Tips and Tricks in Interventional Therapy of
CoronaryBifurcation Lesions
Edited by Issam
D. Moussa Antonio Colombo
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Tips and Tricks in Interventional Therapy of Coronary Bifurcation Lesions
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Tips and Tricks in Interventional Therapy of Coronary Bifurcation Lesions Edited by Issam D. Moussa New York Presbyterian Hospital–Weill Medical College of Cornell University New York, New York, U.S.A.
Antonio Colombo San Raffaele Scientific Institute EMO-GVM Centro Cuore Columbus Milan, Italy
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c 2010 Informa UK Ltd First published in 2010 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-13: 978-1-84184-726-9 Orders Informa Healthcare Sheepen Place Colchester Essex CO3 3LP UK Telephone: +44 (0)20 7017 5540 Email:
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Foreword
Bifurcation PCI is not easy. The decision tree for the approach to bifurcations requires knowledge and experience to move through the procedure with minimal time, effort, and complications. In some cases, avoiding the bifurcation stenting altogether may be the best approach. Although the many ways to perform bifurcation PCI can be simplified into two major approaches—(i) stent with provisional side branch stent and (ii) planned stents from the start—there remains controversy as to the best approach for a particular lesion that has a wide variability of mother/daughter branch size ratio, angulation, ostial atherosclerotic involvement, and potential for extensive myocardial infarction if the technique fails. In the practice of PCI and especially bifurcation PCI, the old adage that there is no such thing as “simple” PCI has never been truer. Bifurcation lesions have the most complex anatomic configurations and hence potential for multiple individualized approaches. One only needs to recall the six or more bifurcation classification schemes, and understand and apply one of the more than eight stent techniques to the particular bifurcation anatomy for the best outcome. Unfortunately, understanding which technique is associated with best outcomes for bifurcation PCI is not that simple. Bifurcation PCI remains more of an art form, struggling to become science. It is here that Moussa and Colombo introduce logic and science into this rarified arena. While I, like many others, believe the simple approach is the best approach, in practice this is not always true. Complex interventions are required for some complex circumstances. The field of bifurcation PCI has taken on a life of its own in the recent years as evidenced in 2004 by the birth of the European Bifurcation Club (EBC), with sessions at scientific meetings dedicated to bifurcation PCI management. The “Tips and Tricks” book dedicated to bifurcation PCI is a unique offering, addressing this important clinical PCI subset. Its importance is supported by the industrial development of novel side branch stents and further emphasizes the common and difficult problem that side branch management represents. Drs. Moussa and Colombo have assembled a unique book dedicated to understanding and managing this critically challenging PCI problem. It is a first of its kind in the interventional world. Because of the numerous configurations of a bifurcation involving the aorto-ostia, the main branch and side branch relationship, as well as the distal left main, the PCI approach requires careful classification, categorization, and technique selection based on the best studies (randomized, multicenter, etc.). Validation of the outcomes from the studies reporting the numerous approaches to these treatments is hard to come by. Drs. Moussa and Colombo, experts in their own right, have assembled a stellar team of coauthors who cover the universe of bifurcation PCI. For example, in the first section, the reader will be introduced to the evidence and studies on which most initial decisions are based. Moussa and Colombo ask: Are the trials on which we have based our current approaches to this point satisfactory? Are they large enough? Is there enough detail and division of the types of bifurcations studied to appreciate outcomes related to therapy? These questions and more are addressed in detail. While one cannot generalize these introductory remarks to all bifurcation procedures, the subsequent chapters on the bifurcation anatomy by Drs. Costa, Russell, and Moussa set the groundwork for understanding classifications and hence techniques. The anatomy and physiology resulting in unique stress patterns of specific angulations of the side branches provide insight into the role of stenting and carina reconstruction. To understand the anatomy, the routine incorporation of the imaging modalities as well as physiologic assessment is warranted and addressed. Importantly, because obviously not all bifurcations are the same, the left main coronary artery bifurcation is discussed in a separate set of chapters later in the book.
