke as compared to Elgiloy, although current data does not have the power to demonstrate a statistically significant difference. Furthermore, data demonstrating differences in restenosis rates among these two stent materials is lacking. More recent data has shown that self-expanding stents possessing a closed cell design have fewer adverse neurological events as compared to open cell stents - the improved flexibility of the open cell stents seems most suited for asymptomatic patients with particularly tortuous vasculature. Tapered stents may have lower rates of asymptomatic occlusion or restenosis, but perioperatively there is little difference as compared to their non-tapered counterparts. Overall, intraoperative stroke rate of carotid artery stenting with EPDs is lower than without neuroprotective devices; however a larger majority of strokes tend to occur post-procedurally creating a universal limitation to all EPDs. Self-expanding stent fracture in the carotid vasculature is relatively unknown; yet two recently published case reports of fractures presenting as early restenotic lesions are discussed in Chapter 2. Lastly, we assess the role of diffusion weighted MRI as a diagnostic tool in evaluating the incidence of clinically and radiographic ischemic events following CAS with the use of EPDs. Cerebral protection devices (CPD) in carotid artery stenting (CAS) have gained a large popularity despite the lack of randomized studies to authenticate their clinical benefit. Carotid filters (CF) are commonly employed in the current CAS technique. Like other concepts of CPD, filters presents specific advantages and inherent drawbacks. The authors have previously related our initial experience in a hybrid technique of CAS owing a complementary protection during the first passage of filters through the internal carotid artery (ICA) lesions. In Chapter 3, hoping to enhance the ability of CF, the authors have described in a larger group analysis a possible extended application of this filter-based technique of CAS. Percutaneous coronary intervention (PCI) now forms the solid foundation of interventional cardiology. The milestones of therapeutic interventional cardiology have begun with simple balloon inflation, then to bare metal stent deployment, and finally to invention of drug-eluting stents. In fact, PCI with stent implantation has emerged in recent years as a revolutionary treatment of coronary artery disease. Nowadays, coronary stenting is applied in up to 80% of PCIs. However, balloon angioplasty is associated with an increase in inflammatory activity provoked by plaque rupture, arterial wall damage and endothelial injury. Additionally, stent deployment causes greater injury to the arterial wall and a more intense inflammatory response than balloon angioplasty. A number of circulating indicators of vascular inflammatory activity have been proposed as elements of this inflammatory

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Preface

ix

response, such as soluble adhesion molecules, cytokines and chemokines, acute phase reactants (e.g., fibrinogen, serum amyloid A, and high-sensitivity C-reactive protein), and leukocyte count. The clinical significance of this inflammatory response derives from the increasing evidence supporting the role of inflammation in the generation of early and late complications after PCI, including the development of in-stent restenosis that occurs in 30% to 50% of patients after PCI which represents a major clinical limitation of this technique. In patients who have a marked inflammatory response to coronary stent deployment, modulation of the inflammatory response with a potent anti-inflammatory agent may be effective in reducing neointimal proliferation and subsequent clinical/angiographic events. Consequently, extensive clinical and experimental research in the past decade has focused mainly on the following issues: the nature and components of the inflammatory response to PCI, its prognostic significance, and management strategies. Chapter 4 highlights the biochemical and rheological changes associated with PCI, mainly focusing on the inflammatory response following this process. It is designed as an updated review of previous studies on this issue, intended to orient the reader regarding the series of complex reactions following PCI and their clinical and prognostic importance besides therapeutic management. The authors measured coronary pressure in 417 patients with intermediate coronary stenosis, defined as percent diameter stenosis between 40% and 70% by quantitative coronary angiography. Fractional flow reserve (FFR) was calculated at the maximal hyperemia from the aortic (Pa) and distal coronary pressure (Pd) by the ratio of Pd/Pa. Patients with FFR≧0.75 in group A were treated with medical therapy (n=207). Patients with FFR≧0.75 in group B underwent coronary intervention at the physicians' discretion (n=59). Patients with FFR