Atlas of Interventional Cardiology [2nd ed.] 978-1-57340-180-7;978-1-4613-1091-4

This second edition of the Atlas of Interventional Cardiology is a reflection of the most recent advances and changes in

1,158 280 45MB

English Pages XI, 187 [196] Year 2003

Report DMCA / Copyright

DOWNLOAD FILE

Polecaj historie

Atlas of Interventional Cardiology [2nd ed.]
 978-1-57340-180-7;978-1-4613-1091-4

Table of contents :
Front Matter ....Pages I-XI
Coronary Arterial Response to Injury (Robert S. Schwartz, Renu Virmani, Andrew Farb)....Pages 1-6
Lesion Assessment (Stuart T. Higano, Amir Lerman)....Pages 7-26
Equipment Selection and Techniques of Percutaneous Coronary Intervention (John D. Altman, Charanjit S. Rihal)....Pages 27-40
Guide Selection (Dieter F. Lubbe, Verghese Mathew)....Pages 41-52
Stent Designs and Implantation Techniques (Mandeep Singh, Verghese Mathew)....Pages 53-60
In-stent Restenosis (Ali E. Denktas, Verghese Mathew)....Pages 61-71
Directional Coronary Atherectomy (David R. Holmes Jr.)....Pages 73-82
Rotational Coronary Atherectomy (Verghese Mathew, Kirk N. Garratt)....Pages 83-93
Cutting Balloon Angioplasty (Verghese Mathew, Anoop Chauhan)....Pages 95-106
Specific Lesion Subsets (Gregory W. Barsness, John F. Bresnahan)....Pages 107-128
Drug-eluting Stents (Anoop Chauhan, Ranjit S. More)....Pages 129-138
Distal Protection Devices (David R. Holmes Jr.)....Pages 139-144
Complications of Percutaneous Coronary Artery Intervention (Kirk N. Garratt, David R. Holmes Jr.)....Pages 145-158
Peripheral Interventions (Farris K. Timimi)....Pages 159-176
Back Matter ....Pages 177-187

Citation preview

Atlas of

INTERVENTIONAL CAR DIOL OGY SecondEdition

Atlas of

INTERVENTIONAL CARDIOLOGY SecondEdition

EDITORS

David R. Holmes, Jr., MD Professor of Medicine Mayo Medical School Director, Cardiac Catheterization Laboratory Consultant, Division of Cardiovascular Diseases Mayo Clinic Rochester, Minnesota

Verghese Mathew, MD Assistant Professor of Medicine Mayo Medical School Consultant, Division of Cardiovascular Diseases and Internal Medicine Mayo Clinic Rochester, Minnesota

With 18 contributors

CM CURRENT. MEDICINE

Springer-Science+Business Media, LLC

CURRENT MEDICINE, INC. 400 Market Street, Suite 700 • Philadelphia, PA 79106

Developmental Editors .................................... Teresa M. Giuliana, Cina F. Scala Editorial Assistant ....................................... .Annmarie D'Ortona Cover Design ......................................... .. William C. Whitman, }r. Cover lllustration ........................................ Wieslawa Langenfe/d Design and Layout ....................................... William C. Whitman, jr. lllustrators ......................................... .... .}ohn McCullough, Marie Dean, Wieslawa Langenfeld, Maureen Looney Assistant Production Manager .............................. .Margaret La Mare lndexing ......................................... ..... .Holly Lukens

Library of Congress Cataloging-in-Publication Data Atlas of interventional cardiology 1 editors, Verghese Mathew, David R. Holmes, Jr.-2nd ed. p. ; cm. -- (Atlas of heart diseases) Rev. ed. of: lnterventional cardiology. c1997. lncludes bibliographical references and index. 1. Angioplasty--Atlases. 2. Cardiac catheterization--Atlases. 3. Stents (Surgery)--Atlases. 4. Coronary heart disease--Surgery--Atlases. 1. Mathew, Verghese. 11. Holmes, David R., 1945- III. lnterventional cardiology. IV. Atlas of heart diseases (Unnumbered) [DNLM: 1. Coronary Disease--therapy--Atlases. 2. Atherectomy, Coronary--methods--Atlases. 3. Coronary Disease--Atlases. 4. Heart Catheterization--mathods--Atlases. 5. Stents--Atlases. WG 17 A88438 2002] RD598.35.A53 .A855 2002 617.4' 12--dc21 2002023773

ISBN 978-1-4613-1091-4 (eBook) ISBN 978-1-4757-0808-0 DOI 10.1007/978-1-4613-1091-4 Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. Products mentioned in this publication should be used in accordance with the prescribing information prepared by the manufacturers. No claims or endorsements are made for any drug or compound presently under investigation. ©Copyright 2003 by Springer Science+Business Media New York Originally published by Current Medicina, lnc in 2003. Softcover reprint of the hardcover 2nd edition 2003

Ali rights reserved. No part of this publication may be reproduced, stored in a retrieval system, ar transmitted in any form by any means electronic, mechanical,photocopying, recording, or otherwise, without prior written consent of the publisher.

10 9 8 7 6 5 4 3 For more information please call1 (800) 427-1796 or (215) 574-2266 or e-mail us at inquiry®phl.cursci.com

www.current-science-group.com

IV

PREFACE Since Andreas Griintzig performed the first coronary angioplasty in 1977, there has been an evolution of technique and technology. Although we take for granted today's vast choices in guiding catheters, balloons, and wires, in the early era of interventional cardiology, catheters and wires were stiff, difficult to maneuver, and unforgiving. In addition to these basic tools, multiple novel interventional devices have been developed, several of which remain in use in current interventional practice. Rotational and directional atherectomy have remained in our armamentarium, although they have been somewhat relegated to niche applications. Extraction atherectomy, on the other hand, had come and gone, but is once again experiencing a resurgence. Laser angioplasty, on the other hand, has virtually disappeared from coronary intervention practice. This second edition of the Atlas of Interventional Cardiology reflects the changes in both techniques and devices that have occurred since the first edition was published. Insofar as all percutaneous coronary intervention results in arterial injury, this edition again begins with an overview of the coronary arterial response to injury. In addition, invasive lesion assessment, which has become an important diagnostic area in the catheterization laboratory (specifically coronary physiologic assessment and intravascular ultrasound), is described in detail. General techniques and equipment selection are outlined. Specific emphasis on the adjunctive modalities of directional and rotational

atherectomy, as well as the cutting balloon, is included. In addition, the text describes the evolution of stent design, and various stents are compared. The important area of in-stent restenosis is discussed at length. Distal protection devices are also discussed, which is particularly relevant in the context of the increasing proportion of vein graft interventions in current practice. Drugeluting stents are of enormous clinical interest currently, and the available data in this area are also presented. Ultimately, we have sought to describe a lesion-specific approach to coronary intervention, which includes our perspective on approaches, techniques, and equipment according to lesion type. Handling the complications associated with percutaneous coronary intervention remains an important aspect of our practice, and this area has been emphasized. Lastly, as the interventional cardiology practice evolves, noncoronary interventions are becoming more commonplace; thus, we have devoted a chapter to peripheral arterial interventions. Current technology, including the latest wave of excitement associated with drug-eluting stents, clearly reestablishes percutaneous coronary intervention as a mainstay in the treatment of coronary artery disease. The contributors who worked to update this edition of the Atlas of Interventional Cardiology have done a wonderful job of distilling the salient features relevant to interventional cardiology practice from a vast body of available information. We hope that the reader will find this volume useful in illuminating both the technical and the cognitive aspects of our field.

DAVID R. HOLMES, JR., MD VERCHESE MATHEW, MD ROCHESTER, MINNESOTA

v

CONTRIBUTORS JOHN D. ALTMAN, MD

KIRK N. GARRATT, MD

Interventional Cardiologist St. Anthony's Hospital Denver, Colorado

Associate Professor Departments of Cardiovascular Diseases and Internal Medicine Mayo Medical School Consultant Mayo Clinic Rochester, Minnesota

GREGORY W. BARSNESS, MD

Assistant Professor Department of Medicine Mayo Graduate School of Medicine Senior Associate Consultant Mayo Clinic Rochester, Minnesota

STUART T. HIGANO, MD

Assistant Professor of Medicine Departments of Cardiovascular Diseases and Internal Medicine Mayo Medical School Consultant Mayo Clinic Rochester, Minnesota

JOHN F. BRESNAHAN, MD

Associate Professor of Medicine Department of Cardiovascular Diseases Creighton University Omaha, Nebraska Consultant Mayo Clinic Rochester, Minnesota

DAVID R. HOLMES, JR., MD

Professor of Medicine Mayo Medical School Director, Cardiac Catheterization Laboratory Consultant, Division of Cardiovascular Diseases Mayo Clinic Rochester, Minnesota

ANOOP CHAUHAN, MD

Regional Cardiac Unit Blackpool Victoria Hospital Blackpool, England

AMIR LERMAN, MD

ALI E. DENKTAS, MD

Professor of Medicine Department of Cardiovascular Diseases and Internal Medicine Mayo Medical School Consultant Mayo Clinic Rochester, Minnesota

Chief Interventional Cardiology Fellow Mayo Clinic Rochester, Minnesota ANDREW FARB, MD

Staff Cardiovascular Pathologist Department of Cardiovascular Pathology Armed Forces Institute of Pathology Washington, DC

VI

DIETER F. LUBBE, MBChB Assistant Professor Department of Medicine Section of Cardiology Co-Director, Cardiac Catheterization Laboratory Houston VA Medical Center Baylor College of Medicine Houston, Texas

MANDEEP SINGH, MD Assistant Professor Departments of Cardiovascular Diseases and Internal Medicine Consultant Mayo Clinic Rochester, Minnesota FARRIS K. TIMIMI, MD Assistant Professor Department of Medicine Division of Cardiovascular Diseases Mayo Medical School Rochester, Minnesota Director, Critical Care and Intensive Care Director, Vascular, Physiologic, and Invasive Laboratory Immanuel St. Joseph's Hospital Mankato, Minnesota

VERGHESE MATHEW, MD Assistant Professor of Medicine Mayo Medical School Consultant, Division of Cardiovascular Diseases and Internal Medicine Mayo Clinic Rochester, Minnesota RANJIT S. MORE, MD St. Mary's Hospital Portsmouth, England

RENU VIRMANI, MD Clinical Professor Department of Pathology Georgetown University Chair, Department of Cardiovascular Pathology Armed Forces Institute of Pathology Washington, DC

CHARANJIT S. RIHAL, MD Associate Professor Department of Medicine Mayo Medical School Consultant Mayo Clinic Rochester, Minnesota ROBERT S. SCHWARTZ, MD Professor of Medicine Department of Cardiology Mayo Medical School Staff Cardiologist Mayo Foundation Rochester, Minnesota

VII

CONTENTS

CHAPTER 1 CORONARY ARTERIAL RESPONSE TO INJURY

Robert S. Schwartz, Renu Vinnani, and Andrew Farb Coronary Artery Responses to Injury .............................................. ...............2 Coronary Artery Injury Caused by Angioplasty .............................................. ...... 3 Histopathology of Neointimal Development Due to Vascular Injury .................................. 3 Histopathologic Results in Patients .............................................. ................ .4 Comparing Stenting in Humans to Experimental Animal Models .................................... 5 Conclusions .............................................. ..................................... 5

CHAPTER 2 LESION AssEsSMENT

Stuart T. Higano and Amir Lennan Beyond Coronary Angiography .............................................. .................... 7 Intravascular Ultrasound .............................................. ......................... 7 Coronary Physiology .............................................. ............................ 15 Conclusions .............................................. ....................................24

CHAPTER 3 EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION

fohn D. Altman and Charanjit S. Rihal Guide Catheters .............................................. ................................ 28 Guidewires .............................................. .................................... 29 Balloons .............................................. ....................................... 32 Catheter Systems .............................................. ............................... 33 Balloon Materials .............................................. ............................... 36 Balloon Sizes and Lengths .............................................. ....................... 37 Procedure .............................................. ...................................... 37 Intervention .............................................. .................................... 37

CHAPTER 4 GUIDE SELECTION

Dieter F. Lubbe and Verghese Mathew Left Anterior Descending Coronary Artery .............................................. ........ .42 Left Circumflex Artery .............................................. .......................... .44 Right Coronary Artery .............................................. .......................... .46 Vein Grafts .............................................. ..................................... 47 Mammary Arteries .............................................. ..............................49 Anomalous Arteries .............................................. ............................. 50 Transradial Coronary Intervention .............................................. ............... .51

VIII

CHAPTER 5 STENT DESIGNS AND IMPLANTATION TECHNIQUES

Mandeep Singh and Verghese Mathew Stent Types and Designs ...................................................................... .54 Balloon-expandable Stents ..................................................................... 55 Self-expanding Stents ......................................................................... 58 Stent Implantation in Specific Lesion Subtypes .................................................... 59

CHAPTER 6 IN-STENT RESTENOSIS

Ali E. Denktas and Verghese Mathew Restenosis ................................................................................... 62 Treatment for Restenosis ....................................................................... 65 Future Approaches ............................................................................ 69

CHAPTER 7 DIRECTIONAL CORONARY ATHERECTOMY

David R. Holmes, Jr. Patient Preparation ............................................................................ 74 Atherocath ................................................................................... 75 Equipment Selection .......................................................................... 75 Performance of Directional Atherectomy ......................................................... 76 Selection for Directional Atherectomy ........................................................... 79 Debulking Prior to Stent Implantation ........................................................... 79 Aorto-ostial Lesions ........................................................................... 80 Left Main Coronary Artery ..................................................................... 80 Bifurcation Lesions ............................................................................ 80 Treatment of In-stent Restenosis ................................................................ 81 Complications ................................................................................ 81 Conclusions .................................................................................. 82

CHAPTER 8 ROTATIONAL CORONARY ATHERECTOMY

Verghese Mathew and Kirk N. Garratt Physical Principles ............................................................................84 Clinical Data ................................................................................. 85 Procedural Aspects and Technique .............................................................. 88 Complications ................................................................................89 Implications of Available Clinical Data and Role of Rotational Atherectomy in Current Clinical Practice .. 89

IX

CHAPTER 9 CUTTING BALLOON ANGIOPLASTY

Verghese Mathew and Anoop Chauhan The Device ................................................................................... 96 Clinical Data ................................................................................. 97 Resistant Lesion Registry ...................................................................... 99 Clinical Use of the Cutting Balloon .............................................................. 99 Complications of the Cutting Balloon ........................................................... 103 Potential Applications of the Cutting Balloon in Current Clinical Practice ............................ 104

CHAPTER 10 SPECIFIC LESION SUBSETS

Gregory W. Barsness and John F. Bresnahan Ostial Lesions ............................................................................... 108 Bifurcations ................................................................................. 109 Total Occlusions ............................................................................. 111 Calcified Lesions ............................................................................. 116 Small Vessels ................................................................................ 117 Diffuse Disease .............................................................................. 117 Thrombotic Lesions .......................................................................... 118 Saphenous Vein Grafts ........................................................................ 120 Internal Mammary Conduit Lesions ............................................................ 124 Conclusions ................................................................................. 124

CHAPTER 11 DRUG-ELUTING STENTS

Anoop Chauhan and Ranjit S. More Pathophysiology Underlying In-stent Restenosis ................................................. 129 Systemic Agents versus Local Delivery ......................................................... 130 Choice of Eluting Agents ...................................................................... 131 Agents and Preclinical Studies ................................................................. 132 Clinical Trials Data ........................................................................... 134 Conclusions ................................................................................. 136

X

CHAPTER 12 DISTAL PROTECTION DEVICES

David R. Holmes, Jr. Conclusions .............................................. ................................... 144

CHAPTER 13 COMPLICATIONS OF PERCUTANEOUS CORONARY ARTERY INTERVENTION

Kirk N. Garratt and David R. Homes, Jr. Inability to Deliver the Therapeutic Device .............................................. ........ 146 Device Malfunction .............................................. ............................ 149 Acute or Threatened Closure .............................................. .................... 150 Side Branch Closure .............................................. ............................ 151 Distal Embolization .............................................. ............................ 153 Perforation .............................................. .................................... 154 Miscellaneous Cardiovascular Complications .............................................. ...... 155 Vascular Access Complications .............................................. .................. 156 Predicting Complications .............................................. ....................... 157

CHAPTER 14 PERIPHERAL INTERVENTIONS

Farris K. Timimi Aorto-iliac Disease .............................................. ............................. 160 Superficial Femoral and Popliteal Disease .............................................. ......... 162 Infrapopliteal Disease .............................................. .......................... 164 Subclavian/ Axillary Arterial Disease .............................................. ............. 165 Renovascular Disease .............................................. .......................... 166 Carotid Artery Disease .............................................. ......................... 171 Conclusions .............................................. ................................... 174 Index ....................................................... ................................................ 177

XI

Coronary Arterial Response to Injury Robert S. Schwartz, Renu Virmani, and Andrew Farb Both stent implantation and simple balloon angioplasty induce marked injury in the coronary artery or peripheral vessels. The artery's response to that injury is critical to the long-term success or failure of the procedures [1-3]. The coronary artery responds to injury incurred during revascularization with neointimal hyperplasia, forming neointima of varying thickness, and with thickening of the adventitia. This latter process frequently caus-

es vessel shrinkage, or negative remodeling, and is a principal cause of restenosis when a stent is not present to resist the constriction [4-8]. When a stent is placed, neointimal hyperplasia is the determining factor for in-stent restenosis and is the major target of drug-eluting stents. Presented in this chapter are animal models and human examples of the coronary artery's response to injury during revascularization procedures.

stent has little biologic activity against neointima and does not limit neointimal thickening. Indeed, stenting is associated with increased neointima compared with balloon angioplasty [7,8]. Only with the advent of brachytherapy and, most recently, drug-eluting stents may restenosis finally be adequately controlled through the elimination of neointimal overgrowth and negative remodeling.

CORONARY ARTERY RESPONSES TO INJURY Several factors affect the- risk of restenosis, including the type of revascularization (stented or not), the site of the lesion (the left anterior descending coronary artery is more susceptible), diabetes, residual stenosis, and the number of stents placed. Systemic drugs have proved ineffective; these include antiplatelet agents [9,10], anticoagulants [11], corticosteroids [12,13], angiotensinconverting enzyme inhibitors [14-16], statins [17-19], calcium channel blockers [20-22], and, most recently, oral tranilast. Hirudin [23,24] and angiopeptin [25-27] have also failed. The intracoronary stent improves long-term minimal luminal diameter and lowers restenosis rates [28-34]. However, the success of the stent is due to achievement of a larger postprocedural lumen, which, despite more late lumen loss, results in lower restenosis rates [6]. A bare (non- drug-eluting)

NEOINTIMAL HYPERPLASIA

Neointimal hyperplasia is the focus of anti-restenosis efforts in arterial stenting. Coronary artery neointima is histopathologically distinct from most primary atherosclerosis and neointimal hyperplasia is clearly a different pathophysiologic process. Microscopically, the atherosclerotic lesion has histologic features of disruption and replication of the internal elastic lamina,

Figure 1-3. Acute pathology specimen of a patient who underwent balloon coronary angioplasty without stent placement. Note the dissection across the superior border of the artery and laceration of the vessel at the plaque site. (Hematoxylin and eosin stain.)

Figure 1-1. Pathology specimen of a coronary artery 30 days after stent placement. Plaque and stent struts are visible. The stent has expanded the vessel, but neointimal ingrowth (quite cellular) has caused severe restenosis.

Figure 1-4. Pathology speciman of a coronary artery long after balloon angioplasty. Renarrowing of the vessel has occurred despite the presence of only a small amount of neointima. The restenosis in this case is probably due to inadequate expansion of the artery and negative remodeling, or shrinkage, of the vessel following the procedure. (Verhoeff- van Gieson elastic stain.)

Figure 1-2. Porcine coronary artery 28 days after balloon angioplasty. Note that neointima has formed along the bottom only at sites where the internal elastic lamina is ruptured. Also note disruption of the external elastic lamina and formation of a new internal elastic lamina along the inferior border, where neointima has formed. (Verhoeff- van Gieson elastic stain.)

ATLAS OF INTERVENTIONAL CARDIOLOGY 2

spindle and smooth cell proliferation, interstitial fibrosis, intracellular and interstitial lipid accumulation, fibrin deposition, calcification, hemorrhage, thrombosis, capillary proliferation, and macrophage collections [35,36]. This process can also be a response to injury. Most atherosclerotic lesions are endothelialized continuously with adjacent vascular endothelium.

CORONARY ARTERY REMODELING Following coronary angioplasty, artery size changes, owins to remodeling or the formation of neointimal hyperplasia. This is a direct result of vessel shrinkage due to thickening of the adventitia [7,37-39]. Stenting prevents negative remodeling, although it does induce more neointimal hyperplasia (Fig. 1-1) [6].

CORONARY ARTERY INJURY CAUSED BY ANCIOPLASTY

Finally, the plug must eventually become permanent, necessitating its replacement with tissue. The hemostatic process must remain localized only to the site of arterial injury. The propagation of thrombi to sites distant from the primary injury can prove quite dangerous and thus must be under rigid control. Clinical diseases related to the failure of hemostasis overwhelmingly occur as the result of too vigorous thriJmbosis, rather than bleeding diatheses. This concept is seen in the high prevalence of myocardial infarction, strokes, and emboli, and the resulting ischemia of vital organ systems. The initial hemostatic event following deep arterial injury is a rapid and explosive activation and deposition of platelets. The accumulation of platelets can easily reach macroscopic proportions. This sequence of histopathologic events has been examined in the porcine coronary artery injured by an oversized coronary stent. The progression of cellular events from thrombus to neointima is summarized according to stages.

STAGE 1: THROMBOTIC PHASE, DAYS 0-3 The first stage consists of rapid thrombus formation shortly after injury. The initial arterial response to injury is the explosive activation, adhesion, and aggregation of platelets. The platelet thrombus can grow large enough to occlude the vessel, as in myocardial infarction. After a short time (generally less than 24 hours), fibrin-rich thrombus accumulates around the platelet site. The two morphologic features in this phase are platelet-fibrin and fibrin-red cell thrombus. The platelets are densely clumped at the injury site, and the fibrin-red cell thrombus is attached to the platelet mass.

Injury to the arterial wall results from balloon angioplasty in both animal models and patients (Figs. 1-2, 1-3). How much neointima forms in the coronary artery undergoing revascularization? In a typical 3.0-mm coronary artery, the neointimal thickness corresponding to a restenotic lesion that reduces lumen diameter by 50% is about 0.75 mm. All angioplasty cases develop neointima and, thus, restenosis to varying degrees. Early reports from studies of balloon angioplasty suggested that plaque compression and movement of plaque were the mechanisms of luminal enlargement. Histopathologic studies of coronary arteries after balloon angioplasty indicated that these mechanisms were not the primary mechanisms of lumen improvement [40,41]. It has been estimated that more than 90% of arteries undergoing angioplasty are characterized by plaque fracture or splitting of the atheromatous plaque or, in cases of eccentric lesions, the media itself. The most common form of injury caused by balloon angioplasty is plaque or intimal laceration (Fig. 1-4). In eccentric lesions, the most common site of splitting occurs at the junction between the plaque and the more normal arterial wall. This site of fracture would be expected based on engineering and mechanical principles, with the highest stress concentration at this location. The length of the fracture varies and is unpredictable and uncontrollable. The split extends frequently through the internal elastic lamina into the media and, rarely, to the adventitia. Medial laceration was involved in about 80% of cases in selected studies [35,36,42].

STAGE II: RECRUITMENT PHASE, DAYS 3-8 In this phase, the thrombus at the site of injury develops a layer of what appear to be endothelial cells. It is unclear whether the cells truly are endothelial cells despite their histopathologic appearance. Shortly after the appearance of these endothelial cells, an intense cellular infiltration occurs. Included in the infiltration are monocytes that become macrophages as they leave the bloodstream and migrate into the subendothelial mural thrombus. Also present are lymphocytes. Like the monocytes, the lymphocytes originate from the bloodstream. This infiltrate thus develops from the luminal side of the injured artery, with these cells migrating progressively deeper into the mural thrombus. Figure 1-5 shows the evolution of thrombus being infiltrated by inflammatory cells in a normal porcine coronary artery that was stented 4 days before euthanasia. In this model, healing progresses from the luminal side inward toward the thrombus.

STAGE Ill: PROLIFERATIVE PHASE, DAY 8-fiNAL HEALING

HISTOPATHOLOGY OF NEOINTIMAL

In this final stage, actin-positive cells colonize the residual, thrombus from the lumen, forming a cap across the top of the mural thrombus. The cells progressively proliferate, moving toward the injured media, resorbing residual thrombus until all thrombus is gone and replaced by the neointimal cells. At this time, the healing is complete. In the pig, this process requires 21 to 40 days, depending on the thickness of the residual thrombus and the rate of cellular growth. The smooth muscle cell migration and proliferation into the degenerated thrombus create substantially increased neointimal volume at this stage, a volume that appears to be greater than that of the thrombus alone. The smooth muscle cells appear to migrate from sites distant from the injury location. The cells that colonize the resorbing thrombus may use it as a bioabsorbable matrix in

DEVELOPMENT DUE TO VASCULAR INJURY The formation of thrombus at the site of injury represents a complex process of positive and negative feedback systems that remains poorly understood [43]. From an evolutionary standpoint, the sealing of sites of vascular injury is a fundamental requirement for survival of the species. From a conceptual point of view, the problem of rapid yet safe sealing of sites of vascular injury has many stringent requirements. The hemostatic plug must form within seconds to minutes and must not occlude the vessel that has sustained only minor injury. Conversely, in cases of complete transection, total sealing must occur, other processes such as vasospasm also interact here.

CORONARY ARTERIAL RESPONSE TO INJURY 3

mural thrombus around the stent strut in a downward fashion. Figure 1-7, with inset, illustrates a similar process in a native coronary artery from a patient. Both sides of the lumen contain mural thrombus that is being organized abluminally. There is an apparent difference in the ages of these mural thrombi, since the thrombus on the lower surface appears less organized and probably occurred more recently than the one on the upper surface. The organization of thrombus is not found routinely in all sections. Thrombus is clearly sufficient to generate neointimal thickening, but it can be found in varying degrees. Several studies chronicle the process of stent histopathology in patients. Farb et al. [44] examined human stent histopathology and reported results over time from implantation. Stents from patients were examined at a mean of 3 days, 4 to 11 days, and 12 to 30 days; 11 stents were examined after more than 30 days. The results showed plaque compression by stent struts in 94% of patients. In 26% of patients, the lipid core was invaded by stent struts. As seen in animal models, platelet-rich thrombi were associated with stent struts and were related to the duration of stent implantation. Fibrin-containing thrombi also occurred at stent struts, especially soon after stenting. Inflammatory cells, principally neutrophils, were found on 79% of stents at day 3 of implantation, 83% at days 4 to 11, and 72% at days 12 to 30; no inflammatory cells were seen on stents implanted for more than 30 days. Conversely, chronic inflammatory cells consisting of lymphocytes and macrophages were seen around stent struts at all points in time. Medial injury was present in about 30% of stent strut sites, and medial compression without laceration of the internal elastic lamina was present in 55%. In 15% of stent strut sites, the media w as not injured at all. The mean arterial injury score for sections w ith medial d amage was 0.73. Neointimal thickness at stent strut sites was greater at sites with medial injury than where struts contacted plaque. Inflammation associated with stents 3 days after implantation in native coronary arteries was related to the underlying arteri-

which to replicate. The thrombus (at least in the case of oversized coil injuries) is colonized at progressively deeper levels until the neointimal healing is complete.

HISTOPATHOLOGIC RESULTS IN PATIENTS Healing progresses in the human coronary artery in a manner similar to that in the pig model [35,37,44]. Figure 1-6 shows a stented section from a saphenous vein graft that was surgically removed. Inflammatory cells from the lumen colonize the

Figure 1-5. Normal porcine coronary artery 4 days after stent placement. The vessel has an accumulation of mural thrombus along the stent strut site (right). The vessel lumen is at the top, while the normal-appearing media is at the lower left. Macrophages and lymphocytes are colonizing the thrombus at this early stage, from the lumen downward toward the media. Endothelialization is present at this early stage, a common finding in the porcine coronary injury model.

Figure 1-6. Saphenous vein graft and stent strut from a patient several months after stent placement. The vein graft itself is quite hypocellular (bottom). A layer of mural thrombus highly reminiscent of the porcine model has formed over and around the stent strut and is being colonized by macrophages and lymphocytes as in the porcine model. (Hematoxylin and eosin stain.)

Figure 1-7. Native coronary artery about 10 months after balloon angioplasty showing mural thrombus accumulating on both the upper and the lower luminal surfaces. Note that mature neointima has already formed beneath the thrombus. Inset, Higher power view of the neointima forming from the layered mural thrombus, also colonized by macrophages and lymphocytes. (Hematoxylin and eosin stain.)

ATLAS OF INTERVENTIO NAL CARDIOLOGY 4

al wall morphology. Only 3% of struts in contact with fibrous plaque had marked inflammation, compared with 44% of struts embedded in a lipid core and 36% of struts in contact with damaged media. Neointima did not appear in any stent implanted for fewer than 11 days. It was found in 45% of patients 12 to 30 days after stent implantation. Inflammation is a clear source of neointimal thickening. Figure 1-8 shows inflammatory cell growth in a stented human section. Figure 1-9 illustrates intentional inflammation in a stent (caused by metallic copper on the stent wire) in a normal porcine coronary artery. Massive amounts of neointima are evident. Many pathologists agree that by 30 days after implantation stent endothelialization in humans is present, though not necessarily complete, and typically a thin neointima is also present by this time. Leukocytes, platelets, and fibrin are present early, and at 3 months developing neointima completely covers the endothelium. Ten months later, atherosclerotic plaque, manifested by foam cells and cholesterol crystals, may be seen.

stent implantation. Experimental studies in animal models suggest important relationships among inflammation, vascular injury, and neointimal growth. These results have been at least partially replicated in patients, specifically those dealing with inflammation and neointimal growth.

CONCLUSIONS The nature of most revascularization strategies imposes injury on the coronary artery. This injury is necessary, given the diameter changes desired for alleviating tight stenoses. The angioplasty balloon causes this injury by lacerating the plaque and vessel. Balloon expansion creates fissures and tissue dissections. Other revascularization technologies, such as laser, directional atherectomy, or high-speed rotational atherectomy, remove plaque. Stenting of a vessel can cause fissure planes to be spread more widely than if vessel recoil was not prevented by the stent. The important common denominator appears to be injury independent of revascularization method: removal of vascular endothelium and exposure of deep tissue components to flowing blood. Potent repair mechanisms that are basic to survival of the species are triggered by these occurrences. Study of morphology after coronary stent placement demonstrates the following sequence of events: thrombus formation and acute inflammation soon after deployment, w ith subsequent neointimal growth. Increased inflammation occuring soon after stenting is associated with medial injury and lipid core penetration by stent struts. Stent oversizing relative to the reference arterial lumen and medial damage are associated with increased neointimal growth. A goal should be to better understand the vascular response to injury at both the cellular and the molecular level. Brachytherapy and drug-eluting stents appear useful in treating restenosis. Thus, these therapies should be better targeted to the neointima within stents. Importantly, the results from animal models appear to concur with those of human studies, but differences must be better understood, and their implications respected.

COMPARING STENTING IN HUMANS TO EXPERIMENTAL ANIMAL MODELS The thrombus found at stent sites within 24 hours of implantation in porcine restenosis models is associated with inflammatory cells [35,36,44--46). The subsequent healing in the pig closely reflects the findings in human coronary stenting soon after implantation. Vascular injury in stented normal arteries of experimental animals differs considerably from that in human atherosclerotic arteries. Stent oversizing in normal pig arteries produces neointima, owing to direct medial injury by the stent struts. By contrast, in humans, about 60% of stent struts are in direct contact with atherosclerotic plaque, rather than media. Moreover, medial compression or other damage associated with struts occurs in about one third of cases of

Figure 1-8. Saphenous vein graft showing neointima forming at a stent site. Note the high cellularity of the neointima (inset) and the virtual acellularity in the vein graft itself. The cellularity is composed of myofibroblasts and inflammatory cells, including macrophages and lymphocytes. This suggests the ability of such neointimal cells to migrate into regions of acellular media to heal a stent segment. (Hematoxylin and eosin stain.)

Figure 1-9. Inflammation in a normal porcine coronary artery induced by a copper-containing stent. Note the voluminous neointima and the aggressive inflammatory response (inset). Subsequent human studies also suggest the importance of minimizing inflammation to reduce neointimal thickening. (Hematoxylin and eosin stain .)

CORONARY ARTERIAL RESPONSE TO INJURY

5

REFERENCES 1. Schwartz RS, Murphy JG, Edwards WD, et al.: Restenosis after balloon angioplasty: a practical proliferative model in porcine coronary arteries. Circulation 1990, 82:2190-2200. 2. Schwartz RS, Murphy JG, Edwards WD, et al.: Restenosis occurs with internal elastic lamina laceration and is proportional to severity of vessel injury in a porcine coronary artery model [abstract]. Circulation 1990, 82:III-656. 3. Schwartz RS, Murphy JG, Edwards WD, et al.: Coronary artery restenosis and the "virginal membrane": smooth muscle cell proliferation and the intact internal elastic lamina. J Invasive Cardio/1991, 3:3-8. 4. Mehran R, Mintz G, Popma Let al.: Mechanisms and results of balloon angioplasty for the treatment of in-stent restenosis. Am J Cardiol1996, 78:618-622. 5. Mintz G, Pichard A, Kent K, et al.: Endovascular stents reduce restenosis by eliminating geometric arterial remodeling: a serial intravascular ultrasound study [abstract]. JAm Coli Cardiol1995, 95:701-705. 6. Mintz GS, Kent KM, Pichard AD, et al.: Intravascular ultrasound insights into mechanisms of stenosis formation and restenosis. Cardia/ Clin 1997, 15:17-29. 7. Mintz GS, Kent KM, Pichard AD, et al.: Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses. An intravascular ultrasound study. Circulation 1997,95:1791-1798. S. Mintz G, Kent K, Pichard A, et al.: Intravascular ultrasound insights into mechanisms of stenosis formation. Cardia/ Clin 1997, 15:17-29. 9. Webster MW, Chesebro ]H, Fuster V: Platelet inhibitor therapy. Agents and clinical implications. Hematol Oneal Clin North Am 1990, 4:265-289. 10. Runge MS, Bode C: Inhibition of platelets and thrombin: implications for treatment of coronary artery thrombosis [review]. Z Kardio/1993, 2:83-88. 11. Thornton MA, Gruentzig AR, Hollman], et al.: Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study. Circulation 1984, 69:721-727. 12. Cariou R, Harousseau JL, Tobelem G: Inhibition of human endothelial cell proliferation by heparin and steroids. Cell Biollnt 1988, 12:1037-1047. 13. Pepine C], Hirshfeld JW, Macdonald RG, et al.: Controlled trial of corticosteroids to prevent restenosis after coronary angioplasty. M-HEART Group. Circulation 1990,81:1753-1761. 14. Does the new angiotensin converting enzyme inhibitor cilazapril prevent restenosis after percutaneous translurnina l coronary angioplasty? Results of the MERCATOR study: a multicenter, randomized, double-blind placebocontrolled trial. Circulation 1992, 86:100-110. 15. Ellis SG: Do ACE inhibitors or ARBs limit restenosis after stenting? Assimilating the data. j Invasive Cardia/ 2001, 13:98-99. 16. Faxon DP: Effect of high dose angiotensin-converting enzyme inhibition on restenosis: final results of the MARCATOR Study, a multicenter, double-blind, placebo-controlled trial of cilazapril. JAm Coli Cardio/1995, 25:362-369. 17. Gilbert SP, Weintraub WS, Talley JD, Boccuzzi SJ: Costs of coronary restenosis (Lovastatin Restenosis Trial). Am J Cardio/1996, 77:196-199. 18. Malik IS, Khan M, Beatt KJ: Effect of statin therapy on restenosis after coronary stent implantation. Am J Cardia/ 2000, 86:810. 19. Serruys PW, Foley DP, Jackson G, el a/.: A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty: final results of the fluvastatin angiographic restenosis (FLARE) trial. Eur Heart J 1999, 20:58-69. 20. Corcos T, David PR, Bal PG, et al.: Failure of diltiazem to prevent restenosis after percutaneous translurninal coronary angioplasty. Am Heart J 1985, 109:926-931. 21. O'Keefe JHJ, Giorgi LV, Hartzler GO, et al.: Effects of diltiazern on complications and restenosis after coronary angioplasty. Am J Cardio/1991, 67:373-376. 22. Unverdorben M, Kunkel B, Leucht M, Bachmann K: Reduction of restenosis after PICA by diltiazem? Circulation 1992, 86:I-53. 23. Serruys PW, Herrman JP, Simon R, et al.: A comparison of hirudin with heparin in the prevention of restenosis after coronary angioplasty. N Engl J Med 1995, 333:757-763. 24. Strauss BH, van der Giessen WJ, Verdouw PD: Hirudin and restenosis. Circulation 1992, 85:1952-1953.