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Foreword
Albiero and Boldi discuss stenting for non–left main coronary artery bifurcations, addressing the advantages and disadvantages of the provisional stent strategy. Drs. Lim and Koo expertly describe physiologic guidance for both provisional stenting and side branch jailing after stenting. Using fractional flow reserve to simplify the approach and demonstrate its longterm outcome for bifurcation lesions with stenting and kissing balloons is described by Dr. Koo, the world’s expert on the physiologic assessment of these jailed side branches using the pressure wire technique. In double stenting rather than provisional stenting, Drs. Favero, Pacchioni, and Reimers provide description of the most suitable anatomy, rationale for patient selection, and technique descriptions covering the complex double stenting nomenclature including T stenting, crush stenting, culotte stenting, and V stenting. The technique and execution of such methodologies is critical to procedure success. Those individuals interested in pursuing complex intervention will find this chapter highly stimulating. Left main coronary interventions are discussed in the third section of this book. Drs. Park and Kim present the evidence from numerous single and multicentered experiences, identifying outcomes for complex stenting of the different regions of the left main artery. Provisional stenting of the left main distal bifurcation constitutes a real challenge. The opinion provided from two of the most experienced interventionalists in the world in treating bifurcation left main stenoses is based on thousands of patients and is well reported in our major journals. Drs. Latib, Chieffo, and Colombo conclude Section 3 with a discussion of double-stenting of the left main coronary artery, providing detailed descriptions of stent technique, the simultaneous kissing strategy. Finally, in the fourth section, the reader will review bench testing and dedicated studies on focused technology, attempting to improve the delivery of existing stents and the manufacture and development of unique dedicated bifurcation stents. Observations gained from the testing involve insights into overlapping metal struts in the wide array of combined methods including crush, T, culotte, and V stenting. In the last chapter of the book, Drs. Latib, Sangiori, and Colombo speculate on the future of dedicated bifurcation stent systems and where our next steps will lead. An intriguing description and categorization of the staged development for many new stents that are soon to be available within the next few years are provided. The regulatory challenge of bringing these to the practicing interventional cardiologists is worth reading. I believe all levels of physicians interested in the practice of interventional cardiology will benefit by reading “Tips and Tricks” with its important lessons for their practice and patients. The Interventional cardiologists, fellow-in-training, the early career interventionalists as well as the seasoned expert can take heart in using this information to support current practice and identify future practices for his best outcomes, especially those regarding the left main coronary bifurcation. My compliments to Dr. Moussa and Dr. Colombo as they bring into focus one of the more difficult aspects of all coronary interventions, that of the bifurcated and branched lesion. Morton J. Kern, M.D., FSCAI, FACC, FAHA Chief Cardiology, Division of Cardiology Long Beach Veterans Administration Hospital Long Beach, California, U.S.A. Associate Chief Cardiology, Professor of Medicine Division of Cardiology University of California Irvine Orange, California, U.S.A.
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Preface
The mark of mediocrity in written material, whether it is literature, politics, or medicine, is to rely heavily on precedents; so whatever is previously written about a topic is written again and again propagating the same narratives. This statement may seem irrelevant to the topic of coronary bifurcation lesions, and to medical writing in general, because we are in the era of “evidencebased medicine” and written medical literature need to be supported by “evidence” and not merely reflect opinions and anecdotal experience. In reality, however, what is occasionally offered as “evidence” does not qualify as an undisputable guide for clinical or technical decision making. There is no topic in Interventional Cardiovascular Medicine where this “disconnect” is more relevant than that of interventional treatment of coronary bifurcation lesions. The narrative that has been propagated in the literature is that provisional stenting (stenting the main vessel, with additional stenting of the side branch only in the case of an unsatisfactory result) is better than elective double stenting of both branches. This narrative states no exceptions to the rule, as it applies to all patients with coronary bifurcation lesions irrespective of bifurcation anatomy. Advocates of this narrative base their supposition on the results of several prospective randomized controlled trials. This narrative, however, overlooks fundamental