25. Emanuelsson H, Beatt KJ, Bagger JP, et al.: Long-term effects of angiopeptin treatment in coronary angioplasty. Reduction of clinical events but not angiographic restenosis. Circulation 1995,91:1689-1696. 26. Rosanio S, Tocchi M, Patterson C, Runge MS: Prevention of restenosis after percutaneous coronary interventions: the medical approach. Thromb Haemost 1999,82 (Suppl1):164-170. 27. Serruys PW: Long-term effects of angiopeptin treatment in coronary angioplasty: reduction of clinical events but not angiographic restenosis [letter; comment]. Circulation 1995, 92:2759-2760. 28. Serruys PW, Juilliere Y, Bertrand ME, eta[.: Additional improvement of stenosis geometry in human coronary arteries by stenting after balloon dilatation. Am J Cardio/1988, 61:71G-76G. 29. Serruys PW, Strauss BH, van Beusekorn HM, van der Giessen WJ: Stenting of coronary arteries: has a modern Pandora's box been opened? JAm Coli Cardio/1991, 17:143B-154B. 30. Serruys PW, Kay IP, Disco C, et al.: Periprocedural quantitative coronary angiography after Palrnaz-Schatz stent implantation predicts the restenosis rate at six months: results of a meta-analysis of the BElgian NEtherlands Stent study (BENESTENT) I, BENESTENT II Pilot, BENESTENT II and MUSIC trials. JAm Coli Cardio/1999, 34:1067-1074. 31. Serruys PW, Foley DP, Jackson G, et al.: A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty: final results of the fluvastatin angiographic restenosis (FLARE) trial. Eur Heart J 1999, 20:58-69. 32. Anderson HV: Restenosis after coronary angioplasty. Dis Man 1993, 39:613-670. 33. Bairn DS, Levine MJ, Leon MB, et al.: Management of restenosis within the Palrnaz-Schatz coronary stent (the U.S. multicenter experience). The U.S. Palmaz-Schatz Stent Investigators. Am J Cardio/1993, 71:364-366. 34. Bruining N, Sabate M, de Feyter PJ; et al.: Quantitative measurements of instent restenosis: a comparison between quantitative coronary ultrasound and quantitative coronary angiography. Catheter Cardiovasc lnterv 1999,48:133-142. 35. Virrnani R, Farb A, Carter A], Jones RM: Comparative pathology: radiationinduced coronary artery disease in man and animals. Semin Interv Cardia/ 1998, 3:163-172. 36. Virmani R, Farb A: Pathology of in-stent restenosis. Curr Opin Lipido/1999, 10:499-506. 37. Sangiorgi G, Taylor AJ, Farb A, et al.: Histopathology of postpercutaneous translurninal coronary angioplasty remodeling in human coronary arteries. Am Heart J 1999, 138:681-687. 38. Lafont A, Guzman L, Whitlow P, et al.: Restenosis after experimental angioplasty. Intimal, medial, and adventitial changes associated with constrictive remodeling. Circ Res 1995, 76:996-1002. 39. Mintz G, Kent K Saller L, et al.: Dimorphic mechanisms of restenosis after DCA and stents: a serial intravascular ultrasound study. Circulation 1995, 92:2610. 40. Waller B: "Crackers, breakers, stretchers, drillers, scrapers, shavers, burners, welders and meltcrs" -the future treatment of atherosclerotic coronary artery disease. A clinical-morphologic assessment. JAm Coli Cardio/1989, 13:969-987. 41. Waller BF: Morphologic correlates of coronary angiographic patterns at the site of percutaneous transluminal coronary angioplasty. Clin Cardio/1988, 11:817-822. 42. Virmani R, Farb A, Carter AJ, Jones RM: Pathology of radiation-induced coronary artery disease in human and pig. Cardiovasc Radial Med 1999, 1:98-101. 43. Schwartz R, Holmes D, Jr, Topol E: The restenosis paradigm revisited: an alternative proposal for cellular mechanisms. JAm Coli Cardiol1992, 20:1284-1293. 44. Farb A Sangiorgi G, Carter AJ, et al.: Pathology of acute and chronic coronary stenting in humans. Circulation 1999, 99:44-52. 45. Bayes-Genis A Carnrud AR, Jorgenson M, et al.: Pressure rinsing of coronary stents immediately before implantation reduces inflammation and neointimal hyperplasia. JAm Coli Cardia/ 2001, 38:562-568. 46. Ishiwata S, Verheye S, Robinson KA, et al.: Inhibition of neointima formation by tranilast in pig coronary arteries after balloon angioplasty and stent implantation. JAm Col/ Cardia/ 2000, 35:1331-1337.

ATLAS OF INTERVENTIONAL CARDIOLOGY 6

Lesion Assessment Stuart T. Higano and Amir Lerman BEYOND CORONARY ANGIOGRAPHY Although coronary angiography remains the principal m ethod for imaging the coronary arteries, it has several limitations [1-3]. As a silhouette image of the vessel lumen, coronary angiography cannot readily image noncircular vessel lumens nor can it image the vessel wall. Noncircular lumens are seen after plaque rupture or percutaneous coronary intervention (PCI) when there are ulcers, dissections, and intraluminal thrombus (often termed hazy appearance). Contrast streaming, ostial lesions, heavy calcification, and bifurcations with overlapping segments further complicate the coronary angiographic assessment of the vessel lumen. An early stage of plaque development results in outward growth, or positive remodeling, and plaque progression occurs without causing an angiographic stenosis. Even when the vessel lumen is well projected and imaged, the physiologic significance of a coronary stenosis cannot always be determined by the angiogram itself, especially for intermediate stenoses of 50% to 70% diameter. The physiologic importance of a coronary stenosis depends in part on the myocardial territory subtended by the coronary stenosis. For example, two identical 70% diameter stenoses may have divergent physiologic effects if one perfuses a hypertrophied myocardium with a high-flow demand and the other perfuses a completely infarcted territory w ith minimal flow demands. Fortunately, new tools are available for the coronary angiographer to move beyond coronary an giography [4]. Intravascular ultrasound (IVUS) is a n ew tool for obtaining high-resolution tomographic images of vessel lumen

and wall. The IVUS catheter incorporates a tiny ultrasound transducer mounted on the tip. Two new tools for assessing coronary flow physiology are the Doppler and pressure guidewires. The Doppler guid ewire h as a p iezoelectric crystal mounted on its tip for measuring blood flow velocities in the vessel lumen. The pressure guidewire has a piezoelectric crystal mounted 3 em from the wire tip to measure intraluminal coronary pressures and translesional pressure gradients. IVUS and Doppler and pressure guidewires improve the angiographcr's assessment of coron ary a therosclerosis.

INTRAVASCULAR ULTRASOUND HISTORY Initial research in intraluminal ultrasound was begun in the mid-1950s by Cieszynski [St who used a single-element ultrasound crystal mounted perpendicularly on a catheter tip to measure the inner walls of the ventricle and pulmonary arteries on an A-mode scan. Technical progress developed slowly until 1969, when Born et al. [6] first introduced a catheter incorporating 32 transducer elements in a cylindrical phased array that could provide real-time tomographic images. In the late 1980s, several commercially available IVUS instruments were introduced in the United States, generating a high level of interest and enthusiasm for this technique. Industry has responded to this enthusiasm with significant advances in catheter technology and image quality.

CATHETER TECHNOLOGY

catheter is attached to a drive motor, which provides torque to the central core. For accurate image reconstruction, the central core must provide a one-to-one rotation correspondence between the drive motor and the tip of the catheter. Deviation from this one-toone rotation results in image distortion. The dynamic aperture array system utilizes a principle similar to the phased-array transducers on a transthoracic echocardiographic system. Multiple piezoelectric crystal elements (up to 64) are located in a circular fashion around the catheter tip. The elements are activated electronically to form an ultrasound beam; appropriate timing of each transducer element allows a uniform ultrasound beam to be directed perpendicular to the catheter. The ultrasound beam is electronically swept around the catheter, creating a 360° image. The ultrasound images are controlled by microprocessors within the catheter tip immediately proximal to the crystal elements. IVUS catheters are delivered to the coronary arteries through a typical 5F to 6F angioplasty-guiding catheter and an angioplasty guidewire, with most catheters using a monorail design. The ultrasound catheter is usually positioned in the coronary artery using fluoroscopic guidance. The ultrasound images are reviewed online using real-time imaging. Videotape recording

The initial catheters used for IVUS were relatively large (SF to 9F) and inflexible, with poor image quality. Recent technologic advances have resulted in much smaller and more flexible catheters, some of which are now down to 2.6F to 3.5F (1.0-1.5 mm in diameter). Image resolution is now of high quality with consistently reliable images obtainable in most instances. To image an arterial structure from within the lumen, it is necessary to have some mechanism to allow for rotation of the ultrasound beam around the circumference of the vessel. Two basic imaging mechanisms, the mechanical system and the dynamic aperture array system, have been incorporated into IVUS catheters. The mechanical scanning system incorporates a method for mechanically rotating the ultrasound beam. The simplest method has a transducer element attached to a rotating central core. Other rotating systems have been developed using a rotating mirror angled at 45°, with either a fixed or a rotating ultrasound transducer. Both systems have been superseded by the simpler rotating central core system. In all of the current methods, the rotating system revolves at 1500 to 3000 rpm, producing a tomographic image perpendicular to the catheter. The proximal end of the

DERIVED MEASUREME IS Le ion atheroma area = EE ar a - lum n ar a (AI o t rmed uplaqu media areawl

Lum n ar a teno i

Lesion lum n

centri it ind

Figure 2-1. Intravascular ultrasound image of a normal left main coronary artery. The catheter is the dark circle at 5 o'clock with a surrounding bright halo, also known as ring-down artifact.

Ath roma + Lum n ar a

Figure 2-2. Direct and derived measurements of quantitative coronary ultrasound (QCU). DMax- maximum lumen diameter; 0Min-minimum lumen diameter; EEM-£xtemal elastic membrane; PTMaxmaximum plaque thickness; PIMin-minimum plaque thickness; SDMax- maximum stent diameter; SD:r-1in- minimum stent diameter; MLA-minimum lumen area; LA-lumen area; NI-neointima.

ATLAS OF INTERVENTIONAL CARDIOLOGY 8

and/ or digital image acquisition is also used for offline review and quantitative measurements.

Atheroma burden refers to the degree of stenosis across the planar cross-section of the vessel, as seen in the pathologic section. The atheroma burden may be associated with lumen area stenosis, depending on the degree and type of remodeling present (positive/ adaptive or negative/ constrictive). Stent measurements, when chronic, also require measurement of the neointimal area. Lumen areas less than 3.5 to 4.0 mm in the proximal to midcoronary arteries are usually associated with ischemia on functional testing, although this does not apply to the left main coronary artery, saphenous vein bypass grafts, or small distal vessels [17-19].

IMAGE INTERPRETATION

An IVUS image represents a tomographic cross-section of a vessel (Fig. 2-1). The catheter itself, which is located within the lumen of the vessel, appears as a black circle. The normal artery was initially thought to have a trilayer appearance. This included an inner bright layer, a middle sonolucent area, and an outer dense layer. These layers were initially believed to represent the intima, media, and adventitia, respectively. Subsequent studies have shown that this three-layered appearance is not always present [7,8]. In young patients with completely normal coronary arteries on histopathologic examination, the inner bright layer is often absent. This inner layer is usually seen in older patients who have an intimal thickness of at least 178 J.lm [9]. The finding of this inner bright layer most likely represents the difference in acoustic impedance that occurs between blood-tissue interface, thickened intima, and ultrasound reflections from the internal elastic lamina. ln the normal artery, a middle sonolucent area may be present and most likely represents media, with the adventitia represented by a dense outer layer. However, not all arteries have this distinct ultrasound appearance of the medial and adventitial layers. The presence or absence of these two layers is dependent on the type of artery (muscular vs elastic) and the composition of each of the layers, as well as the type of instrument used [10]. Instruments with different dynamic ranges and different levels of gray scale may result in different appearances of the multiple layers. The recently published guidelines from the American College of Cardiology I American Heart Association have established standards for the acquisition, measurement, and reporting of IVUS studies, and thus have improved the ability of clinicians to communicate IVUS findings using a common language [11].

QUALITATIVE ASSESSMENT

In the presence of atherosclerotic disease, there will be an increase in thickness of the inner layer on IVUS. IVUS can diagnose early and diffuse atherosclerosis, which may look completely normal by angiographic examination [20]. Although ultrasound has been used to characterize the composition of an atherosclerotic plaque, it cannot be used definitively to diagnose specific histologic components [10,20]. Atheroma morphology can be classified into soft, fibrous, calcific, or mixed plaques. Soft, or echolucent, plaques have a low echogenic acoustic signal owing to the high lipid content in a mostly cellular lesion (Fig. 2-4). However, a zone of reduced echogenicity may also be attributable to a necrotic zone within the plaque, an intramural hemorrhage, or a thrombus. Fibrous plaques have an intermediate echogenicity between soft plaques and highly echogenic calcific plaques (Fig. 2-5). Very dense fibrous plaques may produce sufficient attenuation or acoustic shadowing and may be misclassified as calcific (Figs. 2-6 and 2-7). Plaque calcium has a high reflectivity and can be recognized on the IVUS image as a bright echodensity with acoustic far-field shadowing. Dense calcification can cause reverberations. Reverberations are echoes in the far field at equidistant intervals from the ultrasound catheter due to ringing of the ultrasound signal between the calcium and the catheter. Mixed plaques may be fibrocalcific or fibrofatty, or other combinations (Fig. 2-8). A thrombus is usually seen as an intraluminal mass, often with a layered, lobulated, or pedunculated appearance. The IVUS appearance is often echolucent, although the echogenicity of the thrombus is in part dependent on the red blood cell content of the thrombus. Thrombi may have a granular or heterogeneous appearance with speckling or scintillation (Fig. 2-9) [21,22]. Blood flow in microchannels may also be apparent within some thrombi. However, none of these features is pathognomic for thrombus, and the diagnosis of thrombus by IVUS should always be considered presumptive. Stagnant blood flow can cause spontaneous echo contrast, simulating thrombus. Spontaneous echo contrast likely is caused by an increase in the echoreflectivity of red blood cell rouleaux formation in the setting of stagnant blood and low shear rates. Injection of contrast medium or saline may disperse the stagnant flow, clear the lumen, and allow differentiation of stasis from thrombosis. The intimal hyperplasia or restenosis can have different appearances, depending on the age and histologic composition of the lesion. For example, early in-stent restenosis often has very low echogcnicity, at times less echogenic than the blood speckle in the lumen, making its detection difficult without proper system gain settings or color imaging (Figs. 2-10 and 2-11). Late in-stent restenosis typically appears more echogenic. The variable appearance is probably due to varying amounts of extracellular matrix and fibrous, cellular material in early and late restenosis. Radiated neointima has a very sonolucent appearance and may appear to have "black holes" [23].

QUANTITATIVE ASSESSMENT

Quantitative assessment of TVUS images includes direct and derived measurements (Fig. 2-2). Direct measurements include measurements of the vessel lumen, external elastic membrane (EEM), atheroma, and arc of calcium (Fig. 2-3). The vessel lumen can be easily traced at the blood-intima interface. Prior studies have shown that IVUS provides a highly accurate and reproducible measurement of lumen area [12,13]. This has been shown in in vitro models as well as in comparative histopathologic studies [14-16]. An accurate measurement of lumen area does assume that the catheter is parallel to the long axis of the vessel, because any deviation from this long axis will result in distortion of the lumen area. Fortunately, deviation from the long axis during in vivo imaging is usually negligible and does not significantly affect the measured vessel area. The outer vessel also can be traced along the EEM, which is presumed to lie at the interface between the sonolucent media and brighter adventitia. Derived measurements are calculated from the directly measured values as shown in Figure 2-2. For example, the atheroma area is calculated as the difference between the vessel area (or EEM area) and the lumen area. This area represents the plaque plus media area and is used as a surrogate for the plaque or atheroma area because the internal elastic lamina cannot be imaged easily by IVUS. Lumen area stenosis references the minimal lumen area to the reference lumen area (at a proximal and/ or distal reference site) and is analogous to the angiographic lumen diameter stenosis. Note that the percent diameter stenosis is always smaller than the percent area stenosis, owing to the squared relationship between diameter and area.

LESION ASSESSMENT 9

Figure 2-3. Intravascular ultrasound images from the left anterior descending coronary artery demonstrating quantitative coronary ultrasound measurements. A, Image from minimal lumen area showing calcified and remodeled plaque. B, Image from the proximal reference segment showing mild intimal thickening between 9 and 12 o'clock. C, D, Quantitative measurements from corresponding images. E, Quantitative coronary ultrasound measurements. In this example, note the large atheroma burden with only a small lumen area stenosis, due primarily to arterial remodeling.

BEEEBE Lumen area, mm2 ar a, mm2 a imum thickn , mm , mm a imum diameter, mm inimum diameter, mm Cal ium ar , degree

~E

!IU2l

3.2 0

2. 1 19

10.0 6

.4

plu m dial,

mm2

LESIQt::i !6.Cl 8.0 18.0 1. 0. 3.4 .1 6

9.0 11.1 0.5 0.2

ATLAS OF INTERVEN TIO NAL CARDIOLOGY

10

Dissections can be classified by how deeply they extend into minority of patients, the dissection may not be apparent by IVUS the vessel wall, including dissections that are intimal (limited to because of the scaffolding by the imaging catheter or because the the intima or atheroma, and not extending into the media), medi- dissection is located behind calcium. Dissections not detected by al (extending into the media), and adventitial (extending through ultrasound can usually be demonstrated by angiography. The vulnerable plaque, the unstable atherosclerotic lesion, the EEM). Dissections can also be classified by the circumferential extent (in degrees of arc), using a protractor centered on the and the ruptured plaque all are important lesions to identify lumen, length (using motorized transducer pullback), size of by IVUS. Unfortunately, there are no absolute IVUS features residual lumen (lumen cross-sectional area [CSA]), and CSA of that define a plaque as vulnerable. However, necropsy studies the dissection tissue arm (Fig. 2-12). Additional descriptors may have demonstrated that unstable coronary lesions are usually include the presence of a false lumen, identification of mobile lipid rich, with a thin fibrous cap (Fig. 2-13). Accordingly, flap(s), presence of calcium at the dissection border, and dissec- hypoechoic plaques without a well-formed fibrous cap are pretions in close proximity to stent edges (pocket or margin tears). sumed to represent potentially vulnerable atherosclerotic An intramural hematoma is an accumulation of blood within the lesions. In addition, vulnerable plaques usually are positively vessel wall, displacing the internal elastic membrane inward and remodeled with a high atheroma burden [24-27]. Positive EEM outward. Entry and exit points may be observed. remodeling is defined as a lesion/reference EEM ratio greater Furthermore, there may be separation of neointimal hyperplasia than 1 (Fig. 2-14) . Such positively remodeled plaques are more from stent struts, seen after treatment of in-stent restenosis. In a common in patients presenting with unstable coronary syn-

Figure 2-4. Intravascular ultrasound image of a soft atherosclerotic plaque demonstrating hypoechoic features. The plaque is of lower echocardiographic intensity than the surrounding adventitia.

Figure 2-5. Intravascular ultrasound image of a mild fibrous atherosclerotic plaque between 9 and 11 o'clock. The echocardiographic intensity of the plaque is equal to the surrounding adventitia.

Figure 2-6. Intravascular ultrasound image of a hard atherosclerotic plaque with echocardiographic intensity brighter than the surrounding adventitia.

Figure 2-7. Intravascular ultrasound image of a hard atherosclerotic plaque with echocardiographic intensity brighter than the surrounding adventitia and far-field attenuation, but no reverberations.

Figure 2-8. Intravascular ultrasound image of a mixed atherosclerotic plaque with both hard and soft components.

Figure 2-9. Intravascular ultrasound image of intraluminal thrombus in a patient with acute myocardial infarction. The thrombus has a granular or heterogeneous appearance with speckling or scintillation. The thrombus could be mistaken for fibrous plaque on this image.

LESION ASSESSMENT 11

Figure 2-10. Intravascular ultrasound image of early in-stent restenosis demonstrating hypoechoic neointima.

Figure 2-11. Intravascular ultrasound images of recurrent early in-stent restenosis with hypoechoic neointima. A, Stent within a stent ("stent sandwich") and neointima that is sonolucent and difficult to image. B, Improved lumen definition with Chromaflo (JOMED, Inc, Rancho Cordova, CA).

Figure 2-12. Intravascular ultrasound image of intimal dissection at the margin of a stent. The tissue is seen at 3 to 6 o'clock.

Figure 2-13. Intravascular ultrasound image of soft plaque with thin, fibrous cap, consistent with vulnerable plague.

Figure 2-15. Intravascular ultrasound image of ruptured, ulcerated plaque in a patient with an acute coronary syndrome. The lumen is still widely patent.

ATLAS OF INTERVENTIONAL CARDIOLOGY 12

Figure 2-14. Intravascular ultrasound image of positively remodeled atherosclerotic plaque. The vessel is "ballooning" out along the plaque between 2 and 7 o'clock.

CLINICAL APPLICATIONS dromes and have a higher inflammatory cell count, indicating more plaque instability. It must be kept in mind, however, that the pathophysiology of many unstable coronary syndromes, The clinical applications for IVUS include assessing indeterincluding acute myocardial infarction, is plaque erosion, and minate lesions and guiding percutaneous interventions [29]. The not plaque rupture, and susceptibility to erosion likely is not indeterminate lesion can be either angiographically indeterdetectable by current IVUS imaging methods. Plaque ulcera- minate or physiologically indeterminate. The angiographically tion is defined as a recess in the plaque beginning at the lumi- indeterminate lesion usually is not seen clearly on angiography, nal-intimal border (Fig. 2-15). Plaque rupture is defined as possibly owing to ostial location, catheter damping and contrast plaque ulceration often with a tear detected in a fibrous cap. streaming, branches and overlapping bifurcations, or dense Contrast injections may be used to prove and define the com- calcification. In these lesions, the anatomy of the lesion is not munication point. The presence of thrombi may obscure IVUS well displayed by the angiogram. By contrast, physiologically indeterminate lesions are those intermediate lesions that are detection of plaque fissuring or ulceration Other findings associated with unstable or disrupted clearly seen by angiography but are in the intermediate 50% to plaques include aneurysms, pseudoaneurysms, and true versus 70% diameter stenosis range. In these lesions, the physiologic false lumens [28]. True aneurysm is defined as a lesion that significance is unknown. The prototype angiographically indeincludes all layers of the vessel wall, with an EEM and lumen terminate lesion is the left main lesion [30,31]. As an anatomic area more than 50% larger than the proximal reference segment. imaging method, IVUS is ideal for assessing angiographically A pseudoaneurysm is disruption of the EEM, usually observed indeterminate lesions, such as an indeterminate left main coroafter intervention, with the lumen extending beyond the three nary artery stenosis. Although randomized trials are not possilayers of the vessel wall. A true lumen is surrounded by three ble in this difficult patient subset, it has been shown that layers of the vessel wall, including the intima, media, and patients without significant disease by IVUS can be spared coroadventitia. Side branches generally communicate with the true nary artery bypass grafting with an excellent clinical outcome lumen, but not with the false lumen. A false lumen is a channel, [32]. In most intermediate lesions, a physiologic tool, such as the usually parallel to the true lumen, that does not communicate pressure or Doppler guidewire, is more appropriate, although a minimum lumen area of less than 3.5 to 4.0 mm2 by IVUS is corwith the true lumen over at least a portion of its length.

i ual a m nt el \ all (Fig. _- 1 L or ~ 100% of LA of th LA

m nt with th low t LA

of the reference egment w ith the lowest LA

Figure 2-16. MUSIC criteria for intravascular ultrasound assessment of stent implantation. LA- lumen area; LD- lumen density; MUSIC- Multicenter Ultrasound Stent in Coronary Artery Disease. Figure 2-17. Intravascular ultrasound image during stent implantation demonstrating incomplete stent apposition.

LESION ASSESSMENT 13

related with abnormal physiology and lesion significance [17-19]. Deferring PCI in patients with indeterminate lesions when assessed by IVUS is also associated with an excellent clinical outcome [33]. One of the greatest potential clinical uses of IVUS is to guide PCI by assisting with device selection and assessing and optimizing results. IVUS has the ability to assess the wall morphology and plaque constituents, allowing for the rational selection of a revascularization device utilizing knowledge of device-wall interactions. For example, a plaque with heavy superficial calcification has a high risk of dissection with percutaneous transluminal coronary angioplasty (PTCA) alone, may not allow complete stent expansion, and may not be cut well with directional atherectomy. However, it might be ideal for rotational atherectomy or cutting balloon technologies. One study has shown a marked change in device strategy with IVUS-guided device selection [34]. However, despite the obvious advantages of plaque visualization for device selection, no randomized trials have unequivocally demonstrated improvement in clinical outcome with IVUS-guided device selection.

Percutaneous lRANSLUMINAL

CORONARY ANGIOPLASTY

Typical morphologies have been described by IVUS following PTCA, with dissections being very common, especially in the presence of calcium [35-38]. IVUS has been used to select balloon size with an improved outcome. In order of increasing aggressiveness, balloon size may be determined by reference lumen size (analogous to sizing with angiographic methods), half the difference between the reference lumen and the vessel (termed media to media), and lesion vessel size. In the presence of positive remodeling, the latter strategy could result in tremendous balloon oversizing compared with angiographic methods. In the presence of diffuse disease, or reference segment disease, the intermediate strategy could result in larger balloons compared to angiographic methods. In the absence of diffuse disease, the balloon size would be nearly equivalent to the angiographic method. Utilizing this intermediate strategy, the CLOUT (Core Laboratory Ultrasound Analysis) and SIPS studies demonstrated that balloon size could be increased, resulting in larger lumen

without an increase in dissection score [39,40]. In other words, oversized balloons appear safe when guided by IVUS in the presence of diffuse disease. Post-PTCA morphologies have been described, usually including an intimal tear or dissection [41,42] . The GUIDE II (Guidance by Ultrasound Imaging for Decision Endpoints) study also showed that larger lumen sizes by IVUS are associated with improved clinical outcome [43). STENTS

One of the first clinical uses of IVUS was the guidance of stent implantation. Early studies showed that warfarin anticoagulation could be avoided without increasing subacute thrombosis rates in patients with stents that were adequately deployed by IVUS criteria (Fig. 2-16), thereby reducing bleeding complications and hospital stay [44,45]. The MUSIC (Multicenter Ultrasound Stent in Coronary Artery Disease) criteria were developed as a guide for assessing adequacy of stent implantation (Fig. 2-16) [46]. IVUS systems were rapidly integrated into many interventionallaboratories for this reason. It was subsequently found that combined antiplatelet therapy with aspirin and a thienopyridine resulted in an extremely low subacute thrombosis rate, even without IVUS guidance. Higher balloon pressure and stent size likely also played a role in improving thrombosis rates. These initial studies demonstrated the discrepancies between angiography and IVUS, and they were essential to the subsequent stent deployment technique with larger balloons and stents. The current role of IVUS for stent implantation remains controversial. However, there are several definitive facts that can be derived from the available studies [47-58]. First, the minimal stent area is usually larger when IVUS guidance is used, by approximately 0.5 to 2 mm2 . Second, higher balloon inflation pressures result in larger minimal stent areas. Third, the progressive growth of the stent with higher pressure is usually not apparent by angiography. Fourth, larger minimal stent areas are associated with lower restenosis rates. Fifth, optimal stent deployment by IVUS is difficult to achieve with success rates only in the 30% to 60% range. It has been more difficult to demonstrate a definite clinical benefit with IVUS guidance.

coronary

5.0

4.0

Figure 2-18. Simplified model of the coronary circulation using two-resistance model. The proximal resistance (R1) represents the epicardial conduit vessel, and the distal resistance (R2) represents the resistance vessels, or microcirculation. This model applies to coronary blood flow at steady state.

1.0

.· . . ,.· :.

7~.:.~·: ·.

::0

~ 2.0

O"o~··· ##

8 3.0 c:

/~

Maxomum vasodolato n

'

'.

\

80°o• •: •.•

85%. :". ..

90°o :

•,

Cor n ry pr

ur

Figure 2-19. Coronary pressure-flow relationship at rest and during hyperemia.

ATLAS OF INTERVENTIONAL CARDIOLOGY 14

Figure 2-20. Definition of types of coronary flow reserve. CFR-coronary flow reserve; FFR-fractional flow reserve; RCFR-relative coronary flow reserve.

Potential areas of benefit include reducing subacute stent thrombosis or reducing in-stent restenosis. Because the incidence of subacute stent thrombosis is already so low, IVUS is unlikely to add any major benefit. Whether enlarging the minimal stent area in a given patient improves in-stent restenosis has yet to be shown in randomized trials, although results from recent trials are promising. Despite being in clinical use for over a decade, and despite clear advantages in plaque imaging over angiography, it has been difficult to show a definite improvement in clinical outcome using IVUS in patients undergoing PCI. There are, however, many reasons that IVUS may not have shown definitively an improved clinical outcome. First, IVUS is a moderately difficult technology for the angiographer to learn, incorporating facets of both interventional and ultrasound technologies. Training is required for setup, performance, and interpretation of IVUS images. IVUS training takes time and can be difficult for the busy practicing interventional cardiologist, although accredited interventional cardiology training programs are now required to provide such training. Second, IVUS is only a diagnostic tool and, in and of itself, cannot improve clinical outcome unless coupled to a therapy that can improve clinical outcome. Despite the multitude of tools currently used for PCI, there are in fact a limited number of therapeutic options. Plaques can only be stretched further (bigger balloon), covered with a stent, cut in-situ (cutting balloon), cut and removed (directional coronary atherectomy or transluminal extraction catheter), or sanded or abraded (rotational atherectomy). Either each of these percutaneous therapies has such a good clinical outcome with angiography alone (ie, stents) that added benefit is marginal and difficult to prove, or they have limited additional therapeutic benefit over and above any other therapy used with angiography alone. While an improvement in clinical outcome is certainly the ultimate proof of the utility of a new therapy or diagnostic tool, it is a high standard that admittedly most new diagnostic tools have not met. For example, most angiographic systems incorporate a pulsed fluoroscopy system for reducing radiation exposure, yet no study has shown a clinical benefit for patients or a reduction in radiation-induced disease in operators. However, it is understood that reduced radiation exposure is a worthwhile goal. Additionally, most would agree that a Doppler-derived mitral valve gradient is the gold standard in the diagnosis of mitral stenosis, yet no study has shown an improved clinical outcome using echocardiography when compared with cardiac catheterization. A similar case can be made for IVUS, the gold standard for assessing the degree of atherosclerosis.

Figure 2-21. Enlarged view of the Doppler guidewire tip with piezoelectric crystal.

CORONARY PHYSIOLOGY A basic understanding of coronary physiology is needed before one incorporates physiologic guidewires into clinical practice [59,60]. The coronary circulation can be most simply modeled using a two-resistance model assuming steady state flow conditions (Fig. 2-18). The proximal resistance represents the epicardial conduit vessel (R1); the distal resistance represents the resistance vessels, or microcirculation (R2). The total coronary resistance (RT) is the sum of the proximal (epicardial conduit) and distal (microcirculatory) resistance. In the absence of coronary stenoses, the resistance of the normal epicardial conduit vessel is negligible (< 5% of total coronary resistance) and the proximal resistance can be ignored. In this circumstance, there is only a minimal pressure gradient from the aorta to the distal epicardial vessel. The distal resistance of the microcirculation regulates coronary blood flow (CBF). With increasing myocardial oxygen demands, such as during stress or exercise, CBF rises owing to a reduction in distal resistance. At maximal vasodilation, the distal resistance is at its minimum and CBF is at its maximum, given the available perfusion pressure. In this state, CBF is linearly related to perfusion pressure (defined as P aorta minus P venous)· Alterations in CBF can be understood by considering the tworesistor model. Coronary atherosclerosis typically occurs in the epicardial conduit vessel and contributes to the proximal resistance. The coronary pressure-flow relationship is shown in Figure 2-19. At rest, CBF is maintained at near-constant levels over a wide range of perfusion pressures by a process termed autoregulation [61]. If aortic pressure falls, such as during a major gastrointestinal hemorrhage, resting CBF is maintained at normal levels despite the lower perfusion pressure by dilation of the microcirculation, or resistance vessels. In the presence of an obstructing atherosclerotic stenosis in the epicardial conduit vessel (increased R1), the distal coronary pressure is reduced and the microcirculation undergoes compensatory vasodilation (reduced R2). Resting CBF is maintained at normal levels as the total coronary resistance is normal (RT = R1 + R2). With increasingly severe stenoses, the translesional pressure drop increases and eventually, autoregulation is overcome, as the resistance vessels are unable to further dilate. In this circumstance, CBF may fall below normal resting values. Plaque rupture with either total or subtotal vessel occlusion, as seen in either unstable angina pectoris or acute transmural injury or infarction, would result in the coronary flow physiology described. The development of collaterals may restore the distal

Figure 2-22. Doppler guidewire in vessel lumen. The ultrasound beam diverges 14 degrees from the guide wire axis, resulting in a conical-shaped ultrasound beam. Even if not placed in the center of the vessel, the Doppler guidewire will usually interrogate the highest velocities in the central stream.

LESION ASSESSMENT

15

perfusion pressure, such that resting myocardial blood flow again can be maintained at normal levels, and even low levels of exertion may be tolerated without ischemia. Coronary flow reserve (CFR) is a quantitative measure of the degree to which coronary atherosclerosis impairs hyperemic CBF and myocardial perfusion, and is defined as the ratio of maximal hyperemic blood flow to resting or basal flow [60,61]. Early studies on coronary physiology in an animal model demonstrated that 50% or less lumen diameter stenoses did not impair hyperemic coronary flow. However, 70% or greater lumen diameter stenoses did reduce hyperemic flow and CFR. Conversely, resting coronary flow was not affected until the stenoses diameter was greater than 90%. Interestingly, atherosclerosis may impair CFR even without angiographic stenoses when there is diffuse coronary involvement. Two other types of CFR have also been described, including relative CFR (RCFR) and fractional flow reserve (FFR), as shown in Figure 2-20 [59,62]. Abnormalities in the distal resistance may also impair CBF. The microcirculation may be unable to dilate normally, thereby limiting hyperemic blood flow. For example, patients with syndrome X have been hypothesized to have "pre-arteriolar" disease, causing a reduced CFR even in the presence of normal epicardial coronary arteries [63,64] . Similar abnormalities may be present in hypertension, even in the absence of ventricular hypertrophy, due to small vessel disease [65]. The underlying abnormality may be related to endothelial dysfunction [66]. Furthermore, severe hypotension or marked right atrial hypertension can reduce coronary perfusion pressure and blood flow. DOPPLER

The Doppler guidewire is an angioplasty-style guidewire with a 12.5 MHz piezoelectric crystal in its tip (Fig. 2-21) [67]. Pulsedwave Doppler technology is used with a carrier frequency of 10 kHz, a sample volume 5 mm from the tip of the guidewire, and a

range gate of 1 mm. The ultrasound beam is emitted in a conical shape with divergence of 14° from the axis of the guidewire, allowing the Doppler guidewire to interrogate the highest velocities in the central stream, even if the guidewire is not placed in the center of the vessel (Fig. 2-22). Although a small angle of incidence with the flowing blood may occur, this angle is typically 10° or less, which results in a minimal error (the underestimation of velocity with an angle error of 10° is equivalent to the cosine 10°, or 8% error). Theoretically, the phasic Doppler signal represents all the flow velocities in the flow stream at any given moment in time, resulting in a spectral broadening. The highest velocity represents the flow in the central stream. Care must be taken to orient the wire such that optimal, or maximal, velocities are obtained. If the sample volume is inadvertently placed on the vessel wall, an artifact will occur (often called wall thump). The Doppler system computer incorporates fast Fourier transform (FFT) technology that converts the Doppler shift frequencies into velocities, allowing all velocities throughout the cardiac cycle to be displayed in a phasic pattern. The peak velocity throughout the cardiac cycle is averaged over the two cardiac cycles, giving the average peak velocity (APV). Phasic coronary flow analysis allows systolic and diastolic components to be measured separately. Systolic and diastolic components can be measured separately, and the diastolic to systolic velocity ratio (DSVR) can be calculated [68]. The area under the velocity curve, the diastolic to systolic velocity integral ratio (DSVR1), can also be measured. In the left coronary artery, flow occurs predominantly during diastole (Fig. 2-23). This phenomenon is due to compression of the microcirculation during systole by left ventricular contraction, often termed throttling. The low systolic velocity results in a high DSVR value. Throttling is less apparent in the proximal and middle right coronary arteries supplying predominantly the lower pressure right ventricle. Phasic coronary flow demonstrates nearly equal systolic and diastolic components in these regions, resulting in a DSVR close to unity. Diastolic predominance does reappear in the right posterior descending artery that supplies the inferior wall of the left ventricle.