problems in the design of these clinical trials, which makes its generalizability to all patients with coronary bifurcation lesions problematic. The goal of this book is to present the reader with a patient-centered approach to technical decision making in the interventional treatment of coronary bifurcation lesions. In doing so, we relied on evidence when it was of high quality and relevant, and we relied on experts’ opinion and judgment when high-quality evidence was lacking. The first section of the book is devoted to the fundamentals of decision making with regard to interpretation of the existing evidence (chapter 1) and understanding the role of bifurcation anatomy in impacting technique choice and outcomes (chapter 2). The subsequent chapters are devoted to technical decision making with regard to tailoring technical approaches to bifurcation anatomy for patients with left main and non–left main coronary bifurcation lesions. A particular emphasis is placed on providing practical tips and tricks to optimize the results and deal with complications, all in the context of actual case presentations. The last section of the book is devoted to the role of in vitro bifurcation modeling and the current state of dedicated bifurcation stent systems. Ultimately, we hope that this book will be a useful resource for interventional cardiologists who thrive to treat their patients as unique individuals who may not fit the profile represented in a given randomized clinical trial. Technical decision making in these patients requires individualized judgment, utilizing pragmatic interpretation of the evidence and applying techniques tailored to the individual patient. Issam D. Moussa, MD Antonio Colombo, MD
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Contents
Foreword Morton J. Kern . . . . v Preface . . . . vii Contributors . . . . xi Section 1. Coronary Artery Bifurcation Lesions: The Fundamentals 1. Coronary Artery Bifurcation Interventions: Bridging the Gap Between Research and Practice 1
Issam D. Moussa and Antonio Colombo 2. Coronary Artery Bifurcation Lesions: Anatomy 101
14
Ricardo A. Costa, Hiroyuki Kyono, Marco Costa, Mary E. Russell, and Issam D. Moussa Section 2. Non–Left Main Coronary Artery Bifurcation Interventions 3. Provisional Stenting Technique for Non–Left Main Coronary Bifurcation Lesions: Patient Selection and Technique 48
Remo Albiero and Emiliano Boldi 4. Physiologic Guidance of Provisional Stenting in Coronary Bifurcation Lesions
67
Michael J. Lim and Bon-Kwon Koo 5. Elective Double Stenting for Non–Left Main Coronary Artery Bifurcation Lesions: Patient Selection and Technique 83
Luca Favero, Andrea Pacchioni, and Bernhard Reimers Section 3. Left Main Coronary Artery Bifurcation Interventions 6. Coronary Revascularization for Patients with Unprotected Left Main Coronary Artery Disease: Making Clinical Decisions in the Absence of Definitive Evidence 116
Issam D. Moussa and Ted Feldman 7. Provisional Stenting for Left Main Coronary Artery Bifurcation Lesions: Patient Selection and Technique 134
Seung-Jung Park and Young-Hak Kim 8. Elective Double Stenting for Left Main Coronary Artery Bifurcation Lesions: Patient Selection and Technique 149
Azeem Latib, Alaide Chieffo, and Antonio Colombo
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Contents
x
Section 4. Coronary Bifurcation Interventions: Bench Testing and Dedicated Bifurcation Stents 9. Bench Testing of Coronary Bifurcation Stenting Techniques: How Is It Done? Does It Help Technical Decision Making? 193
Yoshinobu Murasato 10. Current Status and Future of Dedicated Bifurcation Stent Systems
Azeem Latib, Giuseppe M. Sangiorgi, and Antonio Colombo Index . . . . 251
211
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Contributors
Remo Albiero Cath Lab, Clinica San Rocco di Franciacorta, Ome (Brescia), Italy Emiliano Boldi Cath Lab, Clinica San Rocco di Franciacorta, Ome (Brescia), Italy Alaide Chieffo Interventional Cardiology Unit, San Raffaele Scientific Institute, and Interventional Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy Antonio Colombo Interventional Cardiology Unit, San Raffaele Scientific Institute, and Interventional Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy Marco Costa Harrington-McLaughlin Heart and Vascular Institute, University Hospitals, Case Western Reserve University, Cleveland, Ohio, U.S.A. Ricardo A. Costa Instituto Dante Pazzanese de Cardiologia & Cardiovascular Research Center, S˜ao Paulo, Brazil Luca Favero Department of Cardiology, Mirano Hospital, Mirano, Italy Ted Feldman Cardiac Catheterization Laboratory, Cardiology Division, Evanston Hospital, Evanston, Illinois, U.S.A. Young-Hak Kim South Korea
University of Ulsan College of Medicine, Asan Medical Center, Seoul,
Bon-Kwon Koo Seoul National University Hospital, Seoul, South Korea Hiroyuki Kyono Harrington-McLaughlin Heart and Vascular Institute, University Hospitals, Case Western Reserve University, Cleveland, Ohio, U.S.A. Azeem Latib Interventional Cardiology Unit, San Raffaele Scientific Institute, and Interventional Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy Michael J. Lim
Saint Louis University, St. Louis, Missouri, U.S.A.
Issam D. Moussa Cardiac Catheterization Laboratory, New York Presbyterian Hospital–Weill Medical College of Cornell University, New York, New York, U.S.A. Yoshinobu Murasato Department of Cardiovascular Medicine, Heart Center, New Yukuhashi Hospital, Yukuhashi, Japan Andrea Pacchioni Department of Cardiology, Mirano Hospital, Mirano, Italy Seung-Jung Park University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea Bernhard Reimers
Department of Cardiology, Mirano Hospital, Mirano, Italy
Mary E. Russell Ascent Translational Sciences, Inc., Carlisle, Massachusetts, U.S.A. Giuseppe M. Sangiorgi Interventional Cardiology Unit, San Raffaele Scientific Institute, and International Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy
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Coronary Artery Bifurcation Interventions: Bridging the Gap Between Research and Practice Issam D. Moussa Cardiac Catheterization Laboratory, New York Presbyterian Hospital–Weill Medical College of Cornell University, New York, New York, U.S.A.
Antonio Colombo Interventional Cardiology Unit, San Raffaele Scientific Institute, and Interventional Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy
INTRODUCTION The mark of mediocrity in written material, whether it is literature, politics, or medicine, is to rely heavily on precedents; so whatever is previously written about a certain topic gets written again, propagating the same narratives over and over. Of course, this statement may initially seem irrelevant to our topic, and to medical writing in general, because we are in the era of “evidence-based medicine” and written medical literature need to be supported by “evidence” and not merely reflect opinions and anecdotal experience. In reality, however, what is occasionally presented as “evidence” does not qualify as an undisputable guide for clinical or technical decision making. There is no topic in interventional Cardiovascular Medicine where this “disconnect” is more relevant than that of interventional treatment of coronary bifurcation lesions. The narrative that has been propagated in the literature is that provisional stenting (PS) [stenting the main vessel (MV), with additional stenting of the side branch (SB) only in the case of an unsatisfactory result] is better than elective double stenting (EDS) of both branches. This narrative declares no exceptions to the rule and some perceive it as if it applies to “all” patients with coronary bifurcation lesions. Proponents of this narrative base their conclusion on the results of several retrospective registries (1–7) and randomized controlled trials (RCTs) (8–12). The purpose of this chapter is to present a counter perspective to this dominant narrative; namely, that neither approach should be the default strategy in all patients with bifurcation lesions and that a decision as to which approach to use should be based on the patient’s bifurcation anatomy. The majority of patients with bifurcation lesions will have anatomy that can be safely treated with PS (see chap. 3); however, some patients have “at risk” bifurcation anatomy where PS may be associated with high risk of side branch occlusion (see chap. 2). In this chapter, we will I. Critically appraise the “evidence-base” with regard to PCI of bifurcation lesions: 1. Review the evidence-base 2. Discuss the questions that clinicians should ask of the evidence-base to make an informed decision: A. Does the design of the RCTs appropriately address the questions that need to be answered? B. Are the current bifurcation classifications reliable vehicles to tell us what we need to know about bifurcation anatomy? C. How do we apply the results of the RCTs to patient-centered decision making? II. Discuss the “cost” of inappropriate generalizabilty of the results of the RCTs to all patients III. Summary
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MOUSSA AND COLOMBO
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CRITICAL APPRAISAL OF THE EVIDENCE-BASE Review of the Evidence-Base
Retrospective Studies Over the last decade, numerous retrospective studies compared PS with EDS using bare metal stents (BMS) and drug-eluting stents (DES) (1–7). Although a detailed discussion on this topic is beyond the scope of this chapter, all these studies were limited by the systematic bias, favoring the use of PS in less complex bifurcations and EDS in more complex bifurcations. This bias rendered the findings of these studies, namely, lower restenosis and thrombosis with PS, misleading. Despite the obvious limitations of these studies, the debate concerning the role of PS versus EDS has been errounously framed in a manner that ignores the importance of the specific bifurcation anatomy in determining technique choice. RCTs of PS Vs. EDS The conclusions of the above retrospective studies shaped the underlying hypothesis of the subsequent RCTs (8–12). The basic hypothesis was that one technique is better than the other technique in all patients with bifurcation lesions. This chapter addresses the largest RCTs that have been published in peer-reviewed journals, namely, the NORDIC, BBK, and CACATUS trials (10–12). As shown in Tables 1 and 2, these trials demonstrated the following:
r
There is no statistical difference between PS and EDS in main vessel (MV) restenosis or target vessel revascualrization (TVR).