Figure 2-23. Normal phasic flow patterns in the left anterior descending and distal right coronary arteries. Note the predominant diastolic flow in the left anterior descending artery due to "throttling" of the flow during myocardial contraction. Systole and diastole are indicated by the vertical lines (S, onset of systole, D, onset of diastole). Their placement is determined by empirically derived equations using the two most recent R to R intervals (time in milliseconds from Q wave to D equals 490- [1.69 X heart rate]). The electrocardiogram and phasic guiding catheter pressure are also shown, along with corresponding numerical values. The numbers along the right ordinate indicate velocity in em/sec. D-onset of diastole; S--onset of systole.

Figure 2-24. Intracoronary Doppler study demonstrating the measurement of coronary flow reserve. Tracings from the left anterior descending coronary artery before and after 18 ]Jg of intracoronary adenosine show a normal Doppler-derived coronary flow reserve of 3.1. The baseline or resting average peak velocity (APV) was 21 and the hyperemic APV following intracoronary adenosine was 67.

ATLAS OF INTERVENTIONAL CARDIOLOGY 16

CORONARY BLOOD FLOW

Alternatively, IVUS has been used for measuring flow area. CBF is then calculated by combining the Doppler-derived velocities with the directly measured flow area. However, flow area measured by IVUS cannot be located at the same position as the Doppler sample volume, a requirement for the flow equation to be accurate. Therefore, this method is not recommended. The peak velocities measured by Doppler in the center of the stream (represented by the APV measurement) are not equivalent to or representative of all of the velocities flowing within the flow area, as the flow withm the coronary assumes a near parabolic velocity profile. The spatial mean velocity within the flow area must be used for accurately calculating CBF. If the velocity profile is parabolic, then the spatial mean velocity is equivalent to one half the peak velocity in the stream center. Therefore, the CBF equation becomes: CBF = 1/2 X APV X flow area. Note that when one usesAPV (cm/s) instead ofTVI (em) measurements, the heart rate drops out of the flow equation. This equation has been validated to accurately measure CBF in an animal model utilizing a continuous flow femoral artery- to-coronary artery shunting system [67].

Although the phasic pattern of coronary flow velocity is useful, the Doppler guidewire is used primarily for measurement of absolute CBF and coronary flow reserve. Several assumptions must be made in calculating blood flow because the Doppler guidewire measures blood flow velocity only. Theoretically, the hydraulic equation can be used to calculate CBF (Q) as the product of the flow area and velocity as shown: Stroke volume = (flow velocity) X (flow area), or Q = (flow velocity) X (flow area) X (heart rate). The APV is obtained with the Doppler guidewire, but the APV (measured in em/ s) is not equivalent to the time-velocity integral (TVI, measured in em) used in most Doppler echocardiography laboratories. They are related by the heart rate, as follows: TVI = APV x RR interval, or TVI = APV / heart rate. The flow area can be measured in several different ways. Typically, quantitative coronary angiography is used to measure the coronary diameter at the position of the sample volume (5 mm distal to the wire tip). The diameter (d) is then used to calculate the flow area, assuming a circular flow area, using the following equation: Flow area = (1t/ 4) d 2.

CoRONARY FLow RESERVE

Coronary flow reserve in humans has been difficult to measure in the past, owing to difficulties in measuring CBF. Techniques such as videodensitometry, coronary sinus thermodilution, or microspheres were restricted to specialized research centers or animal models. External Doppler probes were useful only during cardiac surgery. The Doppler guidewire has made the measurement of CPR easy and safe in humans. The Doppler-derived coronary flow reserve (CFVR) is measured by inducing maximal vasodilation with intravenous or, more commonly, intracoronary vasodilators (adenosine, papaverine, or ATP) and comparing the maximally stimulated velocities (APVHyperemia) with the resting or basal velocities (APV Basal) (Figs. 2-24 and 2-25), as follows: CFVR = APV Hyr.eremia / APV Basal· Intracoronary adenosine has been shown to induce maximal coronary vasodilation and has an excellent safety profile [69,70]. Papaverine has a longer half-life and can cause QT prolongation and torsade de pointes on rare occasions [71,72]. Adenosine triphosphate is also an excellent vasodilator [73]. In patients with norma 1 coronary angiograms, the normal CFVR is approximately 2.8, although higher values are seen in patients with normal coronary angiograms and intracoronary ultrasound examinations [74].

Figure 2-25. Example of normal Doppler-derived coronary flow reserve using trend display mode. The baseline or resting average peak velocity (APV) was 21 and the hyperemic APV following intracoronary adenosine was 69. A running trend of the APV is shown at the bottom.

STUDIES OF DOPPLER-DERIVED CORO ARY FLOW RESERVE A D

!:..EYE

6UII:iQB Miller el a/. [7 1 a/. [801 D hak 1 a/. [81 1

Jo

0 17 100 30 35

ITY

SE

< 2.0 < 2.0 < 1.8 < 1.8 < 2.0 < 2.0

94 9-l 89 91

5

SPE!:IEICITY

PV+

100 9

100 4 100

4 2 8-l

96

.!:...:: 77

95 91 89 A

CCUB6CY, 0L2 89 94 92 87 8

Figure 2-26. Correlative studies of Doppler-derived coronary flow reserve and noninvasive functional tests. CFVR- Doppler-derived coronary flow reserve; echo--echocardiogram; MIBI- sestamibi; NA- not availab le; Tl- thallium; PV- predictive value.

LESION ASSESSMENT

17

PRESSURE

There are several other types of CFR (see Fig. 2-20). The Doppler guidewire can be used to measure the absolute and relative CFVR, as well as the corrected CFVR [59,75,76]. The absolute C}VR may be reduced, owing to either epicardial stenoses or abnormalities in the microcirculation. For example, in a target vessel with an indeterminate lesion, an abnormal CFVR may be due to the lesion or to abnormal microcirculation. The relative CFVR and the corrected CFVR attempt to correct for abnormalities in the microcirculation in order to make the Doppler measurement more lesion specific. The relative CFVR is the ratio of the CFVR in the target vessel and the CFVR in a normal reference vessel l75,76]. If there is microcirculatory disease, both CFVR measurements will be abnormal and the ratio (relative CFVR) will be near unity. Relative CFVR values less than 0.80 suggest that the epicardial lesion is physiologically significant [74,75]. The relative CFVR is less useful when the target vessel CFVR is normal and cannot be used when there is rnultivessel disease without a reference vessel. The corrected CFVR also takes the microcirculation into account by correcting for age and baseline APV [77]. Multiple studies have shown an excellent correlation of Dopplerderived CFR and noninvasive functional testing during assessment of the functional significance of an intermediate angiographic coronary stenosis (Fig. 2-26) [78-84]. Most clinicians use a cut-off value of 2.0 when deciding the physiologic significance of an indeterminate stenosis, because this value has the greatest predictive accuracy for detecting ischemia by noninvasive tests. This value also corresponds to a lumen area of less than 4.0 mm2 by intracoronary ultrasound [17]. It is safe to defer revascularization in patients with intermediate lesions and normal coronary flow physiology by Doppler guidewire because these patients have a low cardiac event rate [85,86]. Doppler-derived CFR can also be used to assess the result of PCI. Following PTCA, normal physiology by Doppler guidewire (CFVR > 2.5) coupled with an acceptable angiographic result (< 35% diameter stenosis) results in a 16% angiographic restenosis rate and a 16% target lesion revascularization rate [87].

~- 1~ ·-··········

...•

The pressure guidewire is also an angioplasty-style guidewire (0.014 inch) with a pressure sensor near its tip. Both piezoelectric crystal micromanometer and fluid-filled pressure transducer systems have been used to successfully obtain high-fidelity pressure measurements in the distal coronary artery. In most pressure guidewires, the pressure-sensing region is 3 ern from the distal tip of the wire, allowing the pressure sensor to be moved back and forth across the stenosis without actually uncrossing the stenosis. Because pressure is ubiquitous across the diameter of the coronary vessel, it is easily recorded without the steering or manipulating required of Doppler velocity measurements. Unlike Doppler ultrasound, pressure measurements are familiar to most invasive cardiologists. In fact, translesional pressure gradients measured through the PTCA catheter were used in the early days of coronary intervention for assessing results [88]. These pressure measurements were subsequently abandoned, as neither the technology nor the understanding of coronary pressure physiology was fully developed. Early PTCA catheters were too large to accurately measure pressure gradients unless the lumens were quite large. Furthermore, early measurements of translesional pressure gradients at rest did not correlate with other tests of ischemia [89,90]. We now understand that a small resting pressure gradient does not exclude a physiologically significant lesion because a significant gradient may develop with hyperemia (Fig. 2-27). FRACTIONAL FLOW RESERVE

The concept of myocardial FFR was developed to overcome the inherent inaccuracies of the resting gradient [91]. It can easily be derived from pressure measurements from the distal coronary and aortic root during hyperemia. The myocardial FFR is defined as the ratio of hyperemic flow in a target vessel with a stenosis to hyperemic flow in the same target vessel if the stenosis were not present. Theoretically, these flows can be derived mathematically

···-·~········

.•..• ····15 ...

A

ATLAS OF INTERVENTIONAL CARDIOLOGY 18

Figure 2-27. Translesional pressure gradients measured at rest showing no gradient (A), mild (B), Continued on next page

from pressure gradients using Ohm's Law (voltage= resistance x current), or its hydraulic equivalent (pressure gradient = vascular resistance x flow). Myocardial flow at hyperemia can be derived as follows:

QStenosis

= p d -PV RMyo

where Q 5tenosis is the hyperemic flow, possibly reduced by the stenosis, and P d is the distal coronary pressure during hyperemia. The ratio of hyperemic flow in the presence of a stenosis to hyperemic flow without the stenosis, or myocardial fractional flow reserve, becomes:

QN = PA -Py RMyo

where QN is the theoretical normal hyperemic flow, P A and P v are the hyperemic aortic and venous pressures, respectively, and RMyo is the maximally dilated myocardial flow resistance. In the presence of a stenosis,

Pd -Pv FFRMyo =

QStenosis Qn

RMyo PA -Pv

=

pd- Pv PA-Pv

RMyo Figure 2-27. (Continued) moderate (C), and severe (D) gradients . •

·····~···········-··-·

150 ·

c . .' ·····-·-----·------·-----·o------

D

0 ---------··-----~------······- ---

CORRELATIVE STUDIES OF MYOCARDIAL FRACTIO AL FLOW RESERVE A D

ISCtlEMIC IEST

EERMYO

S~ECIEICITY

£Y:±

.eY:: 88

Dobutamin

100 8 0

100

3

< 0. 5 < 0 .72 < 0.68

46

MIBI

t!!..!Tt!QE Pijl eta/. )92 1 D Bru n eta/. )931 Bartun 1-. et a/. I 4)

45 60

100 95

ho

be eta/. )951 hamuleau et a/. 1961

152M D

181

< 0 .76 Dia tali FFR < 0.

Figure 2-28. Correlative studies of myocardial fractional flow reserve and noninvasive functional tests. Echo--echocardiogram; FFR- fractional flow

6 80

reserve; FFRMy0 - myocardial fractional flow reserve; MIBI- sestamibi; NA- not available; MVD- multivessel disease; PV- predictive value.

LESION ASSESSMENT 19

Assuming RM 0 is equivalent for the two conditions (as it should be if Jaximal hyperemia is achieved) and that Pv is small relative to the other pressures, then FFRM .0 simplifies to the ratio of distal coronary to aortic pressures. Stated another way, the FFRMyo value indicates the degree a stenosis limits hyperemic flow. Specifically, the FFRMyo (x 100%) yields the percent of normal hyperemic flow that a vessel with a stenosis can provide. As with Doppler methods, hyperemia can be achieved with a number of intracoronary and intravenous vasodilators, such as adenosine, papaverine, or ATP. A similar analysis of coronary collateral circulation can be performed to estimate the fractional collateral reserve, Qc/ QN [91].

ADVANTAGES AND CLINICAL CORRELATIONS

The pressure-derived FFRMyo has specific advantages over other methods of lesion assessment [78]. It has an unequivocal normal reference value of 1.0, is load-independent, can be used in multivessel disease, and takes into account and assesses the collateral circulation. Pressure-derived FFRMyo has correlated strongly with noninvasive functional tests (Fig. 2-28) [92-96]. In these studies, a value of FFRMyo less than 0.75 correlates with an abnormal noninvasive functional test for ischemia. In other words, if the vessel cannot supply 75% of the expected hyperemic flow, ischemia will usually result with stress. In practice, FFRMyo values in the 0.75 to 0.80 range are considered a gray area, and clinical judgment is

3

15

"

;

t:: ,Ji

> 0.95). In this group, the event rate (death, myocardial infarction, or target vessel revascularization by bypass surgery or percutaneous methods) at follow-up was only 4.9%. In 32% of the patients, the poststent FFR was between 0.90 and 0.95, and event rate was 6.2%. However, in 32% of patients, the poststent FFR was less than 0.90, and event rate was 20.3%. The event rate rose to 29.5% in the 6% of the patients whose FFR was less than 0.80 (Fig. 2-29).

required. PCI can be safely deferred with a low incidence of major adverse cardiac events if the FFRMyo is more than 0.75 [92,97]. PCI can be assessed with the pressure guidewire as well. Following PTCA, a value between 0.75 and 0.90 is considered a borderline result. Although the ischemia may be relieved, the restenosis rate will be high [98]. Conversely, an FFRMyo over 0.90 has a low restenosis rate even without stent placement opening the possibility of provisional stenting. Following stent placement, an FFRMyo value of 0.94 or greater correlated best with optimal stent deployment as judged by NUS [SO]. In addition, FFR after stenting is a strong independent predictor of outcome at 6 months [99,100]. In one study, a multicenter registry of FFR following angiographically successful stent placement, a total of 36% of the

1.30 1.25

1.20

.

Pd 2.0 > 2.0-2.5 and < 35% 0

RCfYR < 0.80

EfR

< 0.75 > 0.75 > 0.90

> 0.94

> 9.0 mm2, > 80% of r f r nee ar a, fu ll appo ilion

ATLAS OF INTERVENTIONAL CARDIOLOGY 22

Figure 2-35. Catheter-based anatomic and physiologic measurements. CFVR- Dopplerderived coronary flow reserve; DS--diameter stenosis; FFR- fractional flow reserve; IVUS-intravascular ultrasound; PCI- percutaneous coronary intervention; PICA- percutaneous transluminal coronary angioplasty; RCFVRrelative coronary flow reserve. (Adapted from Kern and Meier [4].)

include pressure signal drift and guide catheter-induced pressure damping. First-generation pressure guidewire transducer systems were unable to provide a stable pressure signal consistently (Fig. 2-30). The resulting pressure drift made the accuracy of the FFR measurements uncertain. For this reason, pressure recordings are made with the pressure transducer at the tip of the guide catheter both before and after the FFR measurements. It is imperative that the fluid-filled catheter pressures match those of the pressure guidewire. These pressure records need to be taken without a needle introducer device in the hemostatic valve, because such a device will lower the fluidfilled pressures by 5 to 10 mm Hg. If small-lumen guiding catheters are used (such as 6F diagnostic catheters), the radiographic contrast material should be flushed from the system to avoid further damping the fluid-filled pressure-measuring system. Whenever possible, large-lumen guiding catheters should be used, and balloons or other equipment should be removed from the guiding catheter. Ostial disease presents another challenge in the measurement of translesional pressure gradients. Pressure damping with guide catheter engagement typically results in a "ventricularization" of both the aortic and coronary pressures with an impairment of hyperemic and, possibly, resting coronary flow. Guide catheters with side holes can eliminate the distorted pressure tracing, but they should not be used because intracoronary vasodilator may be flushed out the side holes and maximal coronary vasodilation may not occur. The side holes also may not allow for maximal hyperemia, as they also provide a resistance to blood flow. The problem of pressure damping with engagement can easily be overcome with one of two methods. First, the guide catheter can be withdrawn from the ostium, and intravenous vasodilator, such as intravenous adenosine 140 jlg/kg/min, can be used. Second, intracoronary vasodilator can be very gently infused with the catheter slightly engaged and the pressure ventricularized. Immediately after infusion, the guide catheter can be slightly withdrawn to relieve the pressure damping (Fig. 2-31). Care must be taken to avoid vigorous flushing in a highly damped guide catheter position to avoid trauma to the ostium. This maneuver theoretically can also be performed with the Doppler guidewire, but in practice it is rarely successful because of changes in the position of the Doppler sample volume with guide catheter movement and subsequent loss of optimal signal. The former method is preferred for assessing ostial disease. Theoretical limitations to consider when one assesses coronary lesions with the pressure guidewire and the FFR method include right heart failure, tandem lesions, diffuse disease, and microcirculatory disease. In the derivation of the FFRMyo equation, it was assumed that the venous pressures were low and therefore could be ignored. As shown in Figure 2-32, the error in omitting venous pressure from the calculation can be calculated for any venous pressure, given mean aortic and coronary pressures. For typical values, the FFRMyo value will have less than a 10% error. However, if the venous pressure exceeds 15 to 20 mm Hg, the complete equation, including venous pressure, is required to accurately calculate FFRMyo· Tandem lesions may act as resistors in series to limit myocardial perfusion. It is tempting to simply perform individual FFRMyo measurements on each lesion separately to determine the significance of each. However, each lesion may affect the other lesion by limiting hyperemic flow. De Bruyne et al. [102,103] performed an elegant mathematical analysis of the

pressure signals demonstrating how to calculate the FFRMyo of each lesion separately, as shown in Figure 2-33. In these calculations, the Pw (coronary wedge pressure, or distal coronary pressure during total occlusion) must be measured, making them less clinically useful. A practical approach to assessing angiographically indeterminate tandem lesions is to first measure the FFRMyo distal to both lesions. If the FFRMvo is greater than 0.75, the two tandem lesions will not result "in ischemia with stress. No further evaluation or revascularization is needed. If the FFRMvo is less than 0.75, the two lesions in series have the potential for creating ischemia with stress. Next, perform a FFRMyo measurement with the transducer in between the lesions to assess the proximal FFRM 0 . This can be done with either intracoronary or intravenous ~asodilator, although the latter approach allows for assessment of both lesions with a single pullback. The lesion with the larger hyperemic pressure gradient should be intervened on first, followed by repeat hyperemic pressure measurements of the second lesion. If the measurement is still significant, percutaneous intervention of the second lesion should be performed. Diffuse disease can limit myocardial perfusion without any significant focal stenoses. In this situation, the diffusely narrowed vessel imparts increased frictional forces on the flowing blood, resulting in a reduced distal pressure. There will be a diffuse and gradual reduction in pressure from proximal to distal without a discrete drop in pressure. Interestingly, Gould et al. [104] have shown a graded, longitudinal, base-to-apex myocardial perfusion abnormality in patients with diffuse disease representing a progressive reduction in myocardial perfusion along the length of the coronary vessel. Although FFRMyo will be abnormal in these patients, there are no focal stenoses that can be treated and PCI is not indicated. Gradually pulling back the wire from distal to proximal to record pullback pressures during intravenous vasodilator infusion will reveal the gradual nature of the pressure loss [105]. Conversely, if a focal rise in pressure is recorded during the pressure wire pullback, percutaneous interventional treatment of that focal region may improve flow physiology. Perhaps the most important theoretical limitation to consider in assessing coronary lesions with the pressure guidewire and the FFR method is the presence of microcirculatory disease. The derivation of the FFRMyo equation assumes that the resistance in the microcirculation is minimal (ie, maximally dilated) and constant. In the presence of microcirculatory disease, maximal hyperemia will not be achieved and the FFRMyo measurement will overestimate the true FFRM 0 . However, the FFRMyo may still be of value to the interventfonalist trying to decide weather PCI is indicated. For example, consider a patient with longstanding diabetes mellitus and fixed microcirculatory disease with an indeterminate coronary lesion and a FFRMyo of 0.85. The patient's fixed microcirculatory disease may have impaired the CFR. The true FFRMyo may have been much lower (< 0.75) if the patient did not have fixed microcirculatory disease and could augment hyperemic flow. However, PCI is not indicated because the patient will still have fixed microcirculatory disease following the procedure. Removing the epicardial lesion will improve hyperemic flow by only 15% at most. Microcirculatory disease can be more problematic when it is transient, following acute myocardial infarction, rotational atherectomy procedures, saphenous vein graft interventions, or other interventions with no reflow [106]. Furthermore, treat-

LESION ASSESSMENT

23

values of 2.0 and 0.75 for CFVR and FFRMyo' respectively, because these values have been demonstrated to correlate best with noninvasive functional testing. Normal responses would be seen in quadrant 1, where both flow and pressure measurements are normal. Abnormal responses would be seen in quadrant 3, where both flow and pressure measurements are abnormal. Quadrant 2 represents abnormal microcirculation with normal FFRMyo but reduced flow. In these cases, there may also be a significant epicardial lesion with a falsely elevated FFRMyo owing to an impaired hyperemic response. Results in quadrant 4 are nonphysiologic because the flow response is normal, but there is a large hyperemic pressure gradient. Theoretically, such cases should not occur, but undoubtedly they will as our experience grows.

ment with cholesterol-lowering agents, antihypertensives (such as ACE inhibitors), or weight loss may improve endothelial function and microcirculatory disease, and with time hyperemic flow may increase. In cases of transient microcirculatory disease, the FFRMyo may overestimate the true FFRM 0 that may develop with time or medical treatment. A lesionymay seem less significant initially, but the FFRMyo will become more significant as hyperemic flow improves.

COMBINED PRESSURE-fLOW MEASUREMENTS The complete hemodynamic assessment of an obstruction to flow combines both flows and pressure gradient, eg, assessment of an obstructive valve lesion requires both cardiac output and transvalvular pressure gradient measurements [107-109]. When unclear, augmentation of transvalvular flows with exercise or inotropic stimulation is helpful. Obstructive coronary lesions can benefit from a similar analysis of both translesional pressure gradient and CBF. Combined pressure and flow measurements can now be made with a single guidewire. Combined pressure and Dopplertipped guidewires are currently under evaluation. In addition, pressure guidewires can utilize thermal methods for measuring relative coronary flow and coronary flow reserve [110,111]. Although there are many ways of combining pressure and flow data, the simplest model combines the CFVR and FFRMyo data, as shown in Figure 2-34 [112-114]. Four quadrants canoe made, based on normal or abnormal CFVR and FFRMyo responses. For an indeterminate lesion, we would select cut-off

CONCLUSIONS Intravascular ultrasound and physiologic guidewires are new tools that improve the angiographer's assessment of coronary atherosclerosis. In general, IVUS is used to further define the anatomy of the lesion, and physiologic guidewires are used to define the physiologic effect of the lesion (Fig. 2-35). Given the limitations of angiography, it is important that all physicians who perform or interpret coronary angiograms understand these new tools in order to move beyond coronary angiography.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Arnett EN, Isner JM, Redwood DR, et al.: Coronary artery narrowing in coronary heart disease: comparison by cineangiographic and necropsy findings. Ann Intern Med 1979, 91:350-356. Grondin CM, Dyrda I, Pasternac A, et al.: Discrepancies between cineangiographic and postmorten findings in patients with coronary artery disease and recent myocardial revascularization. Circulation 1974,49:703-708. Schwartz JN, Kong Y, Hackel DB, et al.: Comparison of angiographic and postmortem findings in patients with coronary artery disease. Am J Cardia/ 1975, 36:174-178. Kern MJ, Meier B: Evaluation of the culprit plaque and the physiological significance of coronary atherosclerotic narrowings. Circulation 2001, 103:3142-3149. Cieszynski T: lntracardiac method for the investigation of structure of the heart with the aid of ultrasonics. Arch lmmun Ter Down 1960,8:551-557. Born N, Lancee CT, vanEgmond FC: An ultrasonic intracardiac scanner. Ultrasonics 1972, 10:72-76. '\lissen SE, Gurley JC, Grines CL, et al.: Intravascular ultrasound assessment of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation 1991, 84:1087-1099. \Jishimura RA, Edwards WD, Warnes CA, et al.: Intravascular ultrasound imaging: in vitro validation and pathologic correlation. f Am Call Cardio/1990, 16:145-154. Fitzgerald PJ, St Goar FG, Connolly AJ, eta/.: Intravascular ultrasound imaging of coronary arteries. Are three layers the norm? Circulation 1992, 86:154-158. \Jishimura RA, Kennedy KD, Warnes CA, et al.: Intravascular ultrasonography: image interpretation and limitations. Echocardiography 1990, 7:469-474. Mintz GS, Nissen SE, Anderson WD, et al.: American College of Cardiology clinical expert consensus document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. JAm Coli Cardio/2001, 37:1478-1492.

12. Wenguang L, Gussenhoven WJ, Zhong Y, et al.: Validation of quantitative analysis of intravascular ultrasound images. Int 1Card Imag 1991, 6:247-253. 13. Potkin BN, Bartorelli AL Gessert JM, et al.: Coronary artery imaging with intravascular high-frequency ultrasound. Circulation1990, 31:1575-1585. 14. Pandian NG, Kreis A, O'Donnell T: Intravascular ultrasound estimation of arterial stenosis. 1Am Soc Echocardiogr 19S9, 2:390-397. 15. Hodgson J, Graham SP, Savakus AD, et al.: Clinical percutaneous imaging of coronary anatomy using an over-the-wire ultrasound catheter system. Int 1Card Imag 1989,4:187-193. 16. St. Goar FG, Pinto FJ, Alderman EL, et al.: Intravascular ultrasound imaging of angiographically normal coronary arteries: an in vivo comparison with quantitative angiography. 1Am Call Cardiol1991, 18:952-958. 17. Abizaid A, Mintz GS, Pichard AD, et al.: Clinical, intravascular ultrasound, and quantitative angiographic determinants of the coronary flow reserve before and after percutaneous transluminal coronary angioplasty. Am 1Cardia/ 1998, 82(4):423-428. 18. Briguori C, Anzuini A, Airoldi F, et al.: Intravascular ultrasound criteria for the assessment of the functional significance of intermediate coronary artery stenoses and comparison with fractional flow reserve. Am J Cardia/ 2001, 87(2):136-141. 19. Takagi A, Tsurumi Y, Ishii Y, et al.: Clinical potential of intravascular ultrasound for physiological assessment of coronary stenosis: relationship between quantitative ultrasound tomography and pressure-derived fractional flow reserve. Circulation 1999, 100(3):250-255. 20. Mintz GS, Popma JJ, Pichard AD, et al.: Limitations of angiography in the assessment of plaque distribution in coronary artery disease: a systematic study of target lesion eccentricity in 1446lesions. Circulation 1996, 93(5):924-931. 21. Pandian NG, Kreis A, Brockway B: Detection of intra-arterial thrombus by intravascular high-frequency two-dimensional ultrasound imaging: in vitro and in vivo studies. Am 1Cardio/1990, 65:1280-1283. 22. Jain A, Ramee SR, Mesa J, et al.: Intracoronary thrombus: chronic urokinase infusion and evaluation with intravascular ultrasound. Cath Cardiovasc Diag 1992, 26:212-214.

ATLAS OF INTERVENTIONAL CARDIOLOGY 24

23. Castagna MT, Mintz GS, WeissmanN, et al.: "Black hole": echolucent restenotic tissue after brachytherapy. Circulation 2001, 103(5):778. 24. Schoenhagen P, Ziada KM, Kapadia SR, et a/.: Extent and direction of arterial remodeling in stable versus unstable coronary syndromes: an intravascular ultrasound study. Circulation 2000, 101(6):598-603. 25. Rasheed Q, Nair R, Sheehan H, Hodgson JM: Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables. Am J Cardio/1994, 73(11):753-758. 26. von Birgelen C, Klinkhart W, Mintz GS, eta/.: Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study in vivo. JAm Call Cardial2001, 37(7):1864-1870. 27. von Birgelen C, Klinkhart W, Mintz GS, et al.: Size of emptied plaque cavity following spontaneous rupture is related to coronary dimensions, not to the degree of lumen narrowing. A study with intravascular ultrasound in vivo. Heart 2000, 84(5):483-488. 28. Maehara A, Mintz GS, Ahmed JM, et al.: An intravascular ultrasound classification of angiographic coronary artery aneurysms. Am J Cardiol 2001, 88(4):365-370. 29. Nissen SE, Yock P: Intravascular ultrasound: novel pathophysiological insights and current clinical applications. Circulation 2001, 103:604-616. 30. Nishimura RA, Higano ST, Holmes DR Jr: Utility of intracoronary ultrasound in determining the severity of lesions in the left main coronary artery. Mayo C/in Prac 1993,68:134-140. 31. von Birgelen C, Airiian SG, Mintz GS, ct al.: Variations of remodeling in response to left main atherosclerosis assessed with intravascular ultrasound in vivo. Am J Cardio/1997, 80(11):1408-1413. 32. Abizaid AS, Mintz GS, Abizaid A, eta/.: One-year follow-up after intravascular ultrasound assessment of moderate left main coronary artery disease in patients with ambiguous angiograms. JAm Cull Cardio/1999, 34(3):707-715. 33. Abizaid AS, Mintz GS, Mehran R, et al.: Long-term follow-up after percutaneous transluminal coronary angioplasty was not performed based on intravascular ultrasound findings: importance of lumen dimensions. Circulation 1999, 100(3):256-261. 34. Mintz GS, Pichard AD, Kovach ]A, et al.: Impact of preintervention intravascular ultrasound imaging on transcatheter treatment strategies in coronary artery disease. Am J Cardia/ 1994, 73(7):423-430. 35. Tobis JM, Mallery JA, Gessert J, et al.: Intravascular ultrasound cross-sectional arterial imaging before and after balloon angioplasty in vitro. Circulation 1989, 80:873-882. 36. Waller m~ Orr CM, Pinkerton CM, eta/.: Coronary balloon angioplasty dissections: "the good, the bad, and the ugly." JAm Call Cardio/1992, 20:701-706. 37. Fitzgerald PJ, Ports TA, Yock PG: Contribution of localized calcium deposits to dissection after angioplasty. Circulation 1992, 86:64-70. 38. Potkin BN, Keren G, Mintz GS, et al.: Arterial responses to balloon coronary angioplasty: an intravascular ultrasound study. JAm Call Cardio/1992, 20:942-951. 39. Stone GW, Hodgson JM, St Goar FG, ct al.: Improved procedural results of coronary angioplasty with intravascular ultrasound-guided balloon sizing: the CLOUT Pilot Trial. Circulation 1997, 95(8):2044-2052. 40. Frey AW, Hodgson JM, Muller C, et al.: Ultrasound-guided strategy for provisional stenting with focal balloon combination catheter: results from the randomized Strategy for Intracoronary Ultrasound-guided PTCA and Stenting (SIPS) trial. Circulation 2000, 102(20):2497-2502. 41. Honye J, Mahon DJ, Jain A, et al.: Morphological effects of coronary balloon angioplasty in vivo assessed by intravascular ultrasound imaging. Circulation 1992, 85:1012-1025. 42. Gerber TC, Erbel R, Gorge G, et al.: Classification of morphologic effects of percutaneous transluminal coronary angioplasty assessed by intravascular ultrasound. Am J Cardio/1992, 70(20):1546-1545. 43. Fitzgerald PJ, Yock PG: Mechanisms and outcomes of angioplasty and atherectomy assessed by intravascular ultrasound imaging. JClin Ultrasound 1993, 21(9):579-588. 44. Nakamura S, Colombo A, Gaglione A, et al.: Intracoronary ultrasound observations during stent implantation. Circulation 1994, 89(5):2026-2034. 45. Colombo A, Hall P, Nakamura S, et al.: Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995, 91(6):1676-1688. 46. de )aegere P, Mudra H, Figulla H, et al.: Preliminary results of the MUSIC study. J Invasive Cardial1996, 8 (suppl E):12E-15E.

47. Stone GW, St Goar FG, Hodgson JM, eta/.: Analysis of the relation between stent implantation pressure and expansion. Am J Cardio/1999, 83(9):1397-1400. 48. Fitzgerald PJ, Oshima A, Hayase M, et al.: Final results of the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study. Circulation 2000, 102(5):523-530. 49. HurSH, Kitamura K, Morino Y, et al.: Efficacy of postdeployment balloon dilatation for current generation stents as assessed by intravascular ultrasound. Am J Cardio/2001, 88(10):1114-1119. 50. Hanekamp CE, Koolen JJ, Pijls NH, et al.: Comparison of quantitative coronary angiography, intravascular ultrasound, and coronary pressure measurement to assess optimum stent deployment. Circulation 1999, 99(8):1015-1021. 51. Ahmed JM, Mintz GS, Weissman NJ, et al.: Mechanism of lumen enlargement during intracoronary stent implantation: an intravascular ultrasound study. Circulation 2000, 102(1):7-10. 52. Abizaid A, Pichard AD, Mintz GS, et al.: Acute and long-term results of an intravascular ultrasound-guided percutaneous transluminal coronary angioplasty /provisional stent implantation strategy. Am J Cardio/1999, 84(11):1298-1303. 53. Mudra H, di Mario C, de Jaegere P, et al.: Randomized comparison of coronary stent implantation under ultrasound or angiographic guidance to reduce stent restenosis (OPTICUS Study). Circulation 2001, 104(12):1343-1349. 54. Moussa I, Moses J, di Mario C, et al.: Does the specific intravascular ultrasound criteria have an impact on the probability of stent restenosis? Am JCardiol1999, 83:1012-1017. 55. Albiero R, Rau T, Schluter M, et al.: Comparison of immediate and intermediate-term results of intravascular ultrasound versus angiography-guided Palmaz-Schatz stent implantation in matched lesions. Circulation 1997, 96:2997-3005. 56. Leon MB, Bairn DS, Popma JJ, et al.: A clinical trial comparing three anti-thrombotic drug regimens after coronary artery stenting. The Stent Anticoagulation Restenosis Study Investigators. N Eng/ JMed 1998, 339:1665-1671. 57. Oemrawsingh PV, Mintz GS, Schalij MJ, et al.: Intravascular ultrasound guidance improves angiographic and clinical outcome of stent implantation for long coronary artery stenoses: final results of a randomized comparison with angiographic guidance (TULIP Study). Circulation 2003, 107:62-67. 58. McLeod AL, Northridge DB, Uren NG: Ultrasound guided stenting. Heart 2001, 85:605-606. 59. Gould KL, Kirkeeide RL, Buchi M: Coronary flow reserve as a physiologic measure of stenosis severity. JAm Call Cardio/1990, 15(2):459-474. 60. Gould KL, Lipscomb K, Hamilton G: Physiologic basis for assessing critical coronary stenosis. Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol1974, 33(1):87-94. 61. Klocke FJ: Measurements of coronary flow reserve: defining pathophysiology versus making decisions about patient care. Circulatiarz1987, 76(6):1183-1189. 62. Pijls NH, Van Gelder B, Van der Voort P: Fractional flow reserve. A useful index to evaluate the influence of an epicardial coronary stenosis on myocardial blood flow. Circulation 1995, 92(11):3183-3193. 63. Kemp HG Jr, Van Gelder B, VanderVoort P: Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms. Am J Cardia/ 1973, 32(3):375-376. 64. Epstein SE, Cannon RO 3d: Site of increased resistance to coronary flow in patients with angina pectoris and normal epicardial coronary arteries. JAm Call Cardio/1986, 8(2):459-461. 65. Brush JE Jr, Cannon RO 3rd, Schenke WH, et al.: Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy. N Eng! J Mcd 1988, 319(20):1302-1307. 66. Hamasaki S, AI Suwaidi J, Higano ST, et al.: Attenuated coronary flow reserve and vascular remodeling in patients with hypertension and left ventricular hypertrophy. JAm Coil Cardiol2000, 35(6):1654-1660. 67. Doucette JW, Cor! PD, Payne HM, et al.: Validation of a Doppler guide wire for intravascular measurement of coronary artery flow velocity. Circulation 1992, 85(5):1899-1911. 68. Segal J, Kern MJ, Scott NA, eta/.: Alterations of phasic coronary artery flow velocity in humans during percutaneous coronary angioplasty. JAm Col/ Cardial1992, 20(2):276-286. 69. Wilson RF, Wyche K, Christensen BV, et al.: Effects of adenosine on human coronary arterial circulation [see comments]. Circulation 1990, 82(5):1595-1606.