Table 1
Clinical and Angiographic Outcomes in the RCTs of EDS Vs. PS NORDIC Elective (N = 206)
Clinical outcome Death (%) Nonfatal MI (%) Q-wave Non–Q-wave TVR (%) Any MACE (%) Stent thrombosis (%)
Table 2
Provisional (N = 207)
Elective (N = 101)
6 mo 1.5 0.5 0.5 18 1.9 3.4 0.0
Angiographic outcome Restenosis (%) MV SB
BBK Provisional (N = 101)
Elective (N = 177)
1 yr 1 0.0 0.0 8 1.9 2.9 0.5
1 2 NA NA 8.9 11.9 2
8 mo 5.1 11.5
CACTUS
6 mo 2 1 NA NA 10.9 12.9 1
0.0 10.7 1.7 9.0 7.3 15.8 1.7
0.5 8.6 1.1 7.4 6.3 15.0 1.1
9 mo 4.6 19.2
3.1 10.4
Provisional (N = 173)
6 mo 7.3 5.2
4.6 13.2
6.7 14.7
Procedural Details: RCTs of ES Vs. PS NORDIC
Cross over (%) Final kissing (%) Contrast volume (mL) Procedure time (min) Fluoroscopy time (min)
BBK
CACTUS
Elective (N = 206)
Provisional (N = 207)
Elective (N = 101)
Provisional (N = 101)
Elective (N = 177)
Provisional (N = 173)
5 74 283 + 117 76 + 40 21 + 10
4 32 233 + 93 62 + 51 15 + 9
3 100 203 + 109 51 + 23 15 + 9
18.8 100 204 + 86 56 + 25 13 + 7
1 92 NA NA NA
31 90 NA NA NA
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There is no statistical difference between PS and EDS in SB restenosis or TVR (10) [although in the NORDIC trial there was a trend towards higher SB restenosis in the PS arm (19% vs. 11%; p =0.06)]. There is no statistical difference between PS and EDS in stent thrombosis. The NORDIC trial showed increased procedure time and contrast use with EDS compared to PS (10), while other trials did not (11,12). The NORDIC trial showed higher rate of postprocedure cardiac biomarker elevation in the EDS arm but showed no difference in MI at follow-up (10).
These RCTs confirmed that the conclusions drawn from the retrospective studies—namely, that a one stent approach is associated with lower restenosis and thrombosis—are erroneous. Nonetheless, one can fairly propose that although both approaches are equally safe and effective, PS stenting should be the preferred startegy in patients with bifurcation lesions because it is simpler than EDS and uses less resources. Indeed, these were the conclusions made by the authors of the NORDIC study. So, are these conclusions consistent with the application of evidence-based medicine? We propose that they are not! Questions Clinicians Should Ask of the Evidence-Base to Make an Informed Decision? The application of evidence-based medicine findings to clinical practice does not imply the literal adaptation of the conclusions of a given study(s). Evidence-based medicine should be a dynamic process of intelligent decision making that involves critical appraisal of the “evidence” before adapting its results to treat patients. The disconnect between clinical research methodology and patient-centered decision making is undeniable and may even be unavoidable given the logistical difficulty and potential monetary cost involved if we attempt to tackle the complex clinical/technical questions facing the practice of Interventional Cardiology. As caregivers we should always aim to understand the reasons for this disconnect, how to narrow the gap in future evidence collection, and above all how to make sound clinical/technical decisions in the absence of absolute certainty. In that regard, the following are key questions that we need to ask of the RCTs before using them as basis for decision making regarding the treatment of coronary bifurcation lesions.