LESION ASSESSMENT

25

70. Jeremias A, Whitbourn RJ, Filardo SD, et al.: Adequacy of intracoronary versus intravenous adenosine-induced maximal coronary hyperemia for fractional flow reserve measurements. Am Heart J 2000, 140(4):651-657. 71. Wilson RF, White CW: Serious ventricular dysrhythmias after intracoronary papaverine. Am J Cardiol1988, 62(17):1301-1302. 72. Kern MJ, Deligonul U, Serota H, et al.: Ventricular arrhythmia due to intracoronary papaverine: analysis of QT intervals and coronary vasodilatory reserve. Cathet Cardiovasc Diagn 1990, 19(4):229-236. 73. Jeremias A, Filardo SD, Whitbourn RJ, et al.: Effects of intravenous and intracoronary adenosine 5'-triphosphate as compared with adenosine on coronary flow and pressure dynamics. Circulation 2000, 101(3):318-323. 74. Kern MJ, Bach RG, Mechem CJ, et al.: Variations in normal coronary vasadilatory reserve stratified by artery, gender, heart transplantation and coronary artery disease. JAm Call Cardiol1996, 28(5):1154-1160. 75. Baumgart D, Haude M, Goerge G, eta/.: Improved assessment of coronary stenosis severity using the relative flow velocity reserve. Circulation 1998, 98(1 ):40-46. 76. Kern MJ, Puri S, Bach RG, eta/.: Abnormal coronary flow velocity reserve after coronary artery stenting in patients: role of relative coronary reserve to assess potential mechanisms. Circulation 1999, 100(25):2491-2498. 77. Wieneke H, Haude M, Ge J, eta/.: Corrected coronary flow velocity reserve: a new concept for assessing coronary perfusion. JAm Coil Cardia/ 2000, 35(7):1713-1720. 78. Kern MJ, de Bruyne B, Pijls NH: From research to clinical practice: current role of intracoronary physiologically based decision making in the cardiac catheterization laboratory. jAm Call Cardio/1997, 30(3):613-620. 79. Miller DD, Donohue TJ, Younis LT, et al.: Correlation of pharmacological 99mTc-sestamibi myocardial perfusion imaging with poststenotic coronary flow reserve in patients with angiographically intermediate coronary artery stenoses. Circulation 1994, 89(5):2150-2160. 80. Joye JD, Schulman DS, Lasorda D, et al.: Intracoronary Doppler guide wire versus stress single-photon emission computed tomographic thallium-201 imaging in assessment of intermediate coronary stenoses. JAm Coil Cardiol 1994, 24(4):940-947. 81. Deychak YA, Segal J, Reiner JS, et al.: Doppler guide wire flow-velocity indexes measured distal to coronary stenoses associated with reversible thallium perfusion defects. Am Heart J 1995, 129(2):219-227. 82. Heller LI, Cates C, Popma J, et al.: Intracoronary Doppler assessment of moderate coronary artery disease: comparison with 201Tl imaging and coronary angiography. Circulation 1997, 96(2):484-490. 83. Danzi GB, Pirelli S, Mauri L, et al.: Which variable of stenosis severity best describes the significance of an isolated left anterior descending coronary artery lesion? Correlation between quantitative coronary angiography, intracoronary Doppler measurements and high dose dipyridamole echocardiography. JAm Call Cardiol1998, 31(3):526-533. 84. Schulman DS, Lasorda D, Farah T, eta/.: Correlations between coronary flow reserve measured with a Doppler guide wire and treadmill exercise te~ting. Am Heart J 1997, 134(1):99-104. 85. Kern MJ. Donohue TJ, Aguirre FV, eta/.: Clinical outcome of deferring angioplasty in patients with normal translesional pressure-flow velocity measurements. JAm Coil Cardiol1995, 25(1):178-187. 86. Ferrari M, Schnell B, Werner GS, Figulla HR: Safety of deferring angioplasty in patients with normal coronary flow velocity reserve. JAm Call Cardiol1999, 33(1):82-87. 87. Serruys PW, di Mario C, Piek L et al.: Prognostic value of intracoronary flow velocity and diameter stenosis in assessing the short- and long-term outcomes of coronary balloon angioplasty: the DEBATE Study (Doppler Endpoints Balloon Angioplasty Trial Europe). Circulation 1997, 96(10):3369-3377. 88. Anderson HV, Roubin GS, Leimgruber PP, et al.: Measurement of transstenotic pressure gradient during percutaneous transluminal coronary angioplasty. Circulation 1986, 73(6):1223-1230. 89. Wijns W, Serruys PW, Reiber JH, eta/.: Quantitative angiography of the left anterior descending coronary artery: correlations with pressure gradient and results of exercise thallium scintigraphy. Circulation 1985, 71(2):273-279. 90. Peterson RJ, King SB 3rd, Fajman WA, et al.: Relation of coronary artery stenosis and pressure gradient to exercise-induced ischemia before and after coronary angioplasty. JAm Coli Cardio/1987, 10(2):253-260. 91. Pijls NH, Bech GJ, el Gamal MI, et al.: Quantification of recruitable coronary collateral blood flow in conscious humans and its potential to predict future ischemic events. JAm Coli Cardio/1995, 25(7):1522-1528. 92. Pijls NH, De Bruyne B, Peels K, et al.: Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. N Engl f Med 1996, 334(26):1703-1708.

93. De Bruyne B, Bartunek J, Sys SU, Heyndrickx GR: Relation between myocardial fractional flow reserve calculated from coronary pressure measurements and exercise-induced myocardial ischemia. Circulation 1995, 92(1 ):39-46. 94. Bartunek L Van Schuerbeeck E, de Bruyne B: Comparison of exercise electrocardiography and dobutamine echocardiography with invasively assessed myocardial fractional flow reserve in evaluation of severity of coronary arterial narrowing. Am J Cardio/1997, 79(4):478-481. 95. Abe M, Tomiyama H, Yoshida H, Doba N: Diastolic fractional flow reserve to assess the functional severity of moderate coronary artery stenoses: comparison with fractional flow reserve and coronary flow velocity reserve. Circulation 2000, 102(19):2365-2370. 96. Chamuleau SA. Meuwissen M, van Eck-Smit BL, eta/.: Fractional flow reserve, absolute and relative coronary blood flow velocity reserve in relation to the results of technetium-99m sestamibi single-photon emission computed tomography in patients with two-vessel coronary artery disease. JAm Col/ Cardia/ 2001, 37(5):1316-1322. 97. Bech GJ. DeBruyne B, Bonnier HJ. eta/.: Long-term follow-up after deferral of percutaneous transluminal coronary angioplasty of intermediate stenosis on the basis of coronary pressure measurement. JAm Call Cardiol1998, 31(4):841-847. 98. Bech GJ, Pijls NH, DeBruyne B, et al.: Usefulness of fractional flow reserve to predict clinical outcome after balloon angioplasty. Circulation 1999, 99(7) :883-888. 99. Pijls NH, Klauss V, Siebert U, et al.: Coronary pressure measurement after stenting predicts adverse events at follow-up: a multicenter registry. Circulation 2002, 105:2950-2954. 100. Fearon WF, Luna L Samady H, et al.: Fractional flow reserve compared with intravascular ultrasound guidance for optimizing stent deployment. Circulation200l, 104:1917-1922. 10l.Pijls NH, Kern MJ, Yock PG, DeBruyne B: Practice and potential pitfalls of coronary pressure measuremen. Catheter Cardiovasc Interv 2000, 49(1):1-16. 102. DeBruyne B, Pijls NH, Heyndrickx GR, eta/.: Pressure-derived fractional flow reserve to assess serial epicardial stenoses: theoretical basis and animal validation. Circulation 2000, 101(15):1840-1847. 103. Pijls NH, DeBruyne B, Bech GL et al.: Coronary pressure measurement to assess the hemodynamic significance of serial stenoses within one coronary artery: validation in humans. Circulation 2000, 102(19):2371-2377. 104.Gould KL, Nakagawa Y, Nakagawa K, eta/.: Frequency and clinical implications of fluid dynamically significant diffuse coronary artery disease manifest as graded, longitudinal, base-to-apex myocardial perfusion abnormalities by noninvasive positron emission tomography. Circulation 2000, 101(16):1931-1939. 105. DeBruyne B, Hersbach F, Pijls NH, et al.: Abnormal epicardial coronary resistance in patients with diffuse atherosclerosis but "normal" coronary angiography. Circulation 2001. 104(20):2401-2406. 106. DeBruyne B, Pijls NH, Bartunek J. et al.: Fractional flow reserve in patients with prior myocardial infarction. Circulation 2001, 104(2):157-162. 107. DeBruyne B, Bartunek L Sys SU, et al.: Simultaneous coronary pressure and flow velocity measurements in humans. Feasibility, reproducibility, and hemodynamic dependence of coronary flow velocity reserve, hyperemic flow versus pressure slope index, and fractional flow reserve. Circulation 1996, 94(8):1842-1849. 108. Di Mario C. Gil R, de Feyter PJ. et al.: Utilization of translesional hemodynamics: comparison of pressure and flow methods in stenosis assessment in patients with coronary artery disease. Cathet Cardiovasc Diagn 1996, 38(2):189-201. 109. DeBruyne B, Pijls NH, Smith L, et al.: Coronary thermodilution to assess flow reserve: experimental validation. Circulation 2001, 104(17):2003-2006. 110. Pijls NH, DeBruyne B, Smith L, et al.: Coronary thermodilution to assess flow reserve: validation in humans. Circulation 2002, 105:2482-2486. 111. Meuwissen M, Siebes M, Chamuleau AJ, eta/.: Hyperemic stenosis resistance index for evaluation of functional coronary lesion severity. Circulation 2002, 106:441-446. 112. DiMario C, Krams R. Gil R, et al.: Slope of the instantaneous hyperemic diastolic coronary flow velocity-pressure relation: a new index for assessment of the physiological significance of coronary stenosis in humans. Circulation 1994,90:1215-1224. 113. DeBruyne B, Bartunek L Sys SK, eta/.: Simultaneous coronary pressure and flow velocity measurements in humans. Circulation 1996,94:1842-1849. 114. Meuwissen M, Chamuleau SA, Siebes M, et al.: Role of variability in microvascular resistance on fractional flow reserve and coronary blood flow velocity reserve in intermediate coronary lesions. Circulation 2001, 103(2):184--187.

ATLAS OF INTERVENTIONAL CARDIOLOGY

26

Equipment Selection and Techniques of Percutaneous Coronary Intervention John D. Altman and Charanjit S. Rihal When Gruentzig first developed balloon angioplasty in the late 1970s, generally only patients with proximal discrete single-vessel lesions could be approached [1]. As angioplasty techniques, equipment, operator experience, and adjunctive therapies improved over the years, the scope of angioplasty extended to acute coronary syndromes, multivessel disease, and higher risk categories of patients. For each patient, the question posed must be whether relief of a single stenosis or multiple stenoses is

possible and desirable, and whether complete revascularization is achievable. New technology has evolved, and many new devices have been used to treat specific types of lesions. Current devices used in catheterization laboratories include directional, extraction, and rotational atherectomy, stenting (now the most predominant treatment), lasers, and filters. Use of guide catheters, wires, and balloons is necessary, and common to most devices reviewed in this chapter.

of guide catheters. Stainless steel braiding was embedded in the material of the shaft to improve torque control, and to improve lubricity, very thin Teflon liners were added to the internal lumen of the catheter. These two changes also resulted in improved shaft strength. The use of nylon blends, which are stronger than polyurethane, has allowed for a reduction in shaft wall thickness to improve the luminal diameter for a given external size. The addition of radiopaque soft catheter tips has reduced the incidence of ostial trauma and has allowed more manipulation of the guide catheter while seating it in the target artery. Modern guide catheter design incorporates each of these features (Fig. 3-1) and provides excellent back-up for balloon passage by a combination of wall strength, which imparts inherent memory capabilities to hold the predetermined shape, and the ability to brace that shape within the aortic root against the contralateral wall. Coronary guide catheters are provided in shapes similar to diagnostic catheters. The most commonly used catheters are Judkins left and right catheters, Amplatz catheters, and various hybrids (Fig. 3-2). A number of other catheter shapes have been developed for use in coronary bypass grafts (Fig. 3-3). Guide catheters made from polyurethane are generally soft and therefore require more manipulation during balloon passage. Their softness leads to reduced back-up strength, which worsens at body temperature during prolonged procedures. Guide catheters made from nylon blends or polyurethane are intended for placement at the ostium of the target vessel and provide strong back-up without the need for manipulation. As with diagnostic catheters, the recent trend has been toward smaller sizes of guide catheters. Advances in technology have allowed thinner guide catheter walls, which retain intrinsic strength and resist kinking while providing adequate back-up. Guide catheter wall diameter has been reduced to as little as SF. A trend has emerged in interventional cardiology that smaller is better. This trend favors the use of SF and 6F guiding catheters for all coronary interventions, with the rationale that the use of smaller sheaths decreases access site complications. The potential disadvantage of reducing guide catheter size comes at the loss of

GUIDE CATHETERS Angioplasty guide catheters possess several characteristics that differentiate them from diagnostic catheters. The guide catheter lumen must be large and lubricated enough to accommodate the balloon catheter or device to be delivered. The catheter also must have features that enable it to serve as a platform from which the balloon or device may be advanced against resistance into the artery [2]. Because early balloon catheter shafts were large, the initial guide catheters used were also large-approximately 9.4F in external diameter. Balloon catheters were made of polytetrafluoroethylene (Teflon; DuPont Co., Wilmington, DE), which made them very stiff and difficult to maneuver. Polyurethane guide catheters were less rigid but became too soft during prolonged exposure to body temperature. However, a number of changes have been made to improve the performance

Figure 3-1. The features of guide catheters for interventional coronary procedures. The stainless steel braiding improves torque control and the Teflon (DuPont, Wilmington, DE) liner added to the internal lumen improves lubricity. The soft tip reduces the incidence of ostial trauma and allows safer manipulation.

Figure 3-3. Some catheter designs for special circumstances. From left to right, the left venous bypass catheter curve for reaching vein grafts on

the anterior surface of the ascending aorta; the internal mammary artery guiding catheter for selecting the ostium of the left internal mammary artery; the multipurpose catheter used principally for downgoing right coronary arteries and especially for right venous bypass grafts; and the hockey stick catheter useful in some upgoing venous bypass grafts and in small aortic roots.

Figure 3-2. Commonly used angioplasty guide catheters for the native coronary arteries. From left to right, the Judkins left coronary curve, the Judkins right coronary curve, the Amplatz left coronary curve, and the Amplatz right coronary curve.

ATLAS OF INTERVENTIONAL CARDIOLOGY

28

back-up, dye injection flow rates, and the ability to use larger adjunctive devices. In a prospective randomized study, Metz et al. [3] demonstrated a decrease in femoral access site complications with 6F catheters (13.S% with 6F vs 23.5% with 7 /SF), lower contrast volumes (136 + 6S mL with 6F vs 16S + 9S mL with 7 /SF), and reduced procedure times (36 + 22 min with 6F vs 41 + 28 min with 7 /SF). The success rates with 6F, 7F, and 8F guiding catheters were equal. The failure rate for SF guiding catheters was approximately 10%, with the need to increase the size during the intervention. The benefit of SF guiding catheters has yet to be realized, especially in the era of arterial closure devices. Guide catheter selection can be the difference between a successful and a failed intervention. Heavily calcified, tortuous arteries require a guiding catheter with extra support to allow for distal delivery of coronary stents. If balloon angioplasty alone is planned, a less supportive catheter may suffice. Increasing the size of the catheter (6F to SF) will also increase the guide catheter support. Ostial disease can prevent adequate flow around the guide catheter, resulting in ischemia. This problem is improved by the use of side-hole guides (Fig. 3-4). It is important to remember that the recorded pressure from a side-hole guide is in the aorta and it may not reflect the coronary perfusion pressure. Brisk clearance of injected contrast media ensures that coronary flow is satisfactory. Guide catheter selection is discussed in more detail in Chapter 4, Guide Selection.

GUIDEWIRES Simpson introduced guidewires in the early 1980s [4], but these initial wires were extremely stiff and nonsteerable. The introduction of steerable guidewires in 1982 and continued improvements in guidewire construction since then has increased the ability to treat complex and chronically occluded arteries. Guidewires are useful to cross the lesion, to support equipment crossing the lesion, and to minimize trauma to the vessel wall. Crossing the lesion is facilitated by one-to-one torque transmission, giving the operator precise tip control to steer the wire

through the lesion. Special lubricant coatings are applied to reduce wire friction within the arterial plaque. Guidewires are made with a central solid cylindrical core that tapers in thickness for the last 2 to 1S em. A coil or plastic sleeve surrounds the solid core so that the outer wire diameter is consistent. The external coil has a variable length of radiopaque platinum wire at the tip. Tapering of the core is the most important characteristic of a guidewire. The thickness of the core at the tip of the guidewire determines whether a wire is soft or stiff; the thicker the core, the stiffer the wire. Stiff guidewires transmit torque better than soft guidewires and provide excellent crossability in complex lesions and chronic total occlusions. The malleable tip is manufactured by soldering a flattened ribbon to the distal end of the core wire (shaping ribbon construction) or by flattening the central core (core to tip construction) (Fig. 3-S). Core to tip construction, where the central stainless steel core runs the entire length of the guidewire to the distal tip, increases tip stiffness and torquability. The disadvantage of stiff guidewires is an increased risk of wire perforations. A soft guidewire is often the first wire used because it provides good tip control with little risk of injury to the arterial wall. Support guidewires should not be confused with stiff guidewires. Guidewire support is determined by the thickness of the core in the working segment of the wire, from 2 to 1S em. Support guidewires are often constructed with a soft, atraumatic tip so that significant tapering of the core occurs in the last 2 em of the wire. However, unlike stiff guidewires, support wires have significant core tapering at the tip, from 1 to 2 em. This abrupt transition causes the guidewire to prolapse when attempts are made to cannulate severely angled bifurcations (Fig. 3-6). Support wires are usually placed through an over-the-wire balloon or transfer catheter after first crossing the lesion with another wire. Supportive guidewires are ideal for straightening tortuous vessels and for providing a platform for pushing stents in calcified arteries. Guidewires are available in sizes ranging from 0.010 to 0.021 inch in diameter and from very flexible to relatively stiff configurations. Wires can be obtained with or without a preformed distal J curve. Opacity of the distal tip is provided by incorpo-

t rnal w1r

oil

haping ribbon

A

8 Figure 3-4. A Judkins right coronary guide catheter with side holes. These proximal holes provide for blood flow into the artery even though the guide catheter tip may be completely occluding a small right coronary ostium.

u nllal taper

Tip

Figure 3-5. A diagram of guidewire designs. A, Guidewire with a central core that is attached by a shaping ribbon to the wire tip. B, Guidewire with a tapered central core going all the way to the tip. This wire is less flexible but produces a smoother transition between the flexible tip and the stiffer body of the wire.

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION

29

rating platinum and can vary from the distal3 em to 35 em (Fig. 3-7). A short radiopaque tip allows the longer portion of the wire across the lesion to be radiolucent, which can be an ad van-

Ri ht nl rior obliqu

tage when visualization of a lesion is difficult, when the lesion is in a small-diameter vessel, or when two wires are required at one time (Fig. 3-8).

i w

c Figure 3-7. Wire radiopacity. A, Radiopaque guidewire allows clear indication of the path of the artery and minimizes the risk of unrecognized coiling of the wire in the aortic root. Disadvantages are that in small arteries it may obscure either the severity of the lesion or the post-angioplasty result. B, Wire with radiopaque distal tip. This wire allows excellent opacification of the angiographic appearance of the lesion after the procedure.

Figure 3-6. Illustration of the problem of a prolapsing wire tip during

attempts to enter the side branches. A, The guidewire tip enters the circumflex artery. B, The soft tip prolapses out of the circumflex artery carried by the stiffer proximal shaft, the axis of which is directed toward the left anterior descending coronary artery. C, A wire with a smooth transition between the soft tip and the stiffer shaft allows a smooth traverse of the wire into the branch vessel. LAD-left anterior descending coronary artery.

ATLAS OF INTERVENTIONAL CARDIOLOGY 30

The properties and shape of the guidewire play an important role in the cannulation of specific arteries and in the crossing of the lesions. For example, by curving the distal tip of the guidewire in a relatively broad radius or creating a double curve similar to a Judkins catheter, the wire can be directed selectively into the prob-

lematic left anterior descending or circumflex origin. The shaping of the distal tip can be achieved in many ways, ranging from pulling the wire over a needle or introducer tool in a fashion similar to that used for curling decorative ribbon (Fig. 3-9A) to simply bending the tip between the forefinger and thumb (Fig. 3-9B). Figure 3-8. Two minimally opaque wires crossing a bifurcation lesion. Heavily radiopaque wires would significantly impair visualization in this instance.

Figure 3-9. A, The technique of bending the guidewire using a wire

of bending the guidewire between the thumb and index finger. By pressing firml y, a very short radius curve is achieved. By rolling the guidewire, a rather broad curve can be accomplished.

introducer. Bending without moving the wire produces a short radius curve and gently stripping gives a broad radius curve. B, The technique

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION 31

Guidewires are steered using a proximal torquing device (Fig. 3-10). Because modern guidewires are highly responsive, clockwise or counterclockwise rotation of less than one complete turn is generally satisfactory for achieving the desired direction. It is unnecessary and undesirable to turn the wire constantly in one direction because excessive torquing can fracture the internal core wire and unravel the surrounding protective coil. Although various techniques of maneuvering the guidewire have been used successfully, we find that in the most difficult wire placement situations, the optimal technique is for a single operator to move the wire freely with control of both advancement and withdrawal as well as clockwise and counterclockwise rotation. Atraumatic crossing of a lesion avoids any disruption of the plaque that can lead to acute closure or dissection. To achieve this a traumatic crossing, it is important to observe any buckling of the guidewire because this indicates some impedance to smooth progression of the wire past the lesion. Withdrawal and reorientation of the guidewire is required when buckling occurs to obtain a nontraumatic passage of the wire. Repeated rotation of 180° in a clockwise and counterclockwise direction also seems to aid guidewire advancement and reduce subselection of unwanted small branches. Much of guidewire maneuvering is a learned technique that remains something of an art form. Because there are many variations in coronary anatomy and lesion geometry, the operator must have broad experience to be aware of all the possible guidewire maneuvers.

BALLOONS The original balloons used by Gruentzig were made of polyvinyl chloride, which was inherently of low compliance and allowed balloon angioplasty to be performed successfully without excessive stretching of the artery [5]. Previous attempts using slotted catheters with elastic balloons or elastic balloons within nylon mesh constrainers had not been effective. As with other areas of angioplasty, balloon technology has advanced greatly since the early 1990s [6]. Desirable features of modern balloon catheter shafts include low profile, pushability, trackability, and freedom of wire movement. Other features determined by balloon material include compliance, the ability to tolerate high-pressure inflations, and memory to return to their original shape and size. Balloons are considered either compliant or noncompliant. Compliance refers to the growth of the balloon at higher pressures. For example, a 3.0-mm compliant balloon is 3.0 mm at 8 atm, 3.25 mm at 12 atm, and 3.5 mm at 16 atm, while a 3.0mm noncompliant balloon is only 3.1 mm at 20 atm. Compliant balloons are ideal when the artery size is in question; a single balloon will achieve a size from 3.0 to 3.5 mm. Noncompliant balloons are often used in post-stent dilatation, especially when a part of the stent is underexpanded due to lesion calcification.

Figure 3-1 0. Illustration of finger movements for a wire torquing device. A, Neutral position. B, Counterclockwise rotation. C, Clockwise rotation. Further wire rotation is seldom needed.

ATLAS OF INTERVENTIONAL CARDIOLOGY 32

Although there are currently several different designs available, contemporary balloons have certain features in common, including a central wire lumen of varying size and length and an inflation channel coursing through the length of the catheter shaft into the balloon. There are several different balloon materials, which have varying thicknesses, radial strength, and compliance features. The lumen of balloon catheters is designed to accommodate guidewire diameters ranging from 0.010 to 0.018 inch for most balloon systems. The shaft of the catheter is usually made of some relatively stiff material, such as polyethylene or nylon, to provide good pushability, and it varies in outer diameter from 4.3F to as small as 1.7F. Although the larger catheter shafts may provide more pushability, the same characteristics can be included in catheters with smaller shafts. These small shafts also provide more space in the guiding catheter for injection of contrast media, which improves visualization of the lesion. Small shaft catheters also allow the synchronous use of two balloons in complex bifurcation lesions.

exchange, fixed wire, and perfusion. Selection of a balloon catheter system depends partly on lesion characteristics and partly on operator preference and laboratory staffing. OVER-THE-WIRE SYSTEM

The over-the-wire system consists of a balloon catheter with a movable guidewire passing through the entire length of its central lumen (Fig. 3-11). The inflation channel and the lumen for the wire may be formed by coaxial tubes or may lie adjacent in the shaft body in extruded designs. The over-thewire design also allows for exchange of the guidewire while the balloon is in the coronary artery, a maneuver that is not possible with rapid exchange systems. Over-the-wire systems generally provide a slightly better push than do rapid exchange systems owing to the presence of the wire coaxially throughout the entire length of the balloon catheter. RAPID EXCHANGE SYSTEM

The rapid exchange system is popular because it provides for replacement of the balloon catheter over a standard-length guidewire by a single operator. Instead of a central lumen for the guidewire that runs the entire length of the balloon catheter, the wire lumen exits the balloon catheter several centimeters proximal to the distal tip. From this point

CATHETER SYSTEMS Catheter systems for delivering balloons have evolved greatly, and there are now four categories in use: over-the-wire, rapid

lnflation/d flation lum n

Shaft deign A

B Figure 3-11. A, Illustration of the over-the-wire catheter system. Note that the wire passes through the entire length of the balloon catheter and a lumen separate from the balloon inflation lumen. Inset, left, is a coaxial catheter design. It is actually a catheter within a catheter, with the balloon inflation and deflation lumen being the space between the two catheters. Right, an illustration of an extruded catheter design that produces balloon inflation channels within the catheter material while maintaining a separate lumen for the guidewire. B, An example of an over-the-wire balloon catheter tip. C, The assembled over-the-wire balloon and inflation device

attached to the balloon inflation port. Note the guidewire with the rotating adapter attached.

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION

33

FIXED-WIRE SYSTEM

the guidewire travels separately from the balloon catheter (Fig. 3-12A, B) [7,8]. This system allows the operator to fix the wire with one hand and advance the balloon with the other (Fig. 3-12C). The design of these systems allows for smaller catheter shaft diameters, which makes them particularly useful when guide catheter size is limited or when double balloons are required. The rapid exchange system also allows for easy removal and exchange of the balloon, which may result in a reduction in fluoroscopy time.

In the fixed-wire system, the balloon and wire advance as one unit (Fig. 3-13). In some designs, the wire moves freely within the balloon lumen, whereas in others the wire and balloon move and rotate as a single device. Fixed-wire balloons usually have the lowest profiles and are therefore useful in distal locations, in combination with other balloons in bifurcation lesions, and in situations in which very tight lesions prevent passage with any other balloon. Traditionally, these balloons have not been as Figure 3-12. Rapid exchange catheter system. A and B, Note that the wire travels separately from the balloon catheter except in the distal portion of the catheter, where the wire travels within the balloon catheter in its own separate lumen. C, Balloon advancement with one hand while fixing the guidewire in a stationary position with the other.

Balloon mark r

E

A

/

A

11 point of w~r

Balloon marker

Guid wire

c

B

balloon-on-a-wire systems can achieve the lowest crossing profiles and are useful in situations in which over-the-wire or monorail balloon advancement is impossible.

Figure 3-13. A, Fixed-wire catheter system. The balloon and the wire advance as one unit. There is no central lumen for wire placement, and the guidewire is attached directly to the tip of the balloon. B and C, These

ATLAS OF INTERVENTIONAL CARDIOLOGY 34

steerable as over-the-wire systems; however, modern versions have improved torque response. PERFUSION BALLOONS

Perfusion catheters allow flow through the treated artery while dilation is in progress. The catheter shaft just proximal to the balloon has multiple small holes connecting to the central wire lumen and another set of small holes beyond the balloon that allow exit of blood distal to the lesion. Flow is maximized when the wire is withdrawn (Fig. 3-14) [9]. This system allows blood to perfuse the distal artery while the balloon is inflated. The system is used principally for maintaining distal perfusion during balloon inflation and for improving the angiographic appearance of dissected arteries. The catheter also has been used as the primary dilating catheter when coronary artery occlusion seems to be unduly problematic or when a prolonged balloon inflation could be beneficial. Perfusion balloons are available in rapid exchange configurations and with additional length. Figure 3-15 illustrates that the majority

of these balloons have larger crossing profiles; however, recent designs have somewhat lower profiles and excellent push that allow this type of balloon to be considered as a primary device. After placement of the catheter, the guidewire is pulled back beyond the proximal holes to allow maximal flow during inflations. After deflation of the balloon, the guidewire is replaced through the central lumen to a site distal in the artery. During this maneuver, it is important to ensure that the wire does not exit the side holes or become embedded in the arterial wall. When the wire first exits the balloon, even the softest wires will become very stiff, increasing their propensity for arterial dissection. If the wire movement is not free, it is generally better to fix the wire just proximal to the distal end of the balloon catheter (which is distal to the lesion) and withdraw the balloon slightly while advancing the wire. When the balloon is removed further from the wire, the tip will become softer. The artery also will be easier to visualize with injections of contrast media.

A

Figure 3-14. A, Illustration of a perfusion catheter system. Note that holes in the perfusion shaft proximal to the balloon allow flow of blood to enter the catheter lumen and exit from holes distal to the balloon . B, Angiogram of a perfusion catheter inflated in the circumflex artery, with distal flow maintained. C, Illustration of perfusion of a distal arterial segment through a perfusion balloon.

C

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION

35

BALLOON MATERIALS Several balloon materials with differing strengths and compliance features are now available. The three most commonly used plastic materials are polyethylene (PE), polyolefin copolymer (POC), and nylon, each of which has significantly different characteristics. Balloons made of polyethylene terephthalate (PET) are less compliant and are tolerant of high pressures. These balloons typically achieve their nominal dimension early in the inflation period, below 3 atm, and do not change size greatly or burst until they reach pressures greater than 15 atm, or even 20 atm. Nylon (Duralyn; Cordis, Miami, FL) also has low compliance and a tolerance of high pressures but does not reach nominal size until a pressure of 8 atm is achieved. Conversely, the POC family of balloons is more compliant and thicker, and stretches with

4-r------------------------------------~

3.75 E E .: 3.5

/ /// ~p:

E

g

..···~··,.""'

c:

,'.•~

3

~

CD

Duralyn

...........-

~

:.0 3.25

;•;; "" ---~~

2.75

Pr

ur , atm

Figure 3-15. Relationship between inflation pressure and balloon diameter for 3-mm balloons made of polyethylene (PE), polyolefin copolymer (POC), nylon (Duralyn; Cordis, Miami, FL), and polyethylene terephthalate (PET). PET balloons are least compliant at higher pressures; the diameter of roc balloons increases the most with pressure increase.

increasing balloon inflation pressures. Balloons made of POC reach nominal size at 6 atm (POC6) or 8 atm (POC8). POC6 has greater compliance, achieving a larger size for a given pressure. Intermediate in compliance are PE600 and high-density polyethylene (HOPE). The different compliance properties of the various materials are demonstrated in Figure 3-16, indicating the changes in balloon diameter that can be produced by increasing inflation pressure for each material in a 3-mm balloon. It is true that most lesions can be approached and treated successfully with any of the modern balloon catheters. However, there are some situations in which the compliance features of the balloon should be considered. In addition, the ultimate size of the balloon at the pressure that is likely to be required must be considered when judgments are made about balloon size selection. Lesions that are long or have some element of calcification may indicate that there are softer and firmer components at different sites in the lesion. If some portions of the lesion require high pressure, compliant balloons may exceed their nominal dimension in the softer portions of the artery, whereas the harder portion might remain undilated. A less compliant balloon in this situation would be preferred because it would reach nominal size at low pressure and very little change in size would occur regardless of the pressure applied. In this situation, sizing of the balloon would be aimed at approximating the normal segment of the target artery. The age of the patient and the chronicity of symptoms may also indicate the required inflation pressures. Compliant balloons also have their role. The ability of a balloon to cross a lesion depends on the size of the wrapped balloon, the ability to transmit forward push via the shaft, and the balloon material. PE600, POC, and nylon catheter balloon materials wrap very well and seem to offer the least resistance to crossing a tight lesion or tortuous segment. In general, compliant balloons are sized slightly smaller than the target artery size to allow for expansion if higher pressures are required. Because accurate selection of balloon catheter size is difficult, it frequently is helpful to be able to increase the size of the balloon while performing the procedure. In this situation, the size of the more compliant balloon can be increased by raising increments in the pressure if the result achieved at low pressure is unsatisfactory. This "dialing up" the size of the balloon is helpful in many situations, particularly if the initial sizing has been some-

DIAMETERS I MM ACHIEVED BY 3-MM DIAMETER BALLOO S MADE OF VARIO US MATERIALS, ACCORD! C TO THE PRESSURE APPLIED

~RESSURE,

a1a1

POLYOLEFI CQPOLYMER B

2.79 3.00

4

6 8 10 L

14 16 'Durahn

A A Ofdl~.

E.E.f1QQ

l:::liCl:::l-QE SITY POLYETl:::lYLE E

A

2.82

A

-· 0 3.00 3.10 .20 3.29 3.38

3.00 3.11 __ 1 3.33.43

A

POLYETHYLE E IEREPl:::lil:::l LAIE 2.75 2.83 2.92 3.00 .0 3.1 3.26 .35

UREII:::l

2.95 .04 3.08 3.11 .14 3.19 .2 4

M1am1, FL.

Figure 3-16. Diameters in mm achieved by 3-mm diameter balloons made of various materials, according to the pressure applied.

ATLAS OF INTERVENTIONAL CARDIOLOGY 36

.0 .13 3.22 3.30 .36 3.42 3.47

what underestimated. If multiple lesions are to be approached with the same balloon, one must bear in mind that, following high-pressure inflations, some compliant balloons do not return entirely to their preinflated size. Subsequent inflations, even to the lower pressures, may achieve a larger dimension than would have occurred with the initial inflation. If low-pressure angioplasty is contemplated, then noncompliant balloons that reach the desired diameter at 3 to 4 atm are preferred.

pretreatment with acetylcysteine (600 mg orally twice a day) on the day before and day of intervention is useful [10]. Aspirin (325 mg orally) is administered in all patients and clopidogrel (75 mg/ d for 4 days or 300 mg on the day of the procedure) is given if coronary stenting is planned. If a history of allergy to contrast material is known or suspected, steroids and antihistamines should be administered, ideally beginning 12 hours before the procedure. The inguinal region is shaved in preparation for percutaneous transluminal coronary angioplasty (PTCA), an intravenous line is inserted into the left arm, and fluids are administered.

BALLOON SIZES AND lENGTHS Balloons are available in diameters from 1.5 to 6 mm and in lengths from 1 to 4 em. Quarter sizes are available in the smaller balloons. Long balloons are favorable for use in long lesions and do not straighten as easily as shorter balloons, which may have advantages in tortuous arteries.

INTERVENTION VASCUlAR ACCESS

The majority of coronary intervention procedures are performed from the femoral artery, which is cannulated using the Seldinger technique [11]. It is important to puncture the common femoral artery below the inguinal ligament but above the bifurcation into superficial and profunda vessels to ensure that adequate compression of the vessel will be possible when the sheaths are removed. Punctures at or below the bifurcation are more likely to result in arterial laceration, limb ischemia, or both when the vessels are small or diseased . The common femoral artery is located 1 em below the inguinal ligament lateral to the femoral vein (Fig. 3-17). The two popular styles of vascular needles, single-wall and Cournand, are shown in Figure 3-18. The single-wall needle has a greater tendency to plug with subcutaneous tissue than does the Cournand; however, the single-wall needle favors puncturing of only the anterior wall of the artery. Peripheral vascular disease can make insertion of sheaths more difficult. Tortuous vessels and peripheral stenoses can be overcome by using 0.035-inch hydrophilic guidewires and long femoral sheaths. Traversing the tortuous diseased iliac artery can sometimes be accomplished using the Judkins right diagnostic catheter and injecting contrast boluses to visualize the lumen and direct the tip through the narrow-

PROCEDURE PREINTERVENTION

Prior to coronary intervention, patients receive an explanation of the procedure, including the operator's estimate of success, possible complications, risks, and benefits. A booklet, videotape, or both describing the procedure and an explanation by the nursing staff help to ensure that patient and family are well informed and also help to reduce anxiety. PREINTERVENTION PREPARATION

Before coronary intervention, the patient undergoes tests including electrocardiogram , hemoglobin, platelet count, blood urea nitrogen, electrolytes, and creatinine screening. In patients with elevated creatinine, 6 hours of intravenous hydration and

In umal

Pu ' tu r I

·~~··~~/ Profunda f('fll()(.J I a rt

\ Figure 3-17. Anatomic diagram of the relationship of the vascular structures in the inguinal triangle. The femoral artery should be punctured between the inguinal ligament and the bifurcation. Puncture at the carina or below the bifurcation may result in hematoma formation or pseudoaneurysm.

Figure 3-18. Top, Cournand-style needle with a central-style stylette. Bottom, Single-walled needle.

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION 37

ings (Fig. 3-19). The use of a lubricated guidewire such as the Terumo guide (Terumo Corporation, Tokyo, Japan) can facilitate passage across a severely diseased iliofemoral system. If these techniques are unsuccessful or aortic disease is occlusive, the procedure can be performed from the arm after radial or brachial arterial puncture or brachial artery cutdown. More recently, miniaturization of diagnostic and therapeutic catheters has allowed consideration of alternative arterial access sites. Radial catheterization, a recently popularized technique, can be accomplished using SF or 6F catheters. The radial artery in particular offers a number of potential advantages: it is very

Figure 3-19. The Judkins right coronary guide catheter can be torqued, and with injections of small amounts of contrast medium can be directed at the residual lumen in a tortuous iliac system. When this maneuver is performed carefully, prolonged efforts to cannulate a diseased, tortuous iliac system can sometimes be avoided.

superficial, easily evaluable, and compressible. Most importantly, it is not an end-artery, and as long as ulnar artery patency is ensured, no major complications have been reported as a result of occlusion. In contrast, brachial arterial occlusion can be a catastrophic complication and is a surgical emergency. No major nerves or veins are in the anatomic vicinity of the maximal palpated radial artery pulse over the radial styloid, making the likelihood of neuropathies and arteriovenous fistulas extremely small. Infrequently encountered anatomic anomalies that can make brachial procedures problematic do not interfere with passing catheters from the radial artery. Bed rest, frequently a source of significant patient discomfort following cardiac catheterization, is unnecessary. Some disadvantages also exist, including the small caliber and the propensity of the radial artery to spasm, which can result in discomfort upon inserting and removing arterial sheaths. Sublingual nitroglycerin (0.3 to 0.6 1-1g depending on systemic blood pressure) is administered. Verapamil (1-S mg) may be administered intra-arterially, and systemic heparin (2SOO-SOOO U) is also used. A number of commercially available kits specifically designed for facilitating radial access are available (Fig. 3-20A). In most patients, diagnostic angiography can be accomplished with SF catheters; 6F sheaths will allow all types of guiding catheters to be placed. In some patients, 7F sheaths may be placed, although these are rarely necessary. Coronary and graft procedures may be readily performed. In the case of left internal thoracic conduits, the left radial artery is preferred, although it can be cannulated from the right radial with difficulty (Fig. 3208). A long sheath (which extends almost to the level of the brachial artery in most patients) is helpful to avoid spasm of the proximal radial artery during subsequent catheter manipulation. Standard manipulation techniques for brachial catheterization are equally applicable from the radial approach. Following the procedure, verapamil or nitroglycerin may be administered and the sheath is pulled. If necessary, a calcium channel blocker can also be instilled. Due to the small caliber of the radial artery, its superficial location, ease of compression, and surrounding soft tissues, it is not necessary to wait for normalization of anticoagulation parameters; sheath.s may be safely pulled in the presence of systemic anticoagulants, abciximab, and thrombolytic agents. To obtain hemostasis, 1S to 30 minutes of gradually decreasing pressure are generally sufficient, and a mild pressure dressing can be applied if desired. Patients may walk, use their arm, and otherwise care for themselves immediately following the procedure. If patients are on systemic anticoagulants, a mild pressure dressing and wrist splint may be used for 1 to 2 hours.

A coated with a hydrophilic polymer to allow easy passage into the radial artery. B, A long sheath covering the proximal radial artery is helpful in preventing spasm of that segment.

Figure 3-20. Vascular sheath kits. Intravascular access to the radial artery can be readily achieved through the use of specially designed vascular sheath kits. A, The dilator tapers to 0.018-inch diameter, and the sheath is

ATLAS OF INTERVENTIONAL CARDIOLOGY 38

The brachial artery is punctured above the skin crease at the elbow at a point of strong pulsation (Fig. 3-21), or brachial cutdown may be performed. MEDICATION

Procedural medications include sedatives, such as midazolam given intravenously as 0.5 to 1 mg boluses, and narcotics, such as fentanyl given intravenously as 25 to 50 j..lg boluses, to make the patient comfortable. Heparin is administered as a bolus. However, the controversy continues over whether low-dose (5000 IU), weight-adjusted (70 to 100 IU /kg), or high-dose (10,000 IU) heparin is superior. The optimal activated clotting time (ACT) is also unknown, ranging from less than 200 seconds to more than 350 seconds [12-14]. In the setting of glycoprotein IIb/IIIa antagonists, an ACT between 200 to 250 seconds is generally recommended. High- and low-risk patients benefit from the routine use of glycoprotein lib/Ilia antagonists [15,16]. However, the benefit in low-risk nonurgent coronary interventions may not be cost-effective. POSTINTERVENTION

Patient management is directed toward avoidance of dehydration or overhydration in hemodynamically compromised patients and close monitoring for evidence of acute occlusion, which is most likely to occur in the first 4 to 6 hours. Telemetry is used in most patients for the first 12 to 16 hours, and attention is drawn to patients with chest pain or electrocardiographic changes. Figure 3-21. Anatomy of the antecubital fossa. Note that the puncture site is slightly above the brachial crease and opposite the medial condyle of the humerus.

INTRAVENOUS fLUIDS AND HEPARIN

To reduce the incidence of hypotension and aid in the renal clearance of contrast agents, patients are encouraged to drink fluids and are hydrated with intravenous fluid at a rate of 75 to 150 mL/h for 6 to 12 hours. Postprocedure intravenous heparin infusions are not routinely continued. If the heparin infusion is to be prolonged following the intervention, an arterial closure device is often used. If the compression method for sheath removal is used, the heparin infusion is restarted without a bolus 3 to 6 hours after hemostasis is achieved. SHEATH MANAGEMENT

The vascular sheaths should be removed as soon as possible after the procedure to minimize the chance of vascular complications and to enhance patient comfort. The removal generally occurs 4 to 6 hours after the procedure, and we have found it useful to assess bedside parameters of clotting to ensure that hemostasis will not take too long. Sheaths are removed when the ACT is less than 160 seconds. The vagal stimulus from sheath removal should not be underestimated, and atropine should be at hand to correct bradycardia or hypotension. Yawning, nausea, and a relative bradycardia in the presence of mild hypotension may be subtle clues to vagal activity, and liberal use of intravenous atropine (0.4 to 0.6 mg) is encouraged. A number of our patients undergoing routine coronary interventions receive arterial closure devices. All of these sealing devices reduce time to hemostasis, allowing patients to ambulate more quickly. However, none have significantly decreased major access site complications. POSTPROCEDURE TESTS AND MEDICATION

The patient should undergo troponin or creatine kinase testing at 8 hours and 16 hours post procedure, and an ECG should be done immediately after the procedure and repeated the next day. All patients receive aspirin (81 to 325 mg/ d). Clopidogrel (75 mg/ d) is essential if a coronary stent is used or if in-stent restenosis was treated. Clopidogrel is typically used for 28 days because of the low rate of agranulocytosis and the potential for late (greater than 14 days) stent thrombosis. If brachytherapy was performed and a new stent placed, clopidogrel should be continued for 1 year or for at least 3 to 6 months if a new stent is not placed. Cholesterollowering drugs are instituted, as appropriate, as well as antianginal agents if incomplete revascularization has been achieved. ACE inhibitors are often the antihypertensive drug of choice because they may reduce further ischemic events. Prior to discharge, patients receive a thorough indoctrination regarding lifestyle modification (eg, diet, exercise, cessation of smoking), and subsequent pharmacologic therapy and followup plans are discussed.

EQUIPMENT SELECTION AND TECHNIQUES OF PERCUTANEOUS CORONARY INTERVENTION

39

REFERENCES 1. Gruentzig AR: Transluminal dilatation of coronary artery stenosis [letter]. Lancet 1978, II:263. 2. Arani DT: A new catheter for angioplasty of the right coronary artery and aorta-coronary bypass graft. Cathet Cardiovasc Diagn 1985, 11:647-653. 3. Metz D, Meyer P, Elaerts J: Comparison of 6F with 7F and SF guiding catheters for elective coronary angioplasty: results of a prospective, multicenter, randomized trial. Am Heart J 1997, 134:131-137. 4. Simpson JB, Bairn OS, Robert EW, et al.: A new catheter system for angioplasty. Am JCardio/1982, 49:1216-1222. 5. Talley JD, Hurst JW, King SB, et al.: Clinical outcome five years after attempted percutaneous transluminal coronary angioplasty in 427 patients. Circulation 1988, 77:820-829. 6. King SB III: Angioplasty from bench to bedside. Circulation 1996,93:1621-1629. 7. Bonze! T, Wollschlager H, Meinertz T, et al.: The steerable monorail catheter system: a new device for PICA [abstract]. Circulation 1986, 74(suppl):II-459. 8. Bonze! T, Wollschlager H, Kasper W, et al.: The sliding rail system (monorail): description of a new technique for intravascular instrumentation and its application to coronary angioplasty. Z Kardiol1987, 76(suppl 6):119-122. 9. Stack RS, Quigley PJ, Collins G, et al.: Perfusion balloon catheter. Am J Cardia/ 1988, 61:776-806.

10. Tepel M, van der Giet M, Zikek W: Prevention of radiographic contrast-agent-induced reductions in renal function by acetylcysteine. N Engl f Med 2000, 343(3):180-184. 11. Seldinger SI: Catheter replacement of the needle in percutaneous arteriography: a new technique. Acta Radial Scand 1953,39:368. 12. Chew DP, Bhatt DL, Topol EJ: Defining the optimal activated clotting time during percutaneous coronary intervention: aggregate results from six randomized, controlled trials. Circulation 2001, 103:961-966. 13. Kaluski E, Krakover R, Vered Z: Minimal heparinization in coronary angioplasty-how much heparin is really warranted? Am J Cardia/ 2000, 85:953-956. 14. Koch KT, Piek JJ, Lie KI: Safety of low-dose heparin in elective coronary angioplasty. Heart 1997, 778:517-522. 15. O'Shea JC, Hafley GE, Tcheng JE: Platelet glycoprotein lib/lila integrin blockade with eptifibatide in coronary stent intervention: the ESPRIT trial: a randomized controlled trial. JAMA 2001, 285:2468-2473. 16. The EPIC Investigators: Use of a monoclonal antibody directed against the platelet glycoprotein lib /lila receptor in high-risk coronary angioplasty. N Eng! J Med 1994,330:956-961.

ATLAS OF INTERVENTIONAL CARDIOLOGY

40

Guide Selection Dieter F. Lubbe and Verghese Mathew The successful interventional treatment of coronary lesions depends on the ability of the operator to direct the equipment to the site. Although the interventional equipment chosen may differ for each lesion, it is necessary to have in one's armamentarium the knowledge and experience to utilize guide catheters, guidewires, balloons, and devices in a way that allows access to all the arterial segments. Guide catheter selection is an important consideration in the planning of percutaneous coronary intervention (PCI), because poor guide selection may prevent successful balloon or stent delivery. Considerations include choice of primary and secondary distal catheter curves, as well as internal guide diameter. The optimal guide catheter shape is determined mainly by aortic root width and angulation, as well as angle of origin of the coronary ostium (Fig. 4-1). Guide diameter should be based on anticipated equipment requirements, as well as the degree of guide catheter support needed. Generally, all percutaneous transluminal coronary angioplasty (PTCA) balloon catheters and all but the largest coronary stents (5.0 mm) can be delivered with most 6F guiding catheters. If cutting balloon angioplasty is anticipated, a 7F or SF guide may be required, depending on the nominal balloon size. Most giant lumen SF guides can accommodate rotational atherectomy burrs up to 2.15 mm in

»

.I

-----

-

-......-. ---~ -->-~~~----

-

....... ~

-----

diameter, and a 7F or SF guide should also be used if "kissing" balloon angioplasty is anticipated. Guides as small as SF are now available, through which most coronary stents can be delivered. Although larger diameter catheters generally provide more support for balloon catheter or stent advancement, smaller guiding catheters may provide more support in selected cases by allowing atraumatic deep engagement into the coronary artery, particularly in the right coronary artery (RCA). The standard 100-cm-long guiding catheter is suitable for PCI in most lesion subsets. However, when one treats a distal lesion in the native vessel through a saphenous vein bypass graft, or when a distal left anterior descending coronary artery (LAD) lesion is approached through a tortuous left internal mammary artery (LIMA) graft, PTCA or stent catheters may not reach the target lesion. In these cases, use of a shorter, 90cm guiding catheter allows most lesions to be reached. Compared with diagnostic coronary catheters, guiding catheters have a stiffer shaft, a larger internal diameter, which may be standard, large, or giant lumen, and a reinforced, threelayer construction. The outer layer consists of either polyurethane or polyethylene for improved stiffness. The middle layer is a wire matrix that allows for torque generation, and the inner layer consists of a smooth Teflon coating (Fig. 4-2).

\ -~ """:'-:-. f • .

.,

..

-· "::

- ~- - ,__, ~ · ~-~ · .... -=~.....

'

-

_,

~ i;,~>W_•I

,&.·

i' .. ·1 . .

·J~A '.

- ,

.

lEFT ANTERIOR DESCENDING CORONARY ARTERY

JL

JR

XB

AR

AL

HS

IMA

LCB

MP

Although the LAD appears to arise horizontally from the left main coronary artery (LMCA), it actually courses in a superior and an anterior direction (Fig. 4-3). Therefore, guide catheters that point superiorly, such as the Judkins left coronary catheter (Fig. 4-4A), are usually preferred [2]. The tip will point in a greater or lesser cranial direction, depending on the length between the primary and secondary curves and how far the heel or secondary curve is advanced into the aortic root. If the distance between the primary and secondary curves is long, the catheter remains in the axis of the aorta and cannot be advanced very far down into the aortic root. In this case, the tip of the catheter points more inferiorly (Fig. 4-4B). If the distance between the primary and secondary curves is short, the catheter can be advanced farther into the aortic root, allowing the tip to point in a more cranial direction (Fig. 4-4C). For the average aortic root, a 4-cm Judkins left catheter is appropriately sized, but the 3.5-cm Judkins curve may be more effective for patients with the LAD in a very superior direction or in those with a narrow aortic root. If the aorta is enlarged-as in patients with hypertension or long-standing aortic valve disease-a larger Judkins curve, such as the 4.5-cm or larger, may be required (Fig. 4-4D). In difficult cases, the orientation of the LAD can be appreciated best in the left anterior oblique (LAO) view with caudal angulation, known as the spider view (Fig. 4-5). In this view, the LMCA and its bifurcation into the LAD and left circumflex (LCX) arteries can be seen by "looking up" from under the LMCA. The LAD courses toward the top of the image, and the

Figure 4-1. Commonly used coronary guiding catheters. AR-Amplatz right; AL-Amplatz left; XB-extra back-up; H5-hockey stick; IMAinternal mammary; JL-Judkins left; JR-Judkins right; LCB-left coronary bypass; MP- multipurpose. (Adapted from Safian and Freed [1] .)

Figure 4-2. Guide catheter construction. The outer layer of the guide catheter is polyurethane or polyethylene, the middle layer is a wire matrix, and the inner layer is a smooth Teflon coating.

Figure 4-3. View of the left main coronary artery (LMCA) from the left with the atrial appendage removed and the pulmonary artery divided and lifted up. The left anterior d escending coronary artery (LAD) courses superiorly and anteriorly from the LMCA. LCX- left circumflex artery.

ATLAS OF INTERVENTIONAL CARDIOLOGY 42

LCX courses to the right. When the LMCA is very short, it is preferable to use the short-tip left coronary catheter. By working in the LAO caudal projection, advancement of the guide catheter will bring the tip more superiorly and direct it into the ostium of the LAD (Fig. 4-4C). Obviously, overmanipulation of catheters in the LMCA must be avoided; however, with the softtip guide catheter configuration, gentle manipulation can be performed safely. In addition to the superior or cranial orientation of the LAD, the vessel also proceeds in an anterior direction. To achieve the anterior direction of the tip, the catheter shaft must be rotated in a counterclockwise direction at the groin with the tip located in the ostium of the LMCA. This maneuver may seem paradoxical

because counterclockwise rotation applied to a catheter free in the aorta produces posterior rotation of the tip. However, when the tip of the catheter is entrapped in the ostium of the LMCA, counterclockwise rotation causes the heel or secondary curve of the catheter to be forced in a posterior direction. The fulcrum effect of the LMCA ostium then directs the tip anteriorly (Fig. 4-6). The Amplatz catheter also can be used for selecting the LAD [3]. By selecting the properly sized curve, excellent back-up can be achieved (Fig. 4-7). However, because its primary curve is downward, the Amplatz is usually better suited for selection of the LCX (Fig. 4-7). The recently developed Voda curve provides another option for added back-up, and it is useful in the LCX and ramus intermedius (Fig. 4-8).

c

B

Figure 4-4. A, Judkins left coronary catheter engaging the left main coronary artery (LMCA) with coaxial alignment of the LMCA, pointing toward the left anterior descending coronary artery (LAD). B, Judkins left coronary catheter, pointing downward due to a long secondary curve. This oversized catheter will not adequately engage the LMCA. C,judkins left coronary catheter with a shorter secondary curve, allowing the tip to point upward toward the LAD. D , A long secondary curve segment is necessary for the patient with a widened aorta, a 4.5- or 5-cm Judkins catheter usually is required. LCX- left circumflex artery.

Figure 4-5. The left main coronary artery as seen from the left anterior oblique caudal view (the "spider view"). This view is best for separating the left anterior descending coronary artery (LAD) and the left circumflex artery (LCX) for rapid wire placement.

GUIDE SELECTION 43

LEFT CIRCUMFLEX ARTERY Selection of the LCX usually can be achieved with the Judkins left coronary catheter curve if the length between the two curves is not too short and the catheter is not advanced too far down into the aortic root, so that the tip remains directed inferiorly (Fig. 4-9). However, the Amplatz guide is preferred when the angle between the LMCA and LCX approaches 90° (Fig. 410) or when better back-up is needed in the circumflex system. Such situations arise when the lesion is tight and hard to cross, when it is on a curve, or when it is situated distally. The shape of the Amplatz catheter is such that the primary curve points inferiorly and provides not only easier cannulation of the LCX but also improved back-up as the secondary curve is braced against the aortic cusp and against the contralateral aortic wall (Fig. 4-10). The Amplatz catheter can be positioned in any projection by advancing the secondary curve into the coronary cusp to force the primary curve and the tip upward in the direction of the LMCA ostium. Gentle clockwise rotation at the groin

will direct the tip to the ostium. The Amplatz catheter seats quite snugly into the LMCA; thus, its use should be avoided in the presence of LMCA disease to reduce the chance of traumatic dissection during engagement or removal (Fig. 4-11). Extraction of the Amplatz catheter from the LMCA must be undertaken with care. In most cases, disengagement can be achieved by advancing the Amplatz catheter and its secondary curve deeper into the root of the aorta. This forces the tip backward, out of the LMCA (Fig. 4-12). When disengaged, the catheter is rotated to orient it away from the coronary ostium and then withdrawn. When this maneuver does not work and the tip is forced farther into the coronary artery by catheter advancement, the catheter can be pulled straight back in a gentle fashion, disengaging it from the ostium. The soft tip of modern catheters allows this maneuver to be accomplished without undue trauma to the normal LMCA. Intermediate between the Judkins and the Amplatz curves is the Voda curve (Fig. 4-13). This type of catheter enters the LMCA much as does the Judkins catheter. Because there is no curve at the tip, however, the catheter points in a less caudal direction Figure 4-6. View of the left main coronary artery from above. Counterclockwise rotation of the Judkins left coronary catheter forces the body of the catheter in a posterior direction while turning the tip of the catheter toward the left anterior descending coronary artery (LAD) . L-left aortic valve cusp; LCX-left circumflex artery; N-noncoronary aortic valve cusp; R-right aortic valve cusp.

Figure 4-7. A, Amplatz left catheter in the left main coronary artery (LMCA). Note that the tip is naturally directed toward the ostium of the circumflex artery. B, Angiogram showing the Amplatz guide catheter in the LMCA directing a guidewire into the circumflex artery. LAD-left anterior descending coronary artery; LCX-left circumflex artery.

ATLAS OF INTERVENTIONAL CARDIOLOGY 44

Figure 4-8. Voda catheter in the left main coronary artery. Note the neutral position of the tip, which makes it suitable for intervention in the circumflex coronary artery, ramus intermedius, and left anterior descending coronary artery. LAD-left anterior descending coronary artery; LCX-left circumflex artery.

than does the Judkins. The long tip beyond the curve allows the heel of the catheter to offer firm back-up from the contralateral aortic wall. This catheter often provides adequate back-up for circumflex procedures except when the LCX arises at a very severe caudal angle from the LMCA. The extra back-up (XB) shape is similar to the Voda configuration. Occasionally, cases involving the LCX that are initially approached with a Judkins shape may prove impossible because of inadequate back-up. Rather than immediately changing to an Amplatz or Voda catheter, several maneuvers may be helpful. Withdrawal of the catheter to direct the tip inferiorly may restore coaxial aligrunent and allow advancement of the balloon. An alternative approach is to advance the guide catheter farther, well down into the aortic root. This causes the tip to ride superiorly, creating a U-tum between the tip of the guide catheter in the LMCA and the

LCX. If this is unsuccessful in providing adequate back-up, further advancement of the Judkins catheter may cause the entire tip of the catheter to prolapse into the aortic root, turning the primary curve over and pointing downward, simulating the position achieved with the Amplatz catheter. This maneuver is seldom needed. Changing to an Amplatz or Voda catheter usually solves the backup problem and is usually the preferred maneuver (Fig. 4-14). Changing a guide catheter becomes more difficult if the lesion has already been crossed by a guidewire. If guidewire placement was difficult, it is desirable not to recross the lesion. Techniques have been developed to allow exchange of guide catheters over angioplasty guidewires. The use of exchange wires with long radiopaque tips facilitates this procedure by minimizing the chance of failing to notice an overly redundant loop of radiolucent wire in the aortic root. Long extra-support

Figure 4-9. Judkins left coronary catheter with a long secondary curve segment, creating an inferior direction of the tip in the left main coronary artery. This sizing is correct for intubating the left circumflex coronary artery. LCXleft circumflex artery.

Figure 4-11. Use of the Amplatz catheter should be avoided in the presence of disease of the left m ain coronary artery (LMCA). There is the potential for trauma as the catheter is pulled out of the coronary artery, creating a fulcrum effect during which the tip penetrates the inferior wall of the LMCA.

Figure 4-10. Amplatz catheter placed in the left main coronary artery. Note the inferior direction of the tip pointed toward the left circumflex coronary artery. LCX-left circumflex artery.

Figure 4-12. Correct removal technique for the Amplatz catheter. Pushing the catheter forward frequently allows the tip to prolapse out of the left main coronary artery, and then rotation of the catheter allows the tip to be directed away from the orifice. It can then be removed.

GUIDE SELECTION 45

Figure 4-13. Proper positioning of the Voda catheter in the left main coronary artery. N ote the excellent back-up orientation for cannulation of the circumflex artery. Also note the potential for a traumatic removal of the catheter simply by p ulling it back, because there is no terminal downward curve.

wires also can help. Once the guide catheter is withdrawn from the coronary ostium, it can be helpful to pass a 0.035- or a 0.038inch guidewire beside the angioplasty wire up the descending aorta and around the arch to support the exchange (Fig. 4-15).

coaxial to the RCA (Fig. 4-19). In this situation, back-up will be inadequate for advancement of the balloon catheter. In order to achieve adequate back-up, the catheter should be aligned by

RIGHT CORONARY ARTERY The right coronary artery usually arises anterolaterally from the right coronary cusp (Fig. 4-16A). However, many minor variations can make cannulation and co-axial alignment of catheters difficult, including a more anteriorly placed origin (Fig. 4-16A) and an acutely angled superior take-off "shepherd's crook" (Fig. 4-16B). Most RCAs are entered effectively with the Judkins right coronary guide catheter (Fig. 4-17). The 4-cm Judkins catheter is appropriately sized for most aortic roots, although small aortic roots may require the 3.5-cm size. With the horizontal or moderately down-going or moderately up-going configuration, the Judkins catheter ordinarily is effective. The maneuver for RCA cannulation is identical to that used for the diagnostic RCA catheter. With the catheter in the aortic root, by rotating the shaft clockwise and gently withdrawing it, the tip will select the RCA ostium (Fig. 4-18). When the RCA arises anterior in the right cusp, the tip of the catheter will not be

Figure 4-15. Guide catheter exchange procedure over an angioplasty guidewire using a O.D38-inch guidewire for support. This heavy guidewire provides adequate support for advancing the replacement guide catheter without displacing the coronary guidewire from its position in the coronary artery.

Figure 4-14. The Judkins left coronary catheter can be prolapsed into the coronary root, producing a strong back-up downward curve of the tip. This maneuver is seldom required.

. . '

-i---

Ant rior

I

I

,

A

I

I I

ATLAS OF INTERVENTIONAL CARDIOLOGY 46

Figure 4-16. A, Right coronary artery (RCA) arising normally from the right coronary cusp and more anteriorly (dashed area). B, Acutely angled superior take-off of the RCA ("shepherd's crook"). L-left aortic valve cusp; N-noncoronary aortic valve cusp; R-right aortic valve cusp.

additional clockwise rotation to allow the tip to engage into the ostium (Fig. 4-20A). This maneuver can be appreciated best by viewing the RCA guide catheter in the right anterior oblique (RAO) view [4] (Fig. 4-20B). When the shepherd's crook or a markedly superior take-off of the RCA is encountered, right guide catheters with tips pointing in a cranial direction are necessary. The Judkins right guide catheter, which is adequate for angiography, is often too small to provide back-up, and therefore the Amplatz left 1 catheter usually is selected (Fig. 4-21). A Champs or hockey stick guide are also suitable in this setting. The Arani catheter, with its double-reverse curve, eliminates the need for torque and is particularly useful in patients who are older and have very tortuous iliac arteries, which make catheter torquing very difficult. The secondary curve of the Arani catheter determines the direction of the distal curve. This will cause the tip to lie anteriorly and to the right in the usual location of

the RCA ostium (Fig. 4-22). When the RCA is directed caudally, the multipurpose catheter is ideally suited to provide optimal back-up (Fig. 4-23).

VEIN CRAFTS Surgeons generally anastomose vein grafts to the aorta in relation to the target vessel grafted. The more posterior the destination of the left-sided grafts, the higher they are located on the aorta (Fig. 4-24). The top graft generally goes to the distal LCX, and the lowest graft goes to the LAD. Most left-sided grafts arise in a cranial direction from the aorta. Although the Judkins right coronary or left bypass guiding catheters frequently engage the graft ostium well, support with these guides may be limited, and the Amplatz left 1.5 catheter often provides the best back-up (Fig. 4-25). Because the catheter can enter deep

Figure 4-18. Maneuver for entering the right coronary artery (RCA) with the Judkins right coronary guide catheter. A, The catheter is positioned above the ostium of the RCA pointed toward the left coronary cusp. B, The catheter is rotated clockwise, causing the tip to turn anteriorly and to the right. C, The shaft of the catheter lies against the lesser curve of the aortic arch, pushing the catheter tip in a caudal direction as it descends and enters the RCA. Alternatively, the maneuver can be started below the ostium of the RCA and the catheter withdrawn while the clockwise rotation is being done. Figure 4-19. The aortic root viewed from above. The anterior origin of the right coronary artery (RCA) results in misalignment of the guide catheter tip (dotted figure), and continued clockwise rotation brings the catheter into coaxial alignment (solid figure).

Figure 4-17. Shape of a Judkins right coronary

guide catheter.

GUIDE SELECTION 47

into the ostium, side holes are preferred in most cases. Seating is best achieved by clockwise rotation of the catheter to orient the tip to the ostium of the graft. When the tip of the catheter catches the ostium of the graft the catheter is advanced to obtain the optimal back-up. The multipurpose catheter also can be used for superiorly directed vein grafts by the similar maneuver of engaging the ostium of the graft and advancing the catheter so that it prolapses down into the aortic root, directing the tip superiorly into the target graft (Fig. 4-26). Hockey stick catheters also are helpful occasionally. The most troublesome left vein graft locations are those that are placed far to the left, toward the inner curve of the aortic root. Again, the Amplatz catheters are usually best in selecting these ostia; however, lengthening the tip of a multipurpose catheter with

A

the heat gun can achieve a shape that can reach across the aortic root and cannulate these grafts. Right coronary grafts usually are placed on the anterior aspect of the aorta and travel in a caudal direction. Because of this downward orientation of the graft, the multipurpose guide catheter usually provides excellent coaxial alignment. Right coronary grafts are engaged by applying clockwise rotation to achieve a rightward direction in the LAO projection. It is easy and may be desirable to position the catheter several centimeters into the graft. Obviously, this should be avoided in the presence of proximal graft disease. When approaching a lesion in the native vessel through a saphenous vein bypass graft, a regular 100-cm guide may be too long to allow delivery of equipment to the lesion. A shorter, 90-cm guiding catheter is preferred in this situation.

8

Figure 4-20. A, Right anterior oblique (RAO) view of the intubation of an anterior take-off right

coronary artery (RCA), showing misalignment of the Judkins right coronary catheter. B, After clockwise rotation, appearance of the Judkins catheter as seen from the RAO view.

Figure 4-21. An Amplatz left 1 catheter entering the right coronary artery (RCA) as seen from the left anterior oblique view. This catheter is very suitable for superior take-off of the RCA. Figure 4-22. A, Double-curved Arani catheter positioned in the ostium of the right coronary artery (RCA). This catheter is occasionally helpful in treating patients who have severe aorto-iliac tortuosity. B, Photograph of an Arani curve catheter.

ATLAS OF INTERVENTIONAL CARDIOLOGY 48

more commonly than is the right internal mammary artery, which is sometimes taken as a free graft and attached to the aortic wall. Both vessels arise from the respective subclavian arteries. The left subclavian artery has an independent origin from the aortic arch, and the right subclavian artery arises from the brachiocephalic artery, which usually also gives origin to the right internal carotid artery. Guide catheters for selecting the internal mammary arteries are shaped similarly to diagnostic internal mammary artery catheters and have a very short and severe primary curve (Fig. 4-27). The right internal mammary artery is sometimes better selected with the use of a Judkins right catheter guide. To minimize the chance of ostial dissection, a 6F catheter is preferred. Selection of the subclavian arteries is achieved by placing the catheter, with or without the guidewire protruding, around the arch beyond the origin of the desired artery. The catheter is then gently withdrawn and rotated counterclockwise to direct the tip superiorly until the guidewire or catheter tip enters the subclavian origin (Fig. 4-28). The 0.035- or 0.038inch guidewire is then advanced into the subclavian artery and farther distally in the axillary artery. Next, the guide catheter can be advanced over the guidewire beyond the origin of the internal mammary artery, which is usually situated inferiorly to the thyrocervical trunk and distal to the vertebral artery. Cannulation of the artery is best accomplished in the frontal view, with the patient's arms down by the side. Small flush injections of nonionic contrast medium and gentle withdrawal of the guide catheter can identify the location of the ostium. Gentle counterclockwise rotation of the catheter tip directs it anteriorly and enables it to enter the vessel selectively (Fig. 4-28). In situations where the internal mammary artery is difficult to engage, a coronary guidewire with or without a

MAMMARY ARTERIES With evidence of improved long-term patency rates, the internal mammary artery is now used routinely as a coronary bypass conduit. The left internal mammary artery is used Figure 4-23. Multipurpose catheter entering the right coronary artery (RCA). This catheter is well-suited for supporting interventions in the RCA when the proximal segment is directed caudally.

Figure 4-24. Typical positioning of vein grafts on the aorta for bypassing left coronary artery segments. The more p osterior the d estination of the left-sided grafts, the higher they are located on the aorta .

Figure 4-25. Amplatz left 1.5 catheter selecting vein graft ostium. This curve is usually optimal for vein grafts that have been p laced on the aorta toward the inside of the curvature of the ascending aorta.

GUIDE SELECTION

49

Figure 4-26. Multipurpose guide catheter entering the ostium of the left coronary bypass graft. By advancing this guide catheter, a strong back-up loop against the opposing wall can sometimes be obtained.

balloon catheter or the hydrophilic Terumo wire (Terumo Corp, Tokyo) may be used to select the internal mammary artery; this then functions as a guide rail for cannulation with the angioplasty guide. This has been necessary more commonly in the right internal mammary artery. Figure 4-27. The catheter curve for the left internal thoracic artery. Note that the primary curve has a very short, severe bend for intubating the take-off of the internal thoracic artery from the left subclavian artery. The Judkins right coronary guide catheter is a better choice for the right subclavian artery.

Although disease in the internal mammary artery is rare, lesions at the distal anastomotic site or in the recipient coronary artery are not uncommon. As the internal mammary artery is frequently long and tortuous, a short 90-cm guide may be used to allow the anastomotic lesion, or native LAD lesion, to be reached through the graft.

ANOMALOUS ARTERIES ANOMALOUS LEFT CIRCUMFLEX ARTERY

This vessel usually arises from the very proximal RCA or from a separate orifice in the right cusp and may course in front of or behind the aorta (Fig. 4-29). This is the most common coronary anomaly, and occasionally this artery requires angioplasty. The multipurpose guide catheter is ideally suited for cannulating this vessel and will usually do so selectively, rather than entering the RCA. When there is a common origin for both the RCA and the anomalous LCX, a double-wire technique can be helpful. The first wire is placed into the RCA to stabilize the guide, and the second wire is used to enter and negotiate the anomalous LCX lesion. In situations where the LMCA trunk arises from the right cusp, a multipurpose guide may be used for intervention in the left coronary system. ANOMALOUS RIGHT CORONARY ARTERY

This vessel usually arises from the left coronary cusp and more commonly has an orifice separate from the LMCA. Modifications of the Judkins left guide (Fig. 4-30), with the heat gun used to direct the primary curve anteriorly, can be very helpful. A Judkins left guide with a shorter curve may then be used to cannulate the LMCA. This provides excellent back-up against the contralateral aortic wall. When this vessel cannot be engaged, the Amplatz left 2 or 3 guide may be useful.

Figure 4-28. Maneuver to select the left subclavian and left internal mammary arteries. The guide catheter is placed beyond the take-off of the left subclavian artery. Then, by rotating the catheter counterclockwise, the tip is directed upward to the ostium of the carotid or left subclavian artery. Injections of contrast medium are used to identify entry into the left subclavian artery. If this artery has not been entered, further withdrawal usually results in the tip entering the vessel. The guidewire can then be advanced out of the subclavian artery and the catheter placed over the guidewire beyond the ostium of the left internal thoracic artery. Gently withdrawing the catheter and using small injections of nonionic contrast medium can identify the location of that vessel. ITA- internal thoracic (mammary) artery.

ATLAS OF JNTERVENTIONAL CARDIOLOGY 50

TRANSRADIAL (ORO NARY INTERVENTION With the recent availability of SF and 6F guides, PCI using the transradial approach is increasing in popularity. This approach allows PCI in subsets of patients where a femoral approach may be difficult, eg, in patients with severe peripheral vascula r disease, or pose a high bleeding risk, eg, in patients who are fully anticoagulated. Furthermore, the transradial approach allows early ambulation following PCI and generally causes less patient discomfort. Special guiding catheters have been designed for the transradial approach. The Kimny guide (Boston Scientific, Natick, MA) is a multipurpose guide that can be used for native left and

right coronary interventions as well as vein graft interventions (Fig. 4-31). The primary curve has a 45° angle with a secondary 90° curve, allowing it to support itself on the contralateral aortic wall. Coronary ostial cannulation is best achieved by initially advancing the guide over the 0.035-inch guidewire into the left or right coronary sinus, below the coronary ostium. To engage the left main coronary artery, the guide initially is pushed down into the aortic sinus to turn the tip up in the direction of the left main ostium. Pulling back on the catheter at this point will allow the guide tip to enter the left main ostium. Having the patient take a deep breath may facilitate this maneuver. The guide tip is directed inferiorly and clockwise when engaging the RCA. Coronary intervention can also be performed with conventional guiding catheters. Generally, for the left coronary artery

Figure 4-29. Left anterior oblique view of the right coronary artery with the anomalous circumflex artery arising from its proximal portion.

Figure 4-30. Aortic root viewed from above, showing the origin of an anomalous right coronary artery (RCA) anterior to the take-off of the left main coronary artery. LCA-left coronary artery. Figure 4-31. The Kimny guide. A, B, This multipurpose guide provides adequate support for transradial stent delivery in both the left and right coronary arteries in the majority of patients.

GUIDE SELECTION 51

approached from the right radial artery in a patient with a normal aortic arch, a slightly smaller curve than that normally selected for the femoral approach is used, ie, JL3.5 instead of JL4 (Fig. 4-32A). If half-sizes are not available, a standard JL 4 curve can be used with a short tip. For approaching the right coronary artery, a curve that is approximately 1 em larger (ie, JRS instead of JR4) usually provides a better fit (Fig. 4-32B). When access is achieved from the left radial artery, conventional curves intraditional sizes are used. The XB guide generally provides good support when approaching the left coronary system via the left transradial

A

approach; it can also be used from the right transradial approach. When using a JL, XB, or Amplatz guide for left system interventions from the right transradial approach, an 0.035-inch guidewire should be used to direct the guide toward the left coronary cusp. These guides tend to point rightward or superiorly and are difficult to manipulate toward the LMCA. Once engaged in the LMCA, however, they provide satisfactory support. The hockey stick guiding catheter has a relatively sharp 90° angle and long distal segment, which make it suitable for engaging both the right and the left coronary arteries from the transradial approach (Fig. 4-33).

B

Figure 4-32. A, B, The Judkins guides in percutaneous transradial intervention. When using Judkins guides from the right transradial approach, a 0.5-cm smaller JL guide and 1-cm larger JR guide (smaller and larger than what would typically be used from the femoral artery) usually fit well.

Figure 4-33. The hockey stick guide in percutaneous transradial intervention. The hockey stick's long distal segment and sharp 90-degree angle make it suitable for transradial right coronary artery intervention.

REFERENCES 1.

2.

Safian R, Freed M: The Manual of lnterventional Cardiology, edn 3. Royal Oak, Ml: Physicians' Press; 2001:15. Judkins MP: Selective coronary arteriography. A percutaneous femoral technique. Radiology 1967, 89:815.

3. 4.

Amplatz K, Formanek G, Stranger P, Wilson W: Mechanics of selective coronary artery catheterization via femoral approach. Radiology 1967, 89:1040. King SB, Douglas JS, Gruentzig AR: Percutaneous trans.luminal coronary angioplasty. In Coronary Arteriography and A ngioplasty. Edited by King SB, Douglas J. New York: McGraw-Hill; 1985.

ATLAS OF INTERVENTIONAL CARDIOLOGY 52

Stent Designs and Implantation Techniques Mandeep Singh and Verghese Mathew The introduction of intracoronary stents has significantly influenced the current practice of interventional cardiology. The increase in the use of stents began with the publication of results of the BENESTENT (Belgium Netherlands Stent) and STRESS (Stent Restenosis Study) trials, which demonstrated significant reduction in restenosis rates in patients with discrete stenosis in large native arteries [1,2]. Acute complications of angioplasty, including abrupt vessel closure and emergency coronary bypass surgery, have also been reduced with the use of stents [3]. Similar success with stents has been noted in angiographic subsets of complex lesions (eg, diffuse, tandem, severely calcified, restenotic, thrombotic, or ostial); in total occlusions, bifurcation lesions, saphenous vein grafts, and multivessel interventions, the combination of stenting and abciximab conferred additive long-term benefit with

• ,



~ -

--- -

-

~~--

-

-

-~-

~ . ___.r~

-

' .....

respect to death, myocardial infarction, and target vessel revascularization [4]. The deliverability of newer stents, their application in complex lesion subsets, and significant lowering of procedure-related complications are responsible for the increase in the use of stents. Increased use of stents is likely to increase the potential for stent-related complications, such as acute or subacute stent closure, stent embolization or loss, and in-stent restenosis. Acute and intermediate-term complications can be minimized by careful review of indications for stent placement, appropriate stent selection based on relevant stent and lesion characteristics, and optimizing delivery and deployment of stents. This chapter examines the various stent designs available in the United States and the relevance of certain design characteristics as they apply to specific lesion subsets.

\

..

~ ......_, -- -

~

N~·....

' .L

~' ~:"\ ' I'.

~-.t

'

1 ,

STENT TYPES AND DESIGNS Stents can be classified according to the basic design (slotted tube, coil, ring, mesh, open cell), composition (stainless steel, tantalum, gold, nitinol), and mode of delivery (balloon expandable, self-expanding). None of these designs incorporate all the features of an ideal stent: flexibility, trackability, adequate surface coverage, visibility, radial strength, side branch access, adherence to deployment balloon, low crossing profile, and reliable expandability. The feature common to tubular stents (eg, Palmaz-Schatz) is that they are laser-cut from a continuous cylinder of stainless steel or nitinol. Coverage of the lesion site and resistance to recoil are better in general with a slotted-tube design; however, trackability and flexibility may be compromised, owing to the greater metal content. Coil stents (eg, GR-11, Wiktor) are manufactured from a single strand of metal wire woven into a sinusoidal pattern or ring device with repeating modules of short coils. Both of these designs make the stent extremely flexible and trackable in tortuous lesions. However, these designs share the disadvantage of uneven expansion at the site of resistance. By nature of their design, the self-expanding stents do shorten, making precise placement more challenging than with balloon-expandable stents. More than 55 types of standard and customized coronary artery stents are currently available. The advanced-generation stents are comparable to each other in many ways, although certain distinguishing attributes of each are more advantageous in certain types of lesions. Knowledge of these features facilitates appropriate stent selection on a lesion-specific basis. The ideal stent would have every positive attribute a clinician could desire with no negative features. Several stent manufacturers have made significant advances toward achieving this goal with their advanced-generation stents. However, certain features of stent design or construction that improve one aspect of stent delivery or implantation may, as a result, detract from another. When assessing a lesion for stenting, the clinician should consider which of the following features may be the most important determinants of angiographic and procedural success for that case and tailor stent selection accordingly.

characteristics are ideal for treating proximal discrete lesions and aorta-ostial and coronary-ostial stenoses. Greater metal coverage, however, may result in compromise of flexibility of the delivery system, depending on the design. Coil stents, in general, have less metal coverage; better flexibility is achieved at the potential expense of more frequent plaque prolapse. To optimize metal-to-artery ratio, manufacturers have adopted a varying cell number, depending on nominal stent size (smaller cell number for smaller nominal diameter stents, and larger cell number for larger stents). VISIBILITY

Visibility is a function of the material used to manufacture the stent, as well as strut thickness. Stainless steel is the most common stent material and has relatively poor radiopacity. Tantalum is highly radiopaque, but this degree of radiopacity might obscure lesion assessment. This is particularly true when trying to assess restenosis within a tantalum stent. Platinum has the same disadvantages as tantalum. Gold-plating of stents improves their visibility versus stainless steel, but gold-plated stents are less radiopaque than tantalum stents. Nitinol, a nickel-titanium alloy, provides moderately improved radiopacity compared with stainless steel. Thicker stent struts improve visibility, but they may compromise crossing profile and flexibility. In the ISAR-STEREO (lntracoronary Stenting and Angiographic Results: Strut Thickness Effect on Restenosis Outcome) trial, 651 patients were randomly assigned to receive ACS Multi-Link RX (Guidant, Indianapolis, IN) stent with strut thickness of 50 pm or ACS Multi-Link RX Duet stents with strut thickness of 140 pm [6]. The primary end point of angiographic restenosis was significantly lower in patients assigned to the thin strut group (15%) compared with 25.8% in the thick strut group (RR, 0.58; 95% CI, 0.39-0.87; P = 0.003). RADIAl STRENGTH

Vessel recoil and negative vessel remodeling may result in stent compression if the stent does not possess sufficient radial strength. This is particularly true in aorto-ostial (right coronary, left main, and aorto-coronary saphenous vein grafts) and severely fibrocalcific lesions. Increasing strut thickness helps to improve radial force. The slotted-tube design offers optimal radial strength.

FlEXIBILITY AND lRACKABILITY

The ability of a stent delivery system to access a distal lesion necessitates the negotiation of proximal vessel angulation, tortuosity, and vessel calcification. Important features of the delivery system in this regard would include low crossing profile of the catheter and tapered tip design. Slotted tubular stents tend to straighten out the vessel and may be too rigid for a very tortuous vessel. A stent that is more flexible and conforms to the original anatomy is preferred because implantation of a rigid stent at an arterial hinge point may be associated with increased restenosis [5]. Earlier generation coil stents (eg, GianturcoRoubin, Wiktor, and Wiktor-i) had a marked advantage of flexibility over tubular stents, although current generation stents make this less of an issue. Minimizing the number of connections between cells or segments (open cell design) improves flexibility but may result in less vessel coverage.

SIDE BRANCH ACCESS

The most important considerations in treating a side branch are its size and whether it needs to be stented. The preferred approach is to stent the main artery and to dilate the side branch with or without debulking the parent vessel or side branch. Among currently available stents, there are relative advantages of one stent type versus another. NIR Elite (Boston Scientific, Natick, MA) is less preferred for large side branches; other current generation stents, eg, Multi-Link Penta (Guidant, Indianapolis, IN), S670 (Medtronic AVE, Santa Rosa, CA), and Bx Velocity (Cordis, Miami Lakes, FL), are optimal for side branch access, although stenting over very large side branches with any of these devices is not advocated routinely [7,8]. STENT SHORTENING

ADEQUATE SURFACE COVERAGE

Stent shortening is more a function of individual stent type and geometry than general design and stent material. The expected shortening of most available stent types is relatively low and can be accommodated, if needed, with the wide range of stent

The slotted tube design offers increased lesion coverage, low recoil, and reduced risk of tissue prolapse. Greater metal coverage of the vessel results in better scaffolding of plaque. These

ATLAS OF INTERVENTIONAL CARDIOLOGY 54

lengths available. However, some stents, such as the selfexpanding Magic Wallstent (Boston Scientific, Natick, MA), shorten considerably. It is therefore important that selection of stent length and stent positioning prior to full deployment are appropriate. SECURE ADHERENCE OF STENT TO DEPLOYMENT BALLOON

In extremely tortuous or calcific vessels, stents may be more prone to stripping off the balloon delivery system as force is applied to the balloon catheter to advance the system. This also becomes important if a stent cannot be advanced to the lesion and is brought back into the guide. It is important to keep the guide coaxial with the coronary ostium on withdrawal. Fortunately, this is an infrequent occurrence with the advanced generation of premounted stents.

BALLOON-EXPANDABLE STENTS

endoluminal surface. To improve flexibility, the stent was shortened to 7 mm and two segments were connected with a 1-mm bridge, resulting in a 15-mm articulated stent (PS-153 series). The presence of uncovered segment at the lesion resulted in higher tissue prolapse. The radial strength of this stent made it useful for aorto-ostial, calcific, and extremely fibrotic lesions where vessel recoil is likely. This stent is no longer on the market. CROWN

The Crown (Cordis, Miami Lakes, FL) stent design consisted of a sinusoidal pattern of slots (Fig. 5-1 B). Articulation points were eliminated in this design, and side branch access was much easier than with the earlier versions of the PS stents. An even more flexible version of this stent, the Mini-Crown (Fig. 5-1C), was developed by reducing the number of rows, strut thickness, and width, which also led to a lower optimal expansion range from 2.25 mm to 3.25 mm. This stent is no longer on the market.

PALMAZ -SCHATZ

GIANTURCO-ROUBIN

The Palmaz-Schatz (PS) (Cordis, Miami Lakes, FL) stent was one of the first available stents and is the most widely studied (Figs. 5-1 A, 5-2). The original slotted-tube intracoronary stent, the Palmaz balloon-expandable intraluminal graft, was fashioned from a 15-mm- long solid stainless steel tube with eight rows of offset rectangular slots, each 3.5 mm long. When expanded by balloon inflation, the rectangular slots assumed a diamond configuration, with metal coverage of 20% of the

The Gianturco-Roubin (GR) (Cook, Bloomington, IN) balloonexpandable coil stent was constructed from a single strand of 0.006-inch (0.15-mm) stainless steel wire folded around a compliant balloon catheter to form a series of interdigitating loops in the shape of a cylinder. The second-generation stent, the GR-11, has the same basic design as the Flex-Stent with lower crossing profile achieved by flattening of the stent coils (Fig. 5-3). A longitudinal spine added flexibility with less

Figure 5-1. Evolution of Cordis stents. A, Palmaz-Schatz; B, Crown; C, Mini-Crown; D, Crossflex LC. These stents have been replaced by the Bx Velocity stent (E).

STENT DESIGNS AND IMPLANTATION TECHNIQUES

55

comparing it with the Palmaz-Schatz stent [9]. Stenosis rates comparable to those of the Palmaz-Schatz stent were observed when the appropriate sizing strategy w as used [10]. This stent is no longer on the market.

deformability, and radiopaque gold markers at the ends of the stent allowed more accurate positioning. Failure to adhere to the recommended sizing strategy (sizing the stent to 0.5 mm larger than the reference segment) may have contributed to the higher restenosis rates observed in the GR-II randomized study

TECHNICAl SPECIFICATIONS OF VARIOUS STE TS

TE T

TECH !CAL 5PECIFICAIIO 5

.e5:.l.51

, in

6

G&!l

1&L 20

316L 20

20

316L 16

0.0025 M rat Good Poor

0.0027 M rat Good Good

0.002 M d rate Good Good

0.005 Excel! nt Fair r\ goodt

Poor Minimal

Fair G d Minimal Minimal 15, 19,31 11, 18, -6

~

12-17

1\'

2.5-5.0 A

ood

Good Good IS 3 mml

B

II

ru

S2Z.Q

0.008 Mod rate rygood Good

316 20(- mm I nil 0.0055 od r te ery good ery good

xcellent < 2.0

Ex ell nt 1.0

8.4

0.006

E cellent 9-11 12, 20,40

A

ELOCITY

8, 13, 18, 23, 28,33 2.25- 5.0

2.5--4.0

B

B

A

A

1. B

.0

0.005 Mod rat Very good Excel! nt ! ID 0.03 in I E ellent 3.5 9, 12, 1-, 18, 14, 30 .0

B

0.043-{).044

A

316 1 - -3

0.043

TE T

5 Material compo ilion Metal/art 1\ ratio, "o trut thi kn , in Radiopacit Radial tr ngth ide bran h ace

sz 15 average 0.002 Low/mod rate Fair Fair Good

2

80 80 84.7

22 61

37 21

20

RADIATION Gamma Gamma Gamma Gamma B ta B ta B ta Beta B ta

BERT- Beta Energ\ R t nosos Troal, PREVE 'T- Prolof ratoon Reductoon woth a ular Energ Trial; RIPPS- ropps Coronary Radoatoon to lnhobot Proh eratoon Post tenting; TART- tent and Radoatoon Therapy; WRI T- \ a hington Radoatoon forIn- t nt Rest nosi Troal.

duration of antiplatelet therapy and decreased use of new stents in the more recent trials resulted in lower stent thrombosis rates.

Figure 6-10. Rates of stent thrombosis and the duration of antiplatelet treatmen t and new stent use in brachytherapy trials. Major vascular brachytherapy trials and the stent thrombosis rates show that the longer

Figure 6-11. Stent coatings under investigation for in-stent restenosis.

irolimus Actinom cin 0

ATLAS OF INTERVENTIONAL CARDIOLOGY

68

was 34% in the brachytherapy group when the analysis segment was taken into account. The 6-month MACE was 34% in the brachytherapy group versus 76% in the placebo group of the WRIST trial. The antiplatelet therapy duration for this trial was also short (30 days or less). Consequently, the late thrombosis rate was 10% in the brachytherapy group versus 4% in the placebo group. Late stent thrombosis was more common when a new stent was placed (22% stent thrombosis in patients with new stents vs 3% in patients without new stents). This provides further evidence for the use of long-term antiplatelet therapy and avoiding the use of new stents at the time of vascular brachytherapy. PREVENT (Proliferation Reduction with Vascular Energy Trial) was a randomized prospective study which used a betaemitting source in 105 patients, with 25 patients in the control group [97]. This study included both de novo (60%) and restenotic lesions (30%) as well as ISR (24%). New stent implantation was seen in 61% of the procedures. This study underscores the importance of geographic miss. The binary restenosis rate for the target site was only 8% at 6 months compared to 39% in the control group. However, when the target site and adjacent segments were taken into account, the restenosis rate in the brachytherapy group was 22%, still lower than the 50% in the control group. Nevertheless, this has probably accounted for the increased TVR rate seen in the brachytherapy group (21% vs 32%, NS) despite the impressive difference in the TLR rate (6% vs 24% in favor of brachytherapy group). When investigators studied angiograms of the patients with edge narrowing, it was determined that the injured segment was not completely covered by the radiation source (geographic miss). Another important aspect of this study is the high late stent thrombosis rate of 8%. This may be attributed to the relatively short duration of antiplatelet therapy and the high incidence of new stent deployment. Figure 6-10 summarizes the late thrombosis percentages in the major vascular brachytherapy trials as well as the duration of antiplatelet therapy. The other randomized trial of beta-emitters for ISR is the START (Stents and Radiation Therapy) trial [99]. In this trial476 patients with ISR were randomized to beta radiation versus placebo. The antiplatelet therapy initially consisted of ticlopidine for 14 days but was later changed to ticlopidine or clopidogrel for 60 days. Only 21% of the patients received a new stent. At eight months, TVR and MACE were both significantly lower in the treatment group (TVR 24.1% vs 16.0%, MACE 25.9% vs 18.0%). In this study with longer antiplatelet use and less frequent use of stents, there were no stent thromboses between days 31 and 270. The only stent thrombosis occurred in the placebo group within the first 30 days. The START trial used a 30-mm source train. The START 40 trial used a 40-mm source train and randomized 210 patients. New stents were used in 20% of the patients and the duration of the antiplatelet regimen was 3 months. There was no

stent thrombosis in any patient and the reduction of restenosis, TVR, and TLR were still impressive (TVR 24.1% vs 16%, TLR 22.4% vs 11.1 %, restenosis 45.2% vs 21.9%) [100]. The issue of geographic miss was further clarified by the BRIE (Beta-Radiation in Europe) trial [101]. Geographic miss was present in 41.2% of the patients in the trial. The restenosis rate was 16.3% in the edges that had geographic miss and only 4.3% in the edges without geographic miss. The reasons for geographic miss were reported as lack of accurate matching of the injured length to the radiation source, treatment of long lesions, and lack of long radiation source. Currently, we have a better understanding of the issues related to vascular brachytherapy. Late stent thrombosis seems to have resolved with the use of longer-duration antiplatelet therapy and discouraging the use of new stents at the time of brachytherapy. Geographic miss and edge effect require careful selection of patients suitable for currently available source trains and careful placement of the radiation source to cover the injured segment. The use of devices that limit the vessel injury length, such as the cutting balloon, may be of particular interest in the treatment of ISR.

FUTURE APPROACHES In the years to come the simplest and the most effective methods will survive the test of time. Current area of interest focuses on local drug delivery systems and gene therapy as well as the use of coated or biodegradable stents. Recently, the use of drug-eluting stents sparked much interest as ISR seems to be markedly attenuated with a sirolimus-eluting stent [102]. There are several drug-eluting stents under development (Fig. 6-11). Multicenter randomized studies to further investigate this potential treatment are underway. If this approach proves useful for de novo lesions, the next step may be to use it in restenotic segments. The prevention of restenosis through oral medication would be a simple, attractive solution. Many drugs have been used for this purpose without any success. Tranilast was the latest drug undergoing clinical investigation for this purpose, unfortunately with disappointing results [103,104]. It is unlikely that a cure for ISR will be found in the near future with the currently available techniques. However, drug-eluting stents are emerging as a promising modality for minimizing ISR. Brachytherapy offers a benefit in terms of reducing the incidence of recurrent ISR, although it does not eliminate the problem. Other types of energy-delivery systems are also being investigated for the prevention and treatment of ISR, but none has been proven effective and safe in large clinical trials yet. The available modalities, however, have certainly improved the outcomes of intervention in this challenging lesion subset.

REFERENCES 1.

2.

3.

4.

Heart and Stroke Statistical Update. In: American Heart Association; 2001. Kimura T, Tamura T, Yokoi H, et al.: Long-term clinical and angiographic follow-up after placement of Palmaz-Schatz coronary stent: a single center experience. J Jnterv Cardio/1994, 7:129-139. Mehran R, Dangas G, Abizaid AS, eta/.: Angiographic patterns of in-stent restenosis: classification and implications for long-term outcome. Circulation

5.

1999, 100:1872-187S.

7.

van Beusekom HM, van der Giessen WJ, van Suylen R, et al.: Histology after stenting of human saphenous vein bypass grafts: observations from surgically excised grafts 3 to 320 days after stent implantation. JAm Coil Cardiol1993, 21:45-54.

6.

Mintz GS, Popma JJ, Hong MK, et al.: Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis. Am J Cardiol1996, 78:18-22.

8.

Anderson PG, Bajaj RK, Baxley WA, et al.: Vascular pathology of balloonexpandable flexible coil stents in humans.] Am Coli Cardiol1992, 19:372-381. Gordon PC, Gibson CM, Cohen DJ, eta!.: Mechanisms of restenosis and redilation within coronary stents-quantitative angiographic assessment. JAm Call Cardiol1993, 21:1166-1174. Hoffmann R, Mintz GS, Dussaillant GR, et al.: Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study. Circulation 1996, 94:1247-1254.

IN-STENT RESTENOSIS 69

9. Abizaid A, Kornowski R, Mintz GS, et al.: The influence of diabetes mellitus on acute and late clinical outcomes following coronary stent implantation. JAm Call Cardio/1998, 32:584-589. 10. Carrozza JP Jr, Kuntz RE, Fishman RF, et al.: Restenosis after arterial injury caused by coronary stenting in patients with diabetes mellitus. Ann Intern Med 1993, 118:344-349. 11. Dauerman HL, Bairn DS, Cutlip DE, eta!.: Mechanical debulking versus balloon angioplasty for the treatment of diffuse in-stent restenosis. Am J Cardia/1998, 82:277-284. 12. Kereiakes D, Linnemeier TJ, Bairn DS, eta!.: Usefulness of stent length in predicting in-stent restenosis (the Multi-Link stent trials). Am J Cardia/ 2000, 86:336-341. 13. Lee SG, Lee CW, Hong MK, eta!.: Predictors of diffuse-type in-stent restenosis after coronary stent implantation. Catheter Cardiavasc Interv 1999, 47:406-409, 410. 14. Sheiban I, Leonardo F, Rosano GM, eta!.: Predictors of long-term clinical outcome in patients undergoing multiple vessel stenting for coronary artery disease. Ita! Heart J 2000, 1:480-486. 15. Kastrati A, Schomig A, Elezi S, et al.: Predictive factors of restenosis after coronary stent placement. JAm Call Cardio/1997, 30:1428-1436. 16. Gruberg L, Hong MK, Mintz GS, eta!.: Optimally deployed stents in the treatment of restenotic versus de novo lesions. Am J Cardia/ 2000, 85:333-337. 17. Klugherz BD, Meneveau NF, Kolansky DM, eta!.: Predictors of clinical outcome following percutaneous intervention for in-stent restenosis. Am J Cardia/ 2000, 85:1427-1431. 18. Kasaoka S, Tobis JM, Akiyama T, eta/.: Angiographic and intravascular ultrasound predictors of in-stent restenosis. JAm Call Cardio/1998, 32:1630-1635. 19. Gupta A, Kerkar PG, Vajifdar BU, eta!.: Restenosis after coronary stentingincidence and predictors. J Assoc Physicians India 2001, 49:336-342. 20. Ribichini F, Steffenino G, Dellavalle A, eta/.: Plasma activity and insertion/ deletion polymorphism of angiotensin !-converting enzyme: a major risk factor and a marker of risk for coronary stent restenosis. Circulation 1998, 97:147-154. 21. Mintz GS, Popma JJ, Pichard AD, eta!.: Intravascular ultrasound predictors of restenosis after percutaneous transcatheter coronary revascularization. JAm Call Cardio/1996, 27:1678-1687. 22. Brito FS Jr, Caixeta AM, Rati MA, eta/.: Patient-related and angiographic predictors of restenosis after excimer laser coronary angioplasty. J Invasive Cardia/1998, 10:162-168. 23. Ellis SG, Savage M, Fischman D, eta!.: Restenosis after placement of PalmazSchatz stents in native coronary arteries. Initial results of a multicenter experience. Circulation 1992, 86:1836-1844. 24. Kini A, Marmur JD, Dangas G, eta/.: Angiographic patterns of in-stent restenosis and implications on subsequent revascularization. Catheter Cardiovasc Interv 2000, 49:23-29. 25. Choussat R, Klersy C, Black AJ, eta!.: Long-term (8 years or longer) outcome after Palmaz-Schatz stent implantation. Am J Cardia/ 2001, 88:10-16. 26. Kornowski R, Mehran R, Satler LF, eta/.: Procedural results and late clinical outcomes following multivessel coronary stenting. JAm Col! Cardio/1999, 33:420-426. 27. DeServi S, Mariani G, Bossi I, et a/.: One-year outcome in multi vessel coronary disease patients undergoing coronary stenting. Catheter Cardiovasc Interv 1999, 48:343-349. 28. Hoffmann R, Mintz GS, Mehran R, et al.: Intravascular ultrasound predictors of angiographic restenosis in lesions treated with Palmaz-Schatz stents. f Am Col! Cardio/1998, 31:43-49. 29. Finci L, Ferraro M, Nishida T, eta/.: Coronary stenting beyond standard indications. Immediate and follow-up results. Ita/ Heart J 2000, 1:739-748. 30. Sheiban I, Albiero R, Marsico F, et al.: Immediate and long-term results of "T" stenting for bifurcation coronary lesions. Am J Cardio/2000, 85:1141-1144, A9. 31. Bauters C, Hubert E, Prat A, et al.: Predictors of restenosis after coronary stent implantation. JAm Col! Cardio/1998, 31:1291-1298. 32. Jeong MH, Kim SH, Ahn YK, et al.: Predictive factors for the second restenosis after coronary interventions. Catheter Cardiovasc Interv 2000, 50:34-39. 33. Kastrati A, Schomig A, Elezi S, et al.: Prognostic value of the modified American College of Cardiology I American Heart Association stenosis morphology classification for long-term angiographic and clinical outcome after coronary stent placement. Circulation 1999, 100:1285-1290. 34. Mathew V, Hasdai D, Holmes DR, Jr., eta/.: Clinical outcome of patients undergoing endoluminal coronary artery reconstruction with three or more stents. JAm Call Cardiol1997, 30:676-681. 35. Kastrati A, Dirschinger J, Boekstegers P, et al.: Influence of stent design on 1-ycar outcome after coronary stent placement: a randomized comparison of five stent types in 1,147 unselected patients. Catheter Cardiovasc Interv 2000, 50:290-297.

36. Kobayashi Y, DeGregorio J, Kobayashi N, et a/.: Stented segment length as an independent predictor of restenosis. JAm Call Cardio/1999, 34:651-659. 37. Kornowski R, Bhargava B, Fuchs S, et al.: Procedural results and late clinical outcomes after percutaneous interventions using long (25 mm or greater) versus short (20 mm or less) stents. JAm Coil Cardia/ 2000, 35:612-618. 38. Kastrati A, Elezi S, Dirschinger J, eta/.: Influence of lesion length on restenosis after coronary stent placement. Am J Cardio/1999, 83:1617-1622. 39. Kastrati A, Schomig A, Dirschinger J, el a/.: A randomized trial comparing stenting with balloon angioplasty in small vessels in patients with symptomatic coronary artery disease. Circulation 2000, 102:2593-2598. 40. Kastrati A, Mehilli J, Dirschinger J, eta/.: Restenosis after coronary placement of various stent types. Am J Cardiol 2001, 87:34-39. 41. Park SW, Park HK, Hong MK, eta/.: Comparison of slotted tube versus coil stent implantation for ostial left anterior descending coronary artery stenosis: initial and late clinical outcomes. J Korean Med Sci 1998, 13:483-487. 42. Carrozza JP Jr, Hosley SE, Cohen DJ, eta/.: In vivo assessment of stent expansion and recoil in normal porcine coronary arteries: differential outcome by stent design. Circulation 1999, 100:756-760. 43. HoDS, Liu MW, Iyer S, eta/.: Sizing the Gianturco-Roubin coronary flexible coil stent. Cathet Cardiovasc Diagn 1994, 32:242-248. 44. Vrints CJ, Cools F, Bosmans J, et al.: Acute luminal gain after stenting: comparison of Gianturco-Roubin and Palmaz-Schatz stents. J Invasive Cardiol1996, 8:135-143. 45. Macisaac AI, Ellis SG, Muller DW, et al.: Comparison of three coronary stcnts: clinical and angiographic outcome after elective placement in 134 consecutive patients. Cathet Cardiovasc Diagn 1994, 33:199-204. 46. Silber S, Seidel N, Muehling H, et al.: In-stent restenosis using newer stent designs available in Germany (abstract). JAm Col/ Cardio/1998, 1033-1106. 47. Yokoi H, Kimura T, Hamasaki N, et al.: Coronary stenting for STRESS/ BENESTENT equivalent lesions: Comparison of four different types of stent. JAm Call Cardio/1998, 1137-1164. 48. Kastrati A, Schomig A, Dirschinger J, eta/.: Increased risk of restenosis after placement of gold-coated stents: results of a randomized trial comparing gold-coated with uncoated steel stents in patients with coronary artery disease. Circulation 2000, 101:2478-2483. 49. Kastrati A, Mehilli J, Dirschinger J, et al.: Intracoronary stenting and angiographic results: strut thickness effect on restenosis outcome (ISAR-STEREO) trial. Circulation 2001, 103:2816-2821. 50. Kuntz RE, Gibson CM, Nobuyoshi M, et a/.: Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. f Am Call Cardio/1993, 21:15-25. 51. Hong MK, Park SW, Mintz GS, eta/.: Intravascular ultrasonic predictors of angiographic restenosis after long coronary stenting. Am J Cardia/ 2000, 85:441-445. 52. Hasdai D, Garratt KN, Grill DE, et al.: Effect of smoking status on the longterm outcome after successful percutaneous coronary revascularization. N Eng! J Med 1997, 336:755-761. 53. Jolly N, Ellis SG, Franco I, et a/.: Coronary artery stent restenosis responds favorably to repeat interventions. Am J Cardio/1999, 83:1565-1568, A7. 54. Koch W, Kastrati A, Mehilli J, et al.: Insertion/ deletion polymorphism of the angiotensin !-converting enzyme gene is not associated with restenosis after coronary stent placement. Circulation 2000, 102:197-202. 55. Kastrati A, Schomig A, Seyfarth M, eta/.: PIA polymorphism of platelet glycoprotein Ilia and risk of restenosis after coronary stent placement. Circulation 1999, 99:1005-1010. 56. Hoffmann R, .\1intz GS: Coronary in-stent restenosis-predictors, treatment and prevention. Eur Heart J 2000,21:1739-1749. 57. Carrozza JP, Jr.: ln-stent restenosis: should an old device treat a new problem? f Am Call Cardiol2000, 35:1577-1579. 58. Bairn DS, Levine MJ, Leon MB, eta/.: Management of restenosis within the Palmaz-Schatz coronary stent (the U.S. multicenter experience). Am J Cardia/ 1993, 71:364-366. 59. Reimers B, Moussa I, Akiyama T, et al: Long-term clinical follow-up after successful repeat percutaneous intervention for stent restenosis. JAm Coli Cardia! 1997, 30(1):186-192. 60. Bossi I, Klersy C, Black AJ, et al.: In-stent restenosis: long-term outcome and predictors of subsequent target lesion revascularization after repeat balloon angioplasty. JAm Call Cardia/ 2000, 35:1569-1576. 61. Mehran R, Mintz GS, Popma JJ, et al.: Mechanisms and results of balloon angioplasty for the treatment of in-stent restenosis. Am J Cardio/1996, 78:618-622. 62. Eltchaninoff H, Koning R, Iron C, et a!.: Balloon angioplasty for the treatment of coronary in-stent restenosis: immediate results and 6-month angiographic recurrent restenosis rate. JAm Call Cardiol1998, 32(4):980-984.

ATLAS OF INTERVENTIONAL CARDIOLOGY

70

85. Adamian M, Colombo A, Briguori C, ct al.: Cutting balloon angioplasty for the treatment of in-stent restenosis: a matched comparison with rotational atherectomy, additional stent implantation and balloon angioplasty. JAm Call Cardia/ 2001, 38:672-679. 86. Lauer B, Schmidt E, Stellbring S, et al.: Cutting balloon angioplasty for treatment of in-stent restenosis (abstract). Circulation 2000, 102:II-365. 87. Waksman K Bhargava B, White L, et al.: Intracoronary beta-radiation therapy inhibits recurrence of in-stent restenosis. Circulation 2000, 101:1895-1898. 88. Waksman R, White RL, Chan RC, et al.: Intracoronary gamma-radiation therapy after angioplasty inhibits recurrence in patients with in-stent restenosis. Circulation 2000, 101:2165-2171. 89. Verin V, Popowski Y, de Bruync B, et al.: Endoluminal beta-radiation therapy for the prevention of coronary restenosis after balloon angioplasty. The DoseFinding Study Group. N Eng/ J Med 2001, 344:243-249. 90. Teirstein PS, Massullo V, JaniS, et al.: Catheter-based radiotherapy to inhibit restenosis after coronary stenting. N Engl JMed 1997, 336:1697-1703. 91.Condado JA, Waksman R, Gurdiel 0, et al.: Long-term angiographic and clinical outcome after percutaneous transluminal coronary angioplasty and intracoronary radiation therapy in humans. Circulation 1997, 96:727-732. 92. Malhotra S, Teirstein PS: The SCRIPPS trial-catheter-based radiotherapy to inhibit coronary restenosis. J Invasive Cardia/ 2000, 12:330-332. 93. Waksman R: Intra coronary gamma radiation for diffuse in-s tent restenosis. JAm Coil Cardio/2000, 36:315-316. 94. Leon MB, Teirstein PS, Moses JW, et al.: Localized intracoronary gamma-radiation therapy to inhibit the recurrence of restenosis after stenting. N Eng! J Med 2001, 344:250-256. 95. Teirstein P, Moses JW, Casterella PL et al.: Late thrombosis after coronary radiation may be eliminated by longer antiplatelet therapy and reduced stenting: The Scripps III results. JAm Call Cardia! 2001, 37:60A. 96. King SB 3rd, Williams DO, Chougule P, et al.: Endovascular beta-radiation to reduce restenosis after coronary balloon angioplasty: results of the beta energy restenosis trial (BERT). Circulation1998, 97:2025-2030. 97.Raizner AE, Oesterle SN, Waksman R, et al.: Inhibition of restenosis with betaemitting radiotherapy: report of the Proliferation Reduction with Vascular Energy Trial (PREVENT). Circulation 2000, 102:951-958. 98. Verin V, Urban P, Popowski Y, et al.: Feasibility of intracoronary beta-irradiation to reduce restcnosis after balloon angioplasty. A clinical pilot study. Circulation 1997,95:1138-1144. 99.Kleiman NS, Califf RM: Results from late-breaking clinical trials sessions at ACCIS 2000 and ACC 2000. American College of Cardiology. JAm Coli Cardia/ 2000, 36:310-325. 100. Laskey W: Late clinical and angiographic outcomes after use of Sr-90 beta radiation for the treatment of in-stent restenosis from the START 90 (Stents and Radiation Therapy 90) trial. Paper presented at: Annual Meeting of the American Heart Association; November 12-15, 2000; New Orleans, LA. 101. Sianos C, Kay IP, Costa MA, et al.: Geographical miss during catheter-based intra coronary beta-radiation: incidence and implications in the BRIE study. Beta-Radiation In Europe. JAm Call Cardia/ 2001, 38:415-420. 102. Sousa JE, Costa MA Abizaid A, et al.: Lack of neointimal proliferation after implantation of sirolimus-coated stents in human coronary arteries: a quantitative coronary angiography and three-dimensional intravascular ultrasound study. Cirwlatio11 2001, 103:192-195. 103. Capper EA Roshak AK, Bolognese BL et al.: Modulation of human monocyte activities by tranilast, SB 252218, a compound demonstrating efficacy in restenosis. J Pharmacal Exp Ther 2000, 295:1061-1069. 104.Holmes D, Fitzgerald P, Goldberg S, et al.: The PRESTO (prevention of rcstenosis with tranilast and its outcomes) protocol: a double-blind, placebocontrolled trial. Am Heart J 2000, 139:23-31.

63. Mehran R, Dan gas G, Abizaid A, et al.: Treatment of focal in-stent restenosis with balloon angioplasty alone versus stenting: Short- and long-term results. Am Heart J 2001, 141:610-614. 64. Shiran A, Mintz GS, Waksman R, et al.: Early lumen loss after treatment of in-stent restenosis: an intravascular ultrasound study. Circulation 1998, 98:200-203. 65. Alfonso E Cequier A Zueco J, et al.: Stenting the stent: initial results and long-term clinical and angiographic outcome of coronary stenting for patients with in-stent restenosis. Am J Cardiol2000, 85:327-332. 66. Alfonso F: RIBS: Repeat stenting shows benefits in large but not small vessels. In: American College of Cardiology 50th Annual Scientific Sessions; 2000; Orlando, FL. 67. Radke PW, Klues HG, Haager PK, et al.: Mechanisms of acute lumen gain and recurrent restenosis after rotational atherectomy of diffuse in-stent restenosis: a quantitative angiographic and intravascular ultrasound study. JAm Call Cardiol1999, 34:33-39. 68. Mehran R, Dangas G, Mintz GS, et al.: ln-stent restenosis: "The great equalizer" -s disappointing clinical outcomes with all interventional strategies. In: American College of Cardiology 48th Annual Scientific Session; 1999; New Orleans, LA. Abstract 63A. 69. Sharma SK, Kini A, King T, et al.: Randomized trial of rotational atherectomy versus balloon angioplasty for diffuse in-stent restenosis. Fin a1 results (abstract). Circulation 2000, 102:!T-730. 70. Ferguson JJ: Meeting highlights: highlights of the 22nd Congress of the European Society of Cardiology. Circulation 2001, 103:E41-E45. 71. Kobayashi Y, De Gregorio L Kobayashi N, et al.: Lower restenosis rate with stenting following aggressive versus less aggressive rotational atherectomy. Catheter Cardiovasc Interv 1999,46:406-414. 72. Strauss BH, Umans VA, van Suylen RJ, et al.: Directional atherectomy for treatment of restenosis within coronary stents: clinicaL angiographic and histologic results. JAm Call Cardiol1992, 20:1465-1473. 73. Mahdi NA, Pathan AZ, Harrell L, et al.: Directional coronary atherectomy for the treatment of Palmaz-Schatz in-s tent restenosis. Am J Cardio/1998, 82:1345-1351. 74. Meyer T, Schmidt T, Buchwald A, et al.: Stent wire cutting during coronary directional atherectumy. Clinical Cardiology 1993, 16:450-452. 75. Mehran R, Mintz GS, Saller LF, eta/.: Treatment of in-stent restenosis with excimer laser coronary angioplasty: mechanisms and results compared with PICA alone. Circulation 1997, 96:2183-2189. 76. Giri S, Ito S, Lansky AJ, et a/.: Clinical and angiographic outcome in the laser angioplasty for restenotic stents (LARS) multicenter registry. Catheter Cnrdiovasc Interv 2001, 52:24-34. 77. Mehran R, Dangas G, Mintz GS, et al.: Treatment of in-stent restenosis with excimer laser coronary angioplasty versus rotational atherectomy: comparative mechanisms and results. Circulation 2000, 101:2484-2489. 78. Albiero R, Nishida T, Karvouni E, eta/.: Cutting balloon angioplasty for the treatment of in-stent restenosis. Catheter Cardiovasc Intcrv 2000, 50:452-459. 79. Freitas Junior JO, Berti SL, Bonfa JC, eta/.: Cutting balloon angioplasty for intrastent restenosis treatment. Arq Bras Cardio/1999, 72:615-620. 80. Molstad P, Myreng Y, GolfS, et al.: The Barath Cutting Balloon versus conventional angioplasty. A randomized study comparing acute success rate and frequency of late restenosis. Scand Cardiovasc j 1998, 32:79-85. 81. Muramatsu T, Tsukahara R, HoM, et al.: Efficacy of cutting balloon angioplasty for in-stent restenosis: an intravascular ultrasound evaluation. J Invasive Cardiol 2001, 13:439-444. 82. Chevalier B, Royer T, Guyon P, et al.: Treatment of in-stent restenosis: Short and midterm results of a pilot study between balloon and cutting balloon (abstract). JAm Call Cardio/1999, 33:63A. 83. Mizobe M, Oohata K, Osada T: The efficacy of cutting balloon for in-stent restenosis: Compared with conventional balloon angioplasty (abstract). Circulation 1999, 100:1-308. 84. Adamian M, Marsico F, Briguori C, et al.: Cutting balloon for treatment of in-stent restenosis: A matched comparison with conventional angioplasty and rotational atherectomy (abstract). Circulation 1999, lOO:I-305.

IN-STENT RESTENOSIS 71

Directional Coronary Atherectomy David R. Holmes, Jr. Recognition of the limitations of coronary artery balloon angio- lowing intervention, new trials were designed to take advanplasty fostered the development of nonballoon approaches to tage of the unique properties of DCA for tissue removal [6]. percutaneous coronary revascularization. Directional coronary OARS (Optimal Atherectomy Restenosis Study) [7] was atherectomy (DCA), which received US Food and Drug the first study to evaluate this. In this registry of 199 consecAdministration (FDA) approval in 1990, was the first such tech- utive patients, the aim of the procedure was to achieve a truly nique to be widely applied. The basis for this technique was optimal angiographic result with a residual stenosis of less directionally controlled resection and removal of atheromatous than 15%. Intravascular ultrasound (IVUS) was used for docplaque (Fig. 7-1). DCA, which was limited to proximal and umentation and assessment of plaque burden. A total of 211 midcoronary arterial sites and saphenous vein grafts, produced lesions were treated, 28 with DCA alone and 183 w ith DCA a larger and smoother lumen than that achieved w ith conven- followed by adjunctive PTCA. The initial results were exceltional balloon angioplasty, and it was hoped that this improved lent, with no deaths, Q-wave myocardial infarction in 1.5%, result would translate into fewer complications and even and emergency coronary bypass graft surgery in 1%. The potentially less restenosis. However, initial randomized trials angiographic results documented that a large lumen could be [1- 5] comparing DCA with balloon angioplasty for the treat- achieved safely but that late loss was substantial (1.18 mm). ment of de novo native coronary artery lesions (CAVEAT The 6-month angiographic binary restenosis was 29%. At 1 [Coronary Angioplasty Versus Excisional Atherectomy Trial] year, target vessel revascularization was performed in 21.1 %. and CCAT [Canadian Coronary Atherectomy Trial]) did not Accordingly, in contrast to the previous DCA trials, DCA was show significantly better long-term results with DCA; indeed, safe, better initial angiographic results could be achieved, initial hospital stay was complicated by more non- Q-wave and target lesion revascularization appeared to be somewhat infarctions in the DCA group [1,2]. At 1 year in CAVEAT, a lower than would have been expected. higher mortality was observed in the DCA group (2.2% vs 0.6%; BOAT (Balloon vs Optimal Atherectomy Trial), the second P=0.035). In addition to the initial hospital complication rates randomized trial, was the largest [8]. This study randomly noted with DCA in CAVEAT, the procedures were more assigned 1000 patients with de novo native coronary lesions to complex and hospital charges were higher. It was suggested either optimal atherectomy or balloon dilation. The primary that the atherectomy operators in both CAVEAT and CCAT endpoint was 6-month angiographic restenosis, whereas the practiced conservative atherectomy, as evidenced by a mean secondary endpoint included procedural success, clinical residual stenosis of 29% and 25%, respectively, that might have restenosis, and clinical status over 12 months. The main difbeen improved with adjunctive percutaneous transluminal ference between DCA performance in BOAT and CAVEAT coronary angioplasty (PTCA). was that the DCA devices were more appropriately sized As new information was gathered on the importance of (> 90% were 7F devices), more tissue cuts were obtained, and achieving the greatest immediate postprocedural result fol- approximately 80% of the lesions were dilated after DCA The

procedural success was improved in the DCA patients, at 93% versus 87% (P=0.001). In addition, restenosis was also less with DCA (31.4% vs 39.8%; P=0.016). Despite this angiographic improvement, there was no difference in repeat revascularization (25.4% for DCA vs 28.1% for PTCA; P value not significant) or target vessel revascularization (17.1% vs 19.7%; P=0.33). Therefore, although initial results were superior with DCA in this trial, clinical restenosis was not affected. A final study, ABACAS (Adjunctive Balloon Angioplasty after Coronary Atherectomy Study), evaluated the effect of IVUS guidance [9]. This randomized, multicenter trial evaluated the effects of adjunctive PTCA after DCA versus stand-alone DCA and the outcome of IVUS-guided DCA. Of 225 patients undergoing IVUSguided OCA, optimal debulking was achieved in 214 patients,

who were then randomly assigned to PTCA or no further treatment. Adjunctive PTCA after optimal DCA resulted in a larger minimal luminal diameter and lower residual plaque mass. However, at 6 months there was no significant difference in restenosis rate (23.6% for adjunctive PTCA vs 19.6% for DCA; P value not significant) or target lesion revascularization (20.6% vs 15.2%; P value not significant).

PATIENT PREPARATION Patients undergoing DCA are pretreated with aspirin and often clopidogrel in anticipation of stent implantation. In addition, a Ilb /Ilia receptor inhibitor is typically used. These agents have Figure 7-1. The technique of directional atherectomy. A, The atherocath is positioned across the stenosis and the window is oriented toward the bulk of the plaque. B, The cutting element is withdrawn, allowing invagination of plaque material into the housing. C, The cutter is then activated and advanced slowly. The support balloon holds the window against the wall of the vessel, promoting maximal plaque removal. Shavings are stored in the nose cone and removed later. D, The window is reoriented toward angiographically identified plaque and the sequence is repeated. When the luminal result is judged to be adequate by angiography, ultrasonography, or both, the procedure is complete.

A

B

c

D

Figure 7-2. The assembled atherocath with its motor drive unit.

ATLAS OF INTERVENTlONAL CARDIOLOGY

74

the specific advantage that they result in less periprocedural creatine phosphokinase (CPK) elevation. Following placement of the intravascular sheath in the femoral artery, heparin is administered to achieve an activated clotting time (ACT) of 200 to 250 seconds if a lib /Ilia agent is to be administered or greater than 300 to 350 seconds if no lib /Ilia agent is to be given.

ATHEROCATH The Simpson atherocath (Devices for Vascular Intervention, Redwood City, CA) is a multilumen catheter terminating in a nosecone. This nosecone serves as a collection chamber for shav-

ings that are pushed into it by the cutting element, which spins at approximately 2000 rpm (Figs. 7-1 and 7-2). The cutter is enclosed in a metal housing unit that has a 5- or 9-mm window through which plaque material protrudes when the supporting balloon is inflated to low pressure, pushing the window against the wall of the vessel to be treated. The shaft of the atherocath contains a hollow drive cable that accommodates a 0.014-inch steerable guidewire and a balloon inflation lumen. The proximal portion of the atherocath has a balloon inflation port, a cutter cable-connecting member, and a flush port. A battery-operated motor drive unit is attached to the cutter cable-connecting member. The original FDA-approved atherocath, the SCA-1, had a Surlyn balloon and a 10-mm window, and it was stiff. Subsequent designs had a lower profile and were compatible with 9.5F and lOF guiding catheters (Fig. 7-3). These had 9-mm windows but were still stiff and relatively inflexible, thus limiting their use to proximal nontortuous segments. The Flexi-Cut atherocath (Guidant, Temecula, CA) (Fig. 7-4) represents a significant improvement. It is compatible with SF guiding catheters and is more flexible and trackable than previous devices. GUIDING CATHETERS

The early atherocaths were large and rigid, requiring large lumen guiding catheters (9.5F to llF) that had gentle curves. These were inserted over a 7F or SF introducing catheter and a 0.035- to 0.03S-inch guidewire. With the recent introduction of the Flexi-Cut device, SF guiding catheters can now be used.

EQUIPMENT SELECTION Figure 7-3. Three generations of Simpson atherocaths (Devices for Vascular Intervention, Redwood City, CA).

The size of the aortic root and the position and angle of origin of coronary artery and graft ostia influence atherectomy guide

FLEXI-CUT DIRECTIO Al DEBULKING SYSTEM SPECIFICATIO S Guid cath t r ompatibilit Balloon mat rial Balloon bur t pr lnnallon lime

ur

hape outside diam ter

mark r

8F ompon nt , In .,

!". 7 !". 10 !".lOs lindrical 6F (0.076 inl 6F (0.0 6 in) 0.436 in or 11 .07 mm 12 ° 9mm 304 tainl teel Titanium nitrid oated 420 0.086 in 134 em tainle t I braid 0.076 in PEBA n lon out r lin r with h dro oat hydrophilic coating Tung t n (on no on tip)

2

DIRECTIONAL CORONARY ATHERECTOMY

75

Figure 7-4. Specifications for the most recent debulking device: the Flexi-Cut (Guidant, Temecula, CA) directional debulking system. HTC-housing torque cable.

Care must be taken to avoid trauma to proximal or ostial lesions, and a short tip may be preferred. For left saphenous vein grafts with a horizontal take-off, the left graft catheter will usually suffice, but superiorly oriented left grafts may be difficult to engage, especially if located on the inner curvature of the ascending aorta. In that case, a hockey stick shape may be best (Fig. 7-6).

catheter selection. In the past, 9.5F guides were used for right coronary and saphenous vein graft atherectomy and lOF guides for left coronary artery atherectomy (although llF guides were used if a need for reliable "back-up support" was anticipated). For a right coronary artery atherectomy, the 9.5F right coronary short-tip guide is preferred (Figs. 7-5 and 7-6), especially when lesions are quite proximal and deep engagement is to be avoided. If the right coronary artery has an inferior take-off, the JR4.0 inferior is selected, whereas a superior take-off may require a JR4.0, hockey stick, or left or right graft catheter. For the FlexiCut, SF guide catheters of the same shapes can be used. For a left coronary artery atherectomy, a C-shaped guide catheter is used. When the left main coronary artery is short, undersized guide catheters provide the best coaxial alignment for atherectomy of the left anterior descending (LAD) coronary artery, and slightly oversized guides facilitate DCA in the circumflex artery. Undersized guide catheters may also aid in engaging a posteriorly located and superior left main coronary artery. Saphenous vein grafts to the right coronary artery that arise posteriorly (Fig. 7-6) can usually be engaged with a multipurpose guide catheter, which also works well for other grafts with a downward take-off. For those arising from the lateral wall of the aorta, a right graft catheter is usually selected (Fig. 7-6).

PERFORMANCE OF DIRECTIONAL ATHERECTOMY A guiding catheter is selected that fits optimally within the coronary vessels to be treated. A long-exchange 0.014-inch guidewire is advanced across the lesion into the distal vessel. With the Flexi-Cut atherocath, predilation is seldom performed, and then only in the seting of tortuosity, when difficulty in crossing with the atherocath is anticipated, or if ischemia could be predicted should crossing be prolonged. If the lesion is not calcified and is proximal without any tortuosity, predilation should not be required. The position of the guidewire is then fixed, and the atherocath is advanced under fluoroscopic control. As the Figure 7-5. The available shapes of directional atherectomy guide catheters (Devices for Vascular Intervention, Redwood City, CA). A, The Judkins left coronary catheters (JL) are provided in 3.5, 4, 4.5, and 5 sizes. B, The Judkins right coronary guide (JR) is available in a short tip (ST) and with an inferior orientation (IF). Graft guiding catheters for left (JLGRF) and right (JRGRF) aortic position are also provided.

JLS.O

A

JR4 .0 T

JRGRF

ATLAS OF INTERVENTIONAL CARDIOLOGY 76

A

0

G

B

H

guid

ath I r

lnf rior VG to RCA (multipurpo l

lnf rior right UR4 .01FJ guid cath t r

E

H

c

Right or I ft graft (J R RF r JLGRF) guid cath t r

F

Horizontal or uperior VG to RCA (JRGRF)

Figure 7-6. A-1, Demonstrations of guiding catheter selection for a variety of native coronary and graft problems. LAD- left anterior descending coronary artery; RCA- right coronary artery; SVG-saphenous vein graft.

DIRECTIONAL CORONARY ATHERECTOMY 77

up rior I ft graft (JLGRF, )RGRF. or h l..ev sticl..

Figure 7-7. Left anterior oblique view of the right coronary artery in a 47-year-old man with unstable angina. The extremely eccentric stenosis (A) was successfully treated (B) with a 7F Surlyn cutter without predilating. There were no complications. Histology revealed atheroma and organized thrombus. C, Note the crack of the fibrocollagenous cap (arrow) filled with organizing thrombi. At the site of the crack, there is a mural thrombus. Old hemorrhage within the necrotic lipid core of the plaque is recognized. This patient has remained asymptomatic for 31 months after the procedure. Although eccentricity is only a weak predictor of poor outcome with balloon angioplasty, we believe that extremely eccentric lesions such as this one respond more favorably to directional coronary atherectomy than balloon angioplasty. M-media; OH-old hemorrhage; PC-plaque cap; T-mural thrombus. (Masson's trichrome, X 150.) (From Douglas [20]; with permission.)

Figure 7-8. Proximal left anterior descending coronary artery (LAD) stenosis in a 46-year-old woman with recent-onset angina. A, Note the very long left main coronary artery. Although data from CAVEAT (Coronary Angioplasty Versus Excisional Atherectomy Trial) suggest a similar outcome with directional coronary atherectomy (DCA) and

percutaneous transluminal coronary angioplasty at this site [1], we favor DCA, which was successfully performed (B) in this patient with a 7F Surlyn cutter using a 3.5F guide catheter (C). An elevation of creatine kinase to 272 with 18% MB component occurred. The patient has remained asymptomatic for 3 years following DCA.

ATLAS OF INTERVENTIONAL CARDIOLOGY 78

relatively inflexible atherocath housing passes through the distal portion of the guide catheter, it typically straightens the guiding catheter. This must be compensated for by slight withdrawal of the guide catheter while attempting to maintain coaxial alignment as much as possible with the target vessel. Rotation of the atherocath may facilitate passage into the target vessel and crossing of the lesion. Deep seating of the guide catheter should be avoided. If the lesion cannot be crossed, a balloon is used to pretreat the lesion. Once the atherocath is positioned in the lesion, the window is oriented toward the greatest plaque bulk and the supporting balloon is inflated to 1 atm. The guidewire is then fixed, the cutter is withdrawn, the motor engaged, and the cutter slowly advanced, taking approximately 7 seconds to return it to its most forward position, completing the cut. The balloon is then deflated. The window is then reoriented toward angiographically evident plaque, the supporting balloon is inflated to press the window again against the vessel wall (Fig. 7-7), and the cutter is withdrawn and another cut completed. After six to eight cuts, or when the nosecone appears full, the atherocath is removed and emptied by flushing with saline. A full nosecone may be present when the cutter will not reach its usual most forward position or when guidewire movement is impaired. When removing the atherocath, the guide catheter is withdrawn slightly to prevent deep engagement. Typically, the atherocath is removed over a long 300-cm exchange wire to avoid the need to recross the lesion. If residual stenosis is present after a number of cuts at 1 atm or greater, balloon pressure may be increased in 1-atm increments to 4 atm. If residual plaque still remains, consideration should be given to a larger device or to post-PTCA or post-DCA stenting. Cuts should not be made with the window oriented toward apparently normal segments to avoid coronary perforation. If atherectomy is to be performed, it is important to have as optimal a result as possible. We currently aim to achieve less than 15% residual narrowing with the atherocath (Fig. 7-8). If ultrasound guidance is used, we try to debulk the plaque as completely as possible and then follow with balloon angioplasty or stent implantation. In patients with excellent angiographic results following directional atherectomy and stent implantation, sheath removal

D bulking prior to tent implantation orto-o t1al lc ion !native or v in graft)

0 t1all D with large plaque burden

Figure 7-9. Current potential indications for directional coronary atherectomy. LAD- left anterior descending coronary artery.

is accomplished when the activated clotting time is less than 150 seconds. In some institutions, closure devices are used to decrease the length of time before the patient can ambulate.

SELECTION FOR DIRECTIONAL ATHERECTOMY Directional atherectomy is performed only infrequently. In the multicenter Dynamic Wave Registry from 1999, which tracks procedural performance on an ongoing basis, this technique was used in only 0.3% of patients. This contrasts with the findings of the Northern New England Study Group [10], which documented that of 11,178 patients treated from 1991 to 1994, DCA was used in 10% of cases in 1994. Some centers and operators with specific interest in the technique use it more frequently, whereas other centers and operators may not have any experience a t all with it. The primary use of DCA is for bifurcation lesions, ostial LADs, and in large bulky lesions (see Figs. 7-7 and 7-8). The role of DCA may change with the introduction and more widespread use of the SF compatible Flexi-Cut device, which is much more trackable and more easily delivered. The role will also change, depending on the continued evaluation and testing of the drug-coated stents. Presently, given the lack of data on clinically relevant reduction in restenosis with directional atherectomy, the role of the device is as an adjunctive therapy, particularly in combination with stent implantation (Fig. 7-9).

DEBULKING PRIOR TO STENT IMPLANTATION Multiple studies have found a significant correlation between residual plaque volume after stent implantation and subsequent neointimal area [11- 14]. This finding has formed the basis for several studies. The SOLD (Stenting after Optimal Lesion Debulking) registry studied 71 patients [14] . The procedural success was 96% and the postlesion residual stenosis was 0.4%. During follow-up, the binary restenosis rate was 10.8% and target lesion revascularization (TLR) at 1 year was only 6.7%. Bramucci et al. [12] studied this approach in 100 patients and achieved a final diameter stenosis of 5%. The restenosis rate was only 6.8%. These series formed the basis of the AMIGO (Atherectomy Before Multi-Link Stent Improves Lumen Gain and Clinical Outcomes) trial, which randomized 750 patients with complex native coronary lesions to either DCA plus stent implantation or stent implantation alone. Although this multicenter trial has been completed for some tim e, the results are not yet available. The DESIRE (Debulking and Stenting in Rcstcnosis Elimination) randomized trial compared DCA plus stent with stent alone plus IVUS guidance. This trial, presented at the 2001 American Heart Association conference, included 501 patients who were randomly assigned to either debulking prior to stenting or stenting alone.

DIRECTIONAL CORONARY ATHERECTOMY 79

IVUS was used for assessment of optimal debulking. Although procedural access was similar in both arms, acute gain was greater with DCA/stent (2.09 ± 0.5 vs 1.87 ± 0.5). Of 379 patients with 6-month follow-up, there was a strong trend for less TLR in the DCA/stent arm (9.5% vs 15.8%; P = 0.067). Drug-coated stent technology may have an impact on routine combined DCA/stent application. In selected patients or angiographic subsets, stent implantation yields suboptimal results. These include patients with aorta-ostial lesions, particularly ostial vein graft stenosis (Fig. 7-10), ostial LAD lesions, bifurcations, and chronic total occlusions with large plaque volumes.

increased non-Q-wave infarction and made no improvement in restenosis (48% vs 46% [not significant]). Whether more complete debulking and stent implantation will yield improved outcome has been studied in the AMIGO trial.

LEFT MAIN CORONARY ARTERY Although treatment of left main coronary artery stenoses has been the purview of cardiovascular surgery, there is an increasing amount of data on the percutaneous approaches (Fig. 7-12). Stenoses involving the left main coronary artery (LMCA) are often calcified, which makes DCA very problematic. In patients in whom the LMCA is particularly long and noncalcified, DCA may yield excellent results. Outcomes depend on whether the patient is a good surgical candidate and whether the procedure is elective, in which case the results are excellent. Alternatively, if the patient is a high-risk surgical candidate or the disease is inoperable, the procedural success may be somewhat lower and the long-term success rate is not as favorable. When percutaneous treatment of an unprotected left main trunk is required, DCA with stenting appears to be the preferred technique, if possible. Careful attention must be paid to selecting an optimal guiding catheter that will avoid damaging the LMCA but also allow adequate debulking by DCA. During athercctomy, the gui ding catheter should be withdrawn so that a coaxial alignment can be maintained. In a relatively contemporary multicenter registry of 107 patients [16], 91 were treated electively and 16 for acute infarction. Primary treatment included stents (50%) and DCA (24%). Technical success in elective patients was 98.9%. DCA and stent implantation appeared to have the best results.

AORTO-OSTIAL LESIONS Aorto-ostiallesions are often characterized by large plaque volume, excessive elasticity or rigidity, and increased potential for stent movement during deployment. Some of these lesions, particularly those in the right coronary artery (Fig. 7-11) and left main coronary artery (Fig. 7-12), are often also heavily calcified, which made the older DCA devices unattractive. In some lesions, even with high-pressure dilation greater than 20 atm, the lesion will not fully yield; thus stent deployment will be suboptimal. Use of DCA (especially the Flexi-Cut with the hardened cutter) to debulk the lesion will improve the initial angiographic results. Debulking prior to stent implantation may allow the stent to be more fully deployed and can prevent stent migration during deployment. Left anterior descending coronary artery ostial disease represents a unique subset of patients. These patients present with several problems: 1) the need for precise localization of the stent to avoid acute trapping of the circumflex; 2) the need to avoid damage to the ostium of the circumflex by plaque shift, which may result in the development of a new stenosis during followup; and 3) high restenosis rates. Directional atherectomy is ideally suited for debulking in this anatomic situation because it can be "directed" toward the dominant plaque mass and does not usually result in "no reflow," which is more typically seen with rotational coronary atherectomy. In CAVEAT I [15], 563 patients had proximal LAD lesions, 74 of which were ostial. For the ostial lesions, DCA resulted in a greater initial gain of 1.13 versus 0.56 mm (P < 0.001) but

BIFURCATION LESIONS Treatment of true bifurcation lesions remains difficult. Although stents are widely used, restenosis rates remain high. Dauerman et al. [17] reported on 70 consecutive patients with true bifurcation lesions treated with conventional PTCA or debulking plus adjunctive PTCA. In this study, either directional or rotational atherectomy was used as the approach to debulk. The strategy of debulking resulted in improved proceFigure 7-1 0. A, Extremely eccentric stenosis (arrow) in a saphenous vein graft to the posteri-

or obtuse marginal coronary artery in a 45-yearold man with disabling angina 4 years following coronary artery bypass grafting. Directional coronary atherectomy (DCA) with a 7F atherocath was successful (B, arrow, and note faint p ersisting lucency). Unfortunately, restenosis occurred 8 months later. At that time, a PalmazSchatz stent (Johnson & Johnson Interventional Systems, Warren, NJ) was implanted, and the patient was asymptomatic at 24-month followup. Perhaps the best initial strategy would have been DCA and stenting. (From Douglas [21]; with permission.)

ATLAS OF INTERVENTIONAL CARDIOLOGY

80

dural success (97% vs 73%; P=0.01) and less target vessel revascularization (28% vs 53%; P=O.OS). This has been confirmed in other small series. There are several approaches. First, if both branches have stenoses, both are large vessels, and both can be accessed by the device, both branches could be treated. In general, a safety wire is not used because of the potential for cutting it with the atherectomy device. Second, if the branch vessel is diseased but small, the parent lesion may be treated with DCA. If the branch vessel occludes during DCA, the smooth surface usually allows or may facilitate crossing the occlusion with another wire after the atherocath is removed. The smaller, more flexible Flexi-Cut device should make the approach to bifurcation lesions easier.

TREATMENT OF IN-STENT RESTENOSIS Stent implantation reduces the incidence of restenosis both clinically and angiographically by achieving a larger initial gain and preventing acute recoil [18,19]. Stents do not prevent neointimal hyperplasia and indeed are associated with increased neointimal hyperplasia. In-stent restenosis resulting from this neointimal hyperplasia may be difficult to treat, particularly when it is diffuse. Directional coronary atherectomy may be helpful in debulking these lesions and usually results in improved angiographic outcome. Obviously, the stent size

must allow for passage of the atherectomy device. Great care must be taken to avoid damage to the metal struts. This can be achieved by avoiding oversizing, documenting that the stent had been optimally placed without struts prolapsing into the lumen and using low pressure. If a coil stent design was used, DCA should be avoided.

COMPLICATIONS In the two randomized trials comparing DCA and PTCA (CAVEAT and CCAT), the occurrence rates of major complications (death, Q-wave myocardial infarction, and coronary artery bypass graft [CABG] surgery) and vessel perforation were similar. However, when a composite endpoint of death, emergency CABG surgery, acute myocardial infarction, and abrupt vessel closure was analyzed in CAVEAT, this earlyphase endpoint was encountered more frequently by patients treated with atherectomy (11% vs 5%; P< 0.001). In addition, there appeared to be a higher rate of non- Q-wave myocardial infarction in atherectomy patients in CAVEAT [2], as evidenced by creatine kinase elevation (19% vs 8%; P< 0.001). Other series have similar documented results, but not as striking an increase. In a consecutive patient series from northern New England [10], adverse events were rare: mortality, 0.9%; emergency coronary bypass graft surgery, 2.2%; and nonfatal Figure 7-11. A, Right anterior oblique view of a severe aorto-ostial stenosis (arrow) of the saphenous vein graft to the right coronary artery in a 77-year-old woman with disabling angina that was refractory to medial therapy 4 years after coronary artery bypass grafting. B, Directional coronary atherectomy (DCA) was successful (arrow) using a JR4.0 inferiorly directed guide catheter and 7F atherocath without predilating. The patient developed restenosis 3 months later, with recurrence of unstable angina. DCA was repeated with similar angiographic result and no recurrence of symptoms at 6 months. Unfortunately, restenosis is relatively common at this site with DCA, stents, and laser angioplasty.

Figure 7-12. Severe left main coronary stenosis in a 69-year-old man with disabling angina 12 years following coronary artery bypass grafting. A, Moderate lesion calcification was present on the angiogram. A saphenous vein graft (SVG) to the left anterior descending coronary artery was patent, but SVGs to the right coronary artery and obtuse marginal were occluded. Following predilation to 17 atm, directional coronary atherectomy (DCA) with a 7F atherocath was successful (B). Histology showed calcified atheroma. Catheterization 3 years later showed that the left main artery was widely patent. DCA can often be performed in the presence of mild to moderate calcification, but predilation is usually required. (From Douglas [22]; with permission.)

DIRECTIONAL CORONARY ATHERECTOMY 81

infarction, 2.8%. As was true in CAVEAT, although patients treated with DCA were more likely to have a successful procedure (OR 1.37; 95% CI 1.01-1.88; P< 0.05), they were also more likely to have a nonfatal myocardial infarction (OR 2.0; 95% CI 1.26-3.20; P < 0.01). In BOAT [8], of 1000 patients, lesion success was also improved with DCA (99% vs 97%; P=0.02) and there was no increase in major complications of death, Qwave infarction, or emergency CABG. Again, however, there was an increase in nonfatal myocardial infarction, defined as a CK-MB of greater than three times normal, that occurred in 16% versus 6% (P < 0.0001) of patients. This increase in nonfatal myocardial infarction, however, did not affect 1-year outcome; the 1-year mortality with DCA was only 0.6% versus 1.6% for PTCA (P=0.14). This ubiquitous finding of an increase in CPK elevation with DCA has led many investigators to use adjunctive lib/Ilia receptor inhibitors routinely when treating patients with this device.

CONCLUSIONS Directional coronary atherectomy has been a valuable tool for selected patients with obstructive coronary artery disease. It has allowed investigation of the plaques in these individuals to document the underlying pathophysiology of the disease state. Its role has lessened with the widespread use of stent implantation because the results of the trials performed to date document that DCA does not improve clinical outcome. Currently, DCA is used as an adjunctive therapy to enhance the initial outcome, particularly in patients with aorto-ostiallesions, bifurcation disease, and in-stent restenosis to optimally debulk a lesion prior to definitive therapy. The role this procedure will play in the future will continue to be influenced by ongoing trials, which will assess the outcome of aggressive atherectomy, particularly with the use of smaller, more flexible devices.

REFERENCES 12. Bramucci E, Angoli L, Merlini PA, eta!.: Adjunctive stent implantation follow-

1. Adelman A, Cohen E: A comparison of directional atherectomy with balloon

2.

3.

4.

5. 6.

angioplasty for lesions of the left anterior descending coronary artery. N Eng! JMed 1993, 329:228-233. Topol EJ, Leya F, Pinkerton CA, eta!.: A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease. N Eng! J Med 1993,329:221-227. Holmes, DR, Topol EJ, Adelman AG, et al.: Randomized trials of directional coronary atherectomy: implications for clinical practice and future investigation. JAm Coli Cardio/1994, 24:431-439. Holmes lJR, Topol EJ, CAVEAT-TIInvestigators: A multicenter, randomized tria I of coronary angioplasty versus directional atherectomy for patients with saphenous vein bypass graft lesions. Circulation 1995,91:1966-1974. Holmes DR: Historical background and lessons learned from early randomized trials. Semin Interv Cardia! 2000, 5:163-165. Simonton CA: Directional coronary atherectomy: optimal athcrcctomy trials and new combined strategies with coronary stents. Semin Interv Cardia! 2000,

ing directional coronary atherectomy in patients with coronary artery disease. JAm Coil Cardio/1998, 32:1855-1860. 13. Moussa I, Moses J, Colombo A: Atherectomy plus stenting: what do we gain? Semin Interv Cardio/2000, 5:217-225. 14. Moussa I, Moses J, DiMario C, eta!.: Stenting after optimal lesion debulking (SOLD) registry: angiographic and clinical outcome. Circulation 1998, 98:1604-1609. 15. Boehrer JD, Ellis SG, Pieper K, eta!.: Directional atherectomy versus balloon

angioplasty for coronary ostial and non-ostial left anterior descending coronary artery lesions: results from a randomized multicenter trial. JAm Call Cardio/1995, 24:1380-1386. 16. Ellis SG, Tarnai H, Nobuyoshi M, eta/.: Contemporary percutaneous treatment of unprotected left main coronary stenoses: initia 1 results from a mu IIicenter registry analysis 1994-96. Circulation 1997,96:3867-3872. 17. Dauerman HL, Higgins PJ, Sparano AM, eta!.: Mechanical de bulking yersus balloon angioplasty for the treatment of true bifurcation lesions. JAm Call Cardio/1998, 32:1845-1852. 18. Palacios IF, Sanchez PL, Mahdi NA: The place of directional coronary atherectomy for the treatment of in-stent restenosis. Semin Interv Cardia/ 2000,

5:193-198.

7. Simonton CA, Leon MB, Bairn DS, eta!.: 'Optimal' directional coronary atherectomy: final results of the Optimal Atherectomy Restenosis Study (OARS). Circulation 1998, 97:332-339. 8. Bairn DS, Cutlip DE, Sharma SK, eta!.: Final results of the Balloon vs Optimal Atherectomy Trial (BOAT). Circulation 1998,97:322-331. 9. Suzuki T, Hosokawa H: Effects of adjunctive balloon angioplasty after intravascular ultrasound-guided optimal directional coronary atherectomy: the result of adjunctive balloon angioplasty after coronary atherectomy study (ABACAS). JAm Call Cardio/1999, 34:1028-1035. 10. O'Rourke DJ, Malenka DJ, Robb JF, eta!.: Results of directional coronary atherectomy in northern New England. Am J Cardio/1997, 79:1465-1470. 11. Kiesz AS, Rozek MM: Acute directional coronary atherectomy prior to stenting in complex coronary lesions: ADAPTS Study. Catl!et Cardiovasc Diagn

5:209-216. 19. Haberbosch W, Waas W, Waldecker B, et al.: Directional coronary atherectomy of in-stent restenosis: a two-center experience. J Intervent Cardia/ 2000, 13:93-100. 20. Douglas JS Jr.: Balloon angioplasty: matching technology to lesions. In The

Practice of Interventional Cardiology, edn 2. Edited by Vogel JHK, King SB III. St. Louis: Mosby-Year Book; 1993:85. 21. Douglas JS Jr.: Percutaneous strategies for management of angina pectoris following coronary bypass surgery. ln State-of-the-Art of Invasive Cardiology: Current Diagnostic and Therapeutic Issues. Edited by Vetrovec GW, Carabello BA Mount Kisco, NY: Futura Publishing Company; 1996:483-499. 22. Douglas JS Jr.: Percutaneous coronary intervention after bypass surgery. In Handbook of Cardiovascular Intervention. Edited by Bertrand M, Serruys P, Sievart lJ. London: Churchill Livingstone; 1996.

1998,45:105-112.

ATLAS OF INTERVENTIONAL CARDIOLOGY 82

Rotational Coronary Atherectomy Verghese Mathew and Kirk N. Garratt Rotational atherectomy uses the principle of high-speed abrasive differential cutting to ablate atheromatous plaque. This system, developed by David Auth, was approved for coronary use in 1993. Rotational atherectomy and other newer devices were designed principally to aid in the procedural success of percutaneous coronary intervention and potentially to reduce the occurrence of restenosis compared with that achieved with balloon angioplasty. Obviously, none

of the newer devices (except for stents) have reduced the rates of restenosis, but rotational atherectomy may indeed be useful in certain lesion subsets in clinical practice. This chapter discusses the principles of operation, system and design characteristics, relevant clinical data, technical and procedural issues, and management of complications associated with rotational atherectomy.

and can be ablated by the advancing burr. Conversely, healthy tissue is relatively elastic and therefore is deflected away from the cutting edges of the burr (Fig. 8-2A and B) .

PHYSICAL PRINCIPLES The Rotablator (Boston Scientific, Natick, MA) system is a highspeed, low-powered rotary ablation device (Fig. 8-lA and B). This system operates on the principles of differential cutting and orthogonal displacement of friction. DIFFERENTIAl CUTTING

Differential cutting is the ability to cut one material while sparing another based on differences in composition. Diseased atheromatous tissue, whether composed of calcium, fibrotic tissue, neointima, or lipid-rich material, is relatively inelastic

ORTHOGONAl DISPlACEMENT OF fRICTION

Friction occurs when moving surfaces are in contact, but can be minimized by motion perpendicular (or orthogonal) to the contact surface. The principle of orthogonal displacement of friction permits movement of the burr through tortuous segments of the coronary arterial circulation. At rotational speeds greater than 60,000 rpm, longitudinal friction is minimized, facilitating advancement and withdrawal of the a therectom y burr. Figure 8-1. The Rotablator (Boston Scientific, Natick, MA) system. A, The Rotablator burr and drive shaft function essentially as a rotary sander (inset) . Gentle advancement into the lesion ablates the plaque into microparticles. B, Microparticulate debris. Note the size of the microparticles in relation to erythrocytes and a 5-]lm bead. (B from Reisman [1]; with permission.)

A

Figure 8-2. Differential cutting. The principle of differential cutting allows ablation of diseased (inelastic) tissue and deflection away from healthy (elastic) tissue. A, The elasticity of normal tissue allows it to deflect away from the rotating surface of the advancing burr. B, Diseased (inelastic) tissue is unable to deflect away from the advancing burr; thus, it is ablated by the diamond chips on the distal end of the burr.

ATLAS OF INTERVENTIONAL CARDIOLOGY 84

SYSTEM COMPONENTS The Rotablator system consists of a nickel-plated brass elliptical burr that is coated on the leading edge with diamonds 20 to 30 pm in diameter; the diamond chips protrude approximately 5 pm above the nickel plating to form the abrasive surface that ablates atheromatous plaque. The burr is attached to a flexible drive shaft that is driven by compressed air or nitrogen. A 4.3F sheath covers the drive shaft and protects arterial tissue from injury caused by the spinning drive shaft, and also delivers flush through the system (Fig. 8-3). The proximal end of the drive shaft is attached to the advancer, which provides a mechanism for advancing the drive shaft and rotating burr toward and away from the lesion The rotational speed is regulated by air pressure; depressing the foot pedal activates the burr as well as the locking system to prevent the guidewire from spinning while the burr is rotating. The burr is available for coronary use in 1.25, 1.5, 1.75, 2.0, 2.15, 2.25, 2.38, and 2.5 mm diameters, although larger sizes are available for peripheral vascular use. In general, up to a 1.75-mm burr can be used in a 7F guiding catheter, whereas a 2.38-mm burr requires a 9F system, and a 2.5-mm burr requires a lOF system. An exchangeable drive shaft was designed to simplify the Rotablator procedure and reduce costs. This design allow s the operator to change only the burr I drive shaft if another burr or burr size is required, using the same advancer throughout the procedure regardless of the number of burrs used (Fig. 8-4). The original Rotablator guidewire (C type) is a 0.009-inch stain-

less steel wire with a flexible platinum radiopaque tip 0.017-inch in diameter. The A-type wire is similar to the C type except that the inner core extends to the distal end of the guidewire, adding further stiffness. The RotaWire floppy guidewire (Boston Scientific, Natick, MA) tapers from 0.009 to 0.005 inch in the distal end and has a radiopaque platinum tip 0.014-inch in diameter (Fig. 8-5A and B). The control console provides measures of operation during the procedure. The rotational speed is displayed and controlled by a knob that regulates the pressure of compressed gas. Connections on the front of the console are made to the advancer, whereas connections in the rear of the console are for the compressed gas supply hose and the foot pedal. A recorder jack is also present, which allows for connection of a chart recorder to monitor rotational speed as a paper copy if desired.

CLINICAL DATA Rotational atherectomy was evaluated in a multicenter registry, the findings of which were the basis of US Food and Drug Administration approval of the device. The registry began in 1988, and initially included patients whose anatomy was deemed suboptimal for balloon angioplasty, eg, restenotic lesions after angioplasty or prior angioplasty failures. As experience developed with the device, more complex lesions, including long lesions and calcific lesions, were enrolled. The registry included a total of 2953 procedures (3717lesions). A variety of lesions were treated (Fig. 8-6), with similar procedural success rates, with rotational atherectomy followed by adjunctive balloon angioplasty

Figure 8-3. Burr, drive shaft, and sheath loaded onto a RotaWire (Boston Scientific, Natick, MA).

Figure 8-4. Exchangeable drive shafts. (From Reisman [1]; with permission.)

Figure 8-5. Rotablator (Boston Scientific, Natick, MA) guidewire types. A, Type C. B, Type A. C, RotaWire Floppy. D, RotaWire Extra Support.

B

0

ROTATIONAL CORONARY ATHERECTOMY 85

(Fig. 8-7). Major complications included 1% mortality, 1.2% Qwave myocardial infarction, and 2.5% coronary bypass surgery. Angiographic complications included 13.7% dissection, 1.1% abrupt closure, and 0.7°/r, perforation. In the 50% of patients who had 6-month angiographic follow-up, restenosis was 53%. The ERBAC (Excimer laser, Rotablator and Balloon Comparison) Trial compared rotational atherectomy to other devices in a randomized fashion. Rotational atherectomy had a lower rate of major complications, less residual stenosis, and less crossover to other strategies. At follow-up, rates of death and Qwave myocardial infarction were similar between the groups, and restenosis tended to be higher in the laser angioplasty and rotational atherectomy groups compared with balloon angioplasty, although this was not statistically significant (Fig. 8-8). The STRATAS (Study to Determine Rotablator and Transluminal Angioplasty Sh·ategy) trial randomly assigned

500 patients to an aggressive debulking strategy (burr-to-artery ratio of 0.7 to 0.9) with no- or low-pressure (1 atm) adjunctive angioplasty compared with a moderate debulking strategy (burr-to-artery ratio of 0.5 to 0.7) with conventional angioplasty at routine pressures. The goal was to test the hypothesis that aggressive debulking with minimal vessel stretch would reduce the impetus for restenosis. The acute success rates were similar between the two groups, and 6-month event rates, including restenosis, were comparable. A substudy of this trial demonstrated that decelerations of greater than 5000 rpm for more than 10 seconds or 7000 rpm for more than 5 seconds were associated with an increase in major cardiac events and enzyme elevation after the procedure [2,3]. DART (Dilation vs Ablation Revascularization Trial) compared rotational atherectomy ± adjunctive low-pressure (::::; 1 atm) angioplasty with conventional angioplasty in type Figure 8-6. Lesion types treated in the Multicenter Rotational Atherectomy Registry.

100 0 80 70

c: !;Q..

60

so 40 30 20 10 0 (> 10mm

J1111 100

-

Figure 8-7. Procedural success rates from the Multicenter Rotational Atherectomy Registry.

Rot.lllonal ath 15 mm) in vessels smaller than 3.2 mm in diameter were randomly assigned to angioplasty plus stent or rotational atherectomy plus stent. In-hospital major adverse cardiac events were comparable between the angioplasty plus stent arm and the rotational atherectomy plus stent arm, although rotational atherectomy appeared to yield a higher procedural success rate, greater postprocedural minimum luminal diameter, and greater acute gain (Fig. 8-9). However, at 6 months, target vessel revascularization rates were similar between the two groups (11.5% for angioplasty;

THE ERBAC TRIAL

E.I.M

PI

nt , n

60112 80 15 3 4.8 1-o

68/ 10 6 32 15 6.2 174 85

3. 1/3.8 3 54

010.7

13 91 31 16 __ 3

p

~2

191 81 2.6 3.2 46 62

46 60

< 0.001 < o.os 0.04

0.04

Figure 8-9. Data from the SPORT (Stenting Post-Rotational Atherectomy Trial). NS-not significant; PICA- percutaneous transluminal coronary angioplasty; QCA-quantitative coronary angiography.

THE PORTTRIAL

Les1on length, mm Ret r nc VI ual d1ameter. mm Preprocedure min1mum lum n diameter, mm Diam t r t no i pr pr edur , "n Po tprocedur mm1mum lumen diameter, mm ut gain, mm

2.83 0.88

0.48

2.87

0.4 ~

0.87

0.49 0.38

"' ' '

86.0 9.3 2.-4

85.8 10.4 2.81

0.032

1.86

1.94

0.041 P \~L!...~

ng1ographic Pr edural lini al su

. Ulle ~·

100 88.1 87.3

Figure 8-8. Data from the ERBAC (Excimer laser, Rotablator and Balloon Angioplasty Comparison) triaL ACC-American College of Cardiology; AHA- American Heart Association; CABG-coronary artery bypass grafting; ELCA- excimer laser coronary angioplasty; MI-myocardial infarction; NS-not significant; PTCA- percutaneous transluminal coronary angioplasty; PTRA-percutaneous transluminal renal angioplasty.

100 93.6

0.011-t

91.

ROTATIONAL CORONARY ATHERECTOMY 87

14.4% for rotational atherectomy), as was angiographic restenosis in the 350 patients who had follow-up angiography (27.6% in the angioplasty group; 30.4% in the rotational atherectomy group). The use of debulking strategies, including rotational atherectomy, has been studied in the management of in-stent restenosis. Two large trials were performed regarding this issue and are discussed more extensively in Chapter 6, In-stent Restenosis. The ROSTER (Randomized Trial of Rotational Atherectomy vs Balloon Angioplasty for Diffuse In-stent Restenosis) [7] demonstrated that in the treatment of diffuse instent restenosis, rotational atherectomy resulted in lower rates of dissection and need for repeat stent implantation, and lower clinical restenosis than balloon angioplasty. The ARTIST (Angioplasty vs Rotational Atherectomy for the Treatment of Diffuse In-stent Restenosis) [8] trial actually demonstrated that balloon angioplasty was superior to rotational atherectomy with low-pressure balloon inflations with respect to clinical and angiographic outcome. The discordant results of these two trials are problematic. Possible explanations for these differences include a more aggressive debulking strategy in the ROSTER trial, and exclusion by intravascular ultrasound of inadequately expanded stents. The incidence of this latter category in the ARTIST trial is unclear and was not definitively excluded. It is believed that debulking for suboptimally deployed stents (undersized, poorly apposed) may not afford a substantial clinical benefit. Nonetheless, the role of rotational atherectomy in the treatment of diffuse in-stent restenosis remains equivocal.

PROCEDURAL ASPECTS AND TECHNIQUE Although this chapter is not meant to be a complete instructional manual of rotational atherectomy, a few salient procedural and technical features are highlighted here. Guide sizing should be undertaken, based on the largest anticipated burr size to be used; we generally strive for a burr-to-artery ratio of approximately 0.6 to 0.7. Selection of appropriate guiding catheters based on the aortic root and coronary anatomy is discussed in Chater 4, Guide Selection;

A

one must also bear in mind that guiding catheters with relatively tight curves, such as an Amplatz, may make burr advancement through the guide slightly more difficult, although this can be overcome by using larger diameter guides. If the vessel to be treated supplies the atrial ventricular node (right coronary or circumflex), a temporary transvenous pacemaker should be placed in the right ventricular apex. Alternatively in these situations, the use of intravenous aminophylline (200-300 mg) may preclude the need for temporary pacemaker insertion. Intravenous nitroglycerin is often used to maintain coronary vasodilatation, although care must be taken not to produce systemic hypotension because an adequate mean arterial pressure is desirable to help facilitate flow of microparticles through the microcirculation. In conjunction with this, vasodilators are given through the Rotablator flush, which may include nitroglycerin, verapamil, and adenosine. In the event of hypotension related to rotational atherectomy, vasopressors should be readily available. Clinical considerations include the presence of unstable angina, or angiographic evidence of thrombus, for which rotational atherectomy would not be considered optimal treatment. Patients with congestive heart failure or significant reduction of left ventricular ejection fraction may also pose a greater procedural risk because of the potential for associated transient worsening of left ventricular dysfunction. Measures to provide circulatory support, pharmacologic or mechanical, should be undertaken intraprocedurally. Periprocedural intra-aortic balloon pump support may be required in patients with left ventricular dysfunction. The RotaWire Floppy (Boston Scientific, Natick, MA) is the guidewire most commonly used in our practice. The distal tip can be gently curved by compressing it between the thumb and the forefinger; a "stripping," or "ribboning," technique can stretch the platinum spring and should be undertaken carefully. Occasionally, in lesions that are extremely difficult to cross, another coronary guidewire can be used to cross the lesion and can be changed by withdrawing it over a transfer catheter and replacing it with a rotational atherectomy w ire. It should be noted that a 0.018-inch compatible exchange catheter needs to be used if such an exchange is to be made. The platinum tip of the Rotablator wire must be distal

c

B

Figure 8-10. A, An eccentric lesion on the superior aspect of the left main coronaty artery is depicted. B, Rotational atherectomy over a guidewire positioned in the circumflex results in minimal ablation, because of guidewire

bias directing the burr away from the bulk of the plaque. C, With repositioning of the guidewire into the left anterior descending artery, favorable guidewire bias is achieved. Improved debulking as a result of repositioning.

ATLAS OF INTERVENTIONAL CARDIOLOGY 88

to the lesion because the burr cannot track over this segment of the guidewire. Additionally, the tip should not be placed in a small branch, in the event that the wire would spin along with the burr, which may result in significant vessel trauma if the distal tip is fixed in the small branch. The guidewire should be positioned to optimize the vector of ablation of the lesion to be treated. The interaction of the wire with the vessel wall may result in guidewire bias, which may be favorable or unfavorable (Fig. 8-lOA-C). Once the lesion is crossed, the appropriate burr size is chosen, and the burr is loaded onto the RotaWire, the burr should be platformed outside the body, with the operator taking care to ensure that the wire clip is used (Fig. 8-11). With burr sizes less than 2 mm, we generally platform at 160,000 to 180,000 rpm, although with larger burr sizes, we tend to platform at 150,000 to 160,000 rpm. If the lesion is distal to a particularly tortuous proximal segment, there may be some loss of rpm at the lesion. Care should be taken to avoid substantial drops in rpm during runs (drops < 5000 rpm are desirable). Each run should be for no longer than 30 to 40 seconds, and contrast medium should be injected after each run to check for vessel patency and flow. Intracoronary nitroglycerin, verapamil, and adenosine can also be administered via the guide catheter between runs.

causing obstruction of the distal microcirculation. The incidence of slow or no flow may be reduced by starting with the small burrs and lower speeds and avoiding decreases of more than 5000 rpm. When slow flow occurs, giving intracoronary vasodilators such as nitroglycerin, verapamil, or adenosine through the guiding catheter may be helpful. If prolonged slow flow or no flow occurs, a transfer catheter can be placed in the distal vessel and small doses of nitroprusside, or other vasodilators, can be administered directly into the distal bed through the transfer catheter. Slow or no flow may also be the result of coronary dissection, and therefore the operator must carefully evaluate the possibility of mechanical obstruction due to dissection versus a microvascular problem, because obviously the treatments for the two are vastly different. If dissection does occur, further rotational atherectomy should not be performed, and balloons and stents may be used. Coronary perforation may occur with rotational atherectomy, and appears to be associated with eccentric, tortuous lesions, as well as longer lesions. Unfavorable guidewire bias may straighten out tortuous vessels, directing the rotating burr preferentially into one wall of a vessel versus another [7]. Treatment might include prolonged occlusive balloon dilation and reversal of anticoagulation to seal the perforation, although the approval and availability of covered stents such as the Jomed stent Gomed, Helsingborg, Sweden) makes this a complication that can be dealt with more effectively than in previous years using percutaneous COMPLICATIONS techniques. This is discussed in more detail in Chapter 13, Slow flow or no-reflow may occur when an excessive quantity of Complications of Percutaneous Coronary Artery Intervention. microparticles or excessively large particles result from ablation,

IMPLICATIONS OF AVAILABLE CLINICAL DATA AND ROLE OF ROTATIONAL ATHERECTOMY IN CURRENT CLINICAL PRACTICE From the available data, it appears that rotational atherectomy is a useful technique in the treatment of coronary atherosclerosis, including complex coronary lesions. This can be done with good acute procedural success and satisfactory intermediate term outcome. Randomized trials comparing rotational atherectomy with balloon angioplasty have not shown a clear benefit using this technique, although the ability to treat more complex lesions successfully may be a potential advantage of this approach in certain lesion subsets, such as very rigid fibrocalcific lesions, which cannot be expanded using balloon angioplasty alone. Plaque modification, including the removal of superficial calcification, may

Figure 8-11. WireClip Torquer (Boston Scientific, Natick, MA). (From Reisman [1]; with permission.)

Figure 8-12. Treatment of ostial stenosis. A, A high-grade, focal lesion is evident at the ostium of a right coronary artery. B, C, The lesion is treated first with a small burr, then with a large one. Continued on next page

ROTATIONAL CORONARY ATHERECTOMY 89

improve the likelihood of successful angioplasty or stent deployment. However, it should be made clear that rotational atherectomy has not been demonstrated to afford any benefit with regard to reducing restenosis. In our practice, the use of rota-

tional atherectomy has decreased over the last few years. It is still used for lesions that appear to be heavily calcified, preferably as assessed by intravascular ultrasound. Ostial (Fig. 8-12A-E) and bifurcation lesions (Fig. 8-13A-F) are still

Figure 8-12. (Continued) D, Atherectomy facilitates placement of a coronary stcnt. E, The final result is excellent, with disruption of the aorta-ostium.

the diagonal branch is preserved, without ostial compromise by plaque shifting. D, A safety wire is placed into the diagonal branch, and balloon angioplasty with stent placement is performed in the LAD. E, The ostial lesion in the diagonal branch is treated with balloon angioplasty. F, The final outcome shows excellent results at the LAD and diagonal ostium.

Figure 8-13. Treatment of bifurcation lesions. A, A complex, high-grade stenosis within the left anterior descending artery (LAD), at the bifurcation of a diagonal branch vessel. B, Rotational atherectomy of the LAD lesion; note that a safety wire cannot be placed into the side branch. C Following rotational atherectomy, the LAD is improved and

ATLAS OF INTERVENTIONAL CARDIOLOGY 90

occasionally treated by using rotational atherectomy, particularly to reduce the chance of plaque shift. Rotational atherectomy is often used to treat lesions that are nondilatable, although these lesions are encountered uncommonly (Fig. 8-14A-F). In addition, diffuse lesions are sometimes treated using rotational atherectomy followed by stenting. Rotational atherectomy has been used relatively frequently in the treatment of in-stent restenosis since 1999 (Fig. 8-15A-G). However, with the conflicting data of ARTIST and ROSTER, along with the suggestion that in patients undergoing brachytherapy, rotational atherectomy

did not afford any incremental benefit beyond that provided by balloon angioplasty, a decline in the use of rotational atherectomy for in-stent restenosis has occurred. Rotational atherectomy is rarely used in treating saphenous vein graft lesions; the occasional in-stent restenosis lesion (Fig. 8-16A-F) would be the main indication. Rotational atherectomy, therefore, appears to remain most useful in a subset of patients undergoing coronary interventions that require lesion modification w ith the goal of achieving successful stent deployment.

Figure 8-14. Treatment of nondilatable stenosis. A, Focal, high-grade stenosis in distal right coronary artery. B, Balloon angioplasty is attempted. Appropriately sized balloons will not pass; angioplasty is attempted with a 1.5-mm balloon. C, The 1.5-mm balloon fails to improve the lesion . D, Following exchange of the 0.014-inch coronary guidewire for a rotational atherectomy guide wire, rotational atherectomy is performed using serial burrs. E, Following rotational atherectomy, the lesion is improved and distal blood flow is enhanced. F, After rotational atherectomy, balloon angioplasty with appropriately sized balloon, and stent placement, excellent results are achieved.

ROTATIONAL CORONARY ATHERECTOMY 91

Figure 8-15. Treatment of diffuse coronary artery disease. A, Prior to injection of contrast agent, the positions of several previously placed coronary stents are evident. B, Diffuse disease is present in the diagonal branch, and a tubular lesion is present in the left anterior descending artery (LAD). The disease includes in-stent restenosis and atherosclerosis. C, D, Rotational atherectomy of diagonal disease performed with a small burr, then a large one. E, Following adjunctive percutaneous transluminal coronary angioplasty (PTCA), a nice result is achieved in the diagonal branch. F, Atherectomy of the LAD is performed. G, Following PTCA, an excellent result is achieved.

ATLAS OF INTERVENTIONAL CARDIOLOGY

92

Figure 8-16. Treatment of vein graft lesion. A, A focal in-s tent restenosis lesion in a vein graft. B-D, Serial debulking with increasingly large rotational atherectomy burrs. E, Result after rotational atherectomy alone

is very satisfactory. F, Final results after adjunctive percutaneous transluminal angioplasty is optimal.

REFERENCES 1.

2.

3.

4.

Reisman M: Guide to Rotational Atherectomy. Royal Oak, Ml: Physicians' Press; 1997. Eccleston DS, Horrigan MC, Cowley MJ, eta/.: Is there a role for strip chart recording to guide rotational atherectomy7 Initial findings from STRATAS (abstract). JAm Col/ Cardio/19%, 27:292A. Horrigan MC, Eccleston OS, Williams DO, et a/.: Technique dependence of CKMB elevation after rotational atherectomy (abstract). Circulation 1996, 94:!-560. Reisman M, Buchbinder M, Sharma SK, eta/.: Dilation vs. Ablation Revascularization Trial (DART}. Circulation 1997, 96(suppl A):l-467.

5.

6. 7.

8.

Safian RD, Feldman T, Muller DWM, eta/.: Coronary Angioplasty and Rotablator Athercctomy Trial (CARAT). Catheter Cardiovasc Interv 2001, 53:213-220. Buchbinder M: Paper p resented at the American Heart Association Scientific Session 2000. Sharma SK, Kini A, King T, eta/.: Randomized trial of rotational atherectomy versus balloon angioplasty for diffuse in-stent restenosis. (ROSTER): final results (abstract). Circulation 2000, 102:11-730. Ferguson JJ: Meeting highlights of the 22nd Congress of the European Society of Cardiology. Circulation 2001, 103:E41-E45.

ROTATIONAL CORONARY ATHERECTOMY 93

Cutting Balloon Angioplasty Verghese Mathew and Anoop Chauhan Conventional balloon angioplasty restores coronary blood flow at the expense of some degree of arterial wall injury. The occurrence and degree of vessel wall injury is unpredictable and, in a proportion of cases, results in the complications associated with conventional percutaneous transluminal coronary angioplasty (PTCA). Cutting balloon technology has evolved over nearly a decade. Although initially approved by the U.S. Food and Drug Administration (FDA) in 2000, the cutting balloon has had a rather modest rate of incorporation into interventional practice in the United States. Nonetheless, the cutting balloon may be useful in certain lesion

subsets that respond poorly to conventional PTCA and are also not ideal for stenting. The cutting balloon operates as a microsurgical dilation device, with the objective of scoring atheromatous plaque, which would enable or facilitate angioplasty. The premise behind creating an atherotomy in this fashion is that the creation of controlled endovascular incisions of the atheromatous plaque would reduce the likelihood of severe uncontrolled vessel injury and dissection (Figs. 9-lA and B and 9-2A and B). Scoring the plaque in such a manner may also enable angioplasty to be performed with lower inflation pressures, thus reducing the possibility of barotrauma.

DELIVERABILITY

THE DEVICE The cutting balloon consists of a noncompliant angioplasty balloon on which three (for balloons 3.25 mm or smaller) or four (for balloons 3.5 mm or larger) atherotomes are mounted longitudinally on its outer surface (Fig. 9-3). The height of each atherotome is 0.005 inch. The initial device was released as an over-the-wire version; subsequently, however, a rapidexchange system became available. Cutting balloons are available in quarter sizes from 2.0 to 4.0 mm. Initially, the available device lengths were 10 and 15 mm; now, a 6-mm length is also available.

The longitudinal atherotomes reduce the flexibility and trackability of the balloon, making delivery of the device somewhat reminiscent of first-generation coronary stent systems. In addition, the higher balloon profile (compared with conventional balloons) of the device may preclude crossing of high-grade lesions, and may preclude delivery to a target lesion in the presence of moderate or severe proximal vessel tortuosity or significant calcification. In general, we tend to use the shorter balloon lengths to increase the likelihood of successful device delivery. We reserve the 15-mm length for relatively proximal, less severely stenosed lesions without significant angulation or

Figure 9-1. Conventional angioplasty exerts its force on the entire vessel wall, which in turn yields at the point of least resistance. Lumen enlargement occurs primarily by vessel wall expansion, with a small degree of

plaque compression. A, Perivascular bleeding and denudation of the endothelium occur. B, After 14 days, extensive cellular proliferation and thrombosis are apparent in the lumen.

Figure 9-2. After cutting balloon angioplasty, a relatively smooth incision is made by the atherotome. A, No rips or tears in the media are apparent, no perivascular bleeding is seen, and the endothelium is relatively intact.

B, After 14 days, the artery looks well healed, without significant intimal proliferation or luminal narrowing.

ATLAS OF INTERVENTIONAL CARDIOLOGY

96

proximal vessel tortuosity, and use this size only if the extra balloon length is required. Additionally, resistance to the advancement of the balloon may be encountered in angulated guide catheter configurations. Larger inner diameters of guiding catheters may overcome this resistance. In general, however, devices with diameters less than 3 to 3.25 mm will go through a 6F guiding catheter, whereas larger nominal diameter devices require at least a 7F guide. Any 0.014-inch coronary wire may be utilized; a floppy wire, however, may be helpful in negotiating tortuous segments by reducing wire bias, although, as with conventional PICA or stent delivery, a stiffer wire may be required, along with appropriate guide support (see Chapter 4, Guide Selection). A "buddy" wire may also be used in such cases to facilitate balloon catheter advancement and delivery. If the cutting balloon cannot be advanced through a critical lesion, predilation with a small-diameter conventional balloon may be undertaken to facilitate passage of the device.

IVUS may also be helpful for sizing. A more conservative sizing strategy is generally recommended for ostial lesions, very angulated lesions, or small vessels, to reduce the unpredictable risk of perforation, which has been reported in approximately 1% of cases. Sizing down by 0.25 mm or, certainly, avoiding oversizing in such cases is our practice. Checking the angiographic appearance of the target·lesion in between inflations may guide choice of the inflation pressure utilized, particularly when the operator thinks that the balloon diameter chosen may be at the upper limits of what he or she feels comfortable with in treating a particular lesion. A lower pressure may be initially used; if the operator finds no evidence of perforation after the initial inflation, a higher pressure may be utilized on the subsequent inflation. Early in an operator's experience with the cutting balloon, the avoidance of an aggressive balloon sizing strategy is a reasonable way of becoming comfortable with the device.

PREPARATION AND INFLATION AND DEFLATION

Initial device preparation requires a wet, negative-pressure preparation procedure, similar to conventional PTCA balloons. Initial manufacturer recommendations suggest a more vigorous negative-pressure vacuum utilizing a stopcock, although we do not routinely prepare our balloons in this manner. When positioned at the lesion site, the cutting balloon should be inflated slowly (1 atmosphere per 3 to 5 seconds) to the desired pressure. Deflation should also be carried out at the same rate. More rapid inflation or deflation may increase the likelihood of balloon deformity and rupture, the occurrence of which is of great concern. Although some operators go to relatively high pressures, we generally do not advocate the use of pressures above 10 atmospheres. Multiple (two or three) inflations of 60 to 90 seconds (including inflation and deflation times) are probably better than a single inflation, allowing for more plaque scoring and may improve outcomes [1]. CUTTING BALLOON SIZING

Balloons may be sized 1:1 based on angiographic vessel size, or by media-to-media measurements by intravascular ultrasound (IVUS). Accounting for significant discrepancies in vessel sizing based on angiographic versus IVUS criteria is even more critical than with conventional balloons, since oversizing of the cutting balloon substantially increases the chance of arterial perforation. When such sizing discrepancies occur, a more conservative (smaller) sizing strategy, at least initially, may be reasonable. For in-stent restenotic lesions, most operators recommend oversizing the cutting balloon by 0.25 mm, and some by 0.5 mm, provided that the inflation occurs entirely within the stent. In this regard,

CLINICAL DATA The Global Randomized Trial (GRT), carried out from June 1994 through November 1996, was a multicenter, randomized trial comparing the cutting balloon to conventional PICA. The study included 1245 patients at 31 centers in the United States, Canada, France, Belgium, and The Netherlands. In the cutting balloon arm (622 patients), a single inflation of as much as 8 atmospheres for a maximum of 90 seconds was allowed, and subsequent inflations with a conventional balloon were permitted for residual stenosis of more than 40%. The shortterm and 6-month clinical and angiographic data (unpublished) demonstrated comparable outcomes between the two groups (Figs. 9-4 and 9-5). The Cutting Balloon Versus Angioplasty (CUBA) Trial enrolled 260 patients in 8 centers in Spain. Unlike the GRT, the CUBA Trial permitted as many as three cutting balloon inflations. Use of the cutting balloon resulted in fewer dissections, including complex dissections, than did conventional PTCA, with a trend toward lower angiographic restenosis (30% vs 47%; P = 0.05), without significant impact on the rates of repeat revascularization (Fig. 9-6). An IVUS substudy of the CUBA Trial demonstrated that in hypoechoic (soft) plaques, the mechanism of dilation was plaque compression and redistribution with either cutting balloon or conventional PTCA, whereas in fibrotic or calcific lesions use of the cutting balloon resulted in pie-shaped cuts with an elliptical lumen shape, w ith less dissections than those seen with conventional PTCA. This supports the notion that in fibrotic lesions plaque scoring may be beneficial in reducing vessel injury. Figure 9-3. Cutting balloon.

CUTTING BALLOON ANGIOPLASTY

97

GLOBAL RA DOMIZED TRIAL-Cll ICAL OUTCOMES CUTIIb/G 66LLOO

.

13 .6°1o (84/61 1.3°1o (8/61 ) 4.%(2/6 1 ) 1.5°1o (9/6 171 3.2% 120/61 7) 1.0% (6/61 I 11. 0 (, ( 2/61 71 1.5°'o (9/6 17) 10.5%16 /6 1 ) 1. %18/ 17) O.J 01o (2/6 1 ) 0.3°'o (2/617) 0.8% (5/61 ) )

Ml

Q wa\ ·on-Q wave Ml Em rg nt BG TLR~

BG lper pll PT lper ptl ubacut lo ure Bleeding complication a cular compli ation lini al perforation



0. 01o(21621 1 2 .4 °1o ( 18/62 1) 1. 1°/o (7/62 1I 1.3°io (11 /621) 1.0% 16/62 1 I 14.8°o 19- 162 1) 2. 1°/o (13/6_ 1 )

1.8°o 1-0. 0 o, 3.9°o) 0.3°o l-0.9°1o, 1.6°'o) 1.5°o (-0.3°o, 3.2°o) 0°1o 1-2. 01o, 1.7°JoI -3 .1°o (-6. 0 o, 0.6°o) -0.6°o (-2.1"o, 0.8°o) --.2°o (-5.8°1o, 1.4°o) -0.3°o l-1.5%, 3.0 1o) 0.3°·o l-1.9°1u, 0. 0 o) 0.1 °o )-1. 9°11, l.O'}o) 0.8°o )-0.4°1o, 2.3°o)

12. "" t 9/6211 1.6% (1 0/6_ 1) 0.0°1o (0/6_ 1) 0.2% 11/621 ) 0.0°to 10/6_ 1I

''umbt-1'\ are •. ocounl 's.ampl \ozeo 'Doneren e =[\l'nl.r 8·E,enl rrn Ep,,

=