Does the Design of the RCTs Appropriately Address the Questions that Need to be Answered? The answer is absolutely not. The hypothesis underpinning the design of the RCTs was determined in isolation from clinical reality. The most effective approach to rationalize this answer is to compare the hypothesis underlying the relevant RCTs to the question(s) a physician would ask before making a decision on how to treat a bifurcation lesion: 1. What is the hypothesis underlying the design of the relevant RCTs? The hypothesis of these clinical trials states that one technique should be the preferred, compared to other technique(s), approach in all patients with bifurcation lesions? So what is wrong with this hypothesis? This hypothesis is disconnected from the clinical reality in that no physician would use EDS in all patients with bifurcation lesions but typically select this technique for more complex bifurcations. This hypothesis does not specify “which” bifurcations to be evaluated with the assumption that all bifurcations should similarly respond to various techniques, irrespective of individual variations in SB lesion severity and bifurcation morphology. The study design based on this hypothesis would allow, for example, a patient with a bifurcation lesion 1,1,0 (no SB disease) to be a candidate for randomization. This patient may end up with EDS, even though in clinical practice no rational physician would elect to use EDS in the absence of SB disease. This is just a simple example that illustrate the over simplistic study design underlying some of these clinical trials. 2. What are the question(s) a physician would ask before making a decision how to treat a bifurcation lesion? When a physician is planning to treat an individual patient with a bifurcation lesion, he or she would determine the various anatomic attributes of the bifurcation before deciding which technique to use: (a) How large is the SB (diameter, vessel length, and myocardial territory supplied)? (b) Is the SB ostium diseased? If yes, what is the severity and length of the lesion?
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MOUSSA AND COLOMBO
4
Medina Duke (modified)
D
C
F
G
A
B
E
Sanborn
I
-
-
III
IV
II
IV
Lefevre
1
2
-
4
3
4a
4b
Safian
IA
IB
IIA
IIIA
IIB
IIIB
IV
Movahed
L
S
2
1m
1s
V
T
Staico-Feres
3
2A
2B
2C
1A
1B
1C
Figure 1 Coronary bifurcation classifications.
(c) (d) (e) (f)
Is there severe disease in the SB beyond the ostium? What is the angle of the SB takeoff? Is it difficult to wire/rewire? What is the severity and distribution of the MV lesion? What will happen to the SB after stenting (mild or significant compromise or occlusion)? And what are the consequences of SB occlusion (depend on the territory supplied)? The answer to these questions would determine whether an operator uses PS or EDS (this topic will be extensively covered in the forthcoming chapters). The above discussion clarifying the gap between the design of the RCTs and the process of patient-centered decision making clearly illustrates that the available evidence-base is not sufficient to fill the current knowledge gap. Clinical research can only answer the questions that we pose to it. If we pose the wrong questions we cannot expect to get the right answers!
Are the Current Bifurcation Classifications Schemes Reliable Vehicles to Tell Us What We Need to Know About Bifurcation Anatomy? Unlike non-bifurcation lesions that can be fairly characterized by reference vessel diameter and lesion length, coronary bifurcations have complex anatomic attributes both in the MV and the SB that do not lend itself to simple classifications (see chap. 2). There have been multiple bifurcation classification schemes in an attempt to standardize reporting and guide PCI technique selection (Fig. 1). The most recent and widely used classification is the Medina classification (Fig. 2) (13).
1,1,1
1,1,0
1,0,1
0,1,1
1,0,0
0,0,1
0,1,0 0,1
MV (Distal)
, MV (Proximal)
, SB
0,1 0,1
Figure 2 Medina classification. The Medina classification divides the bifurcation lesion into three segments, the proximal MV, the distal MV, and the SB, and assign each segment a binary value (1, 0) according to the presence or absence of obstruction (DS > 50%). Source: Adapted from Ref. 13.
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Although the Medina classification is intuitive and much easier to remember, it has not added any descriptive elements beyond the other classifications (i.e., it continue to ignore the importance of the size of the SB, the severity and the length of the SB lesion, the SB angle, and the relationship between the SB ostial stenosis and the MV stenosis). A telling example of the limited ability of the Medina classification to provide an accurate anatomic description of bifurcations is found in Figure 3(A) and 3(B). It is clear from these figures that bifurcation lesions with similar Medina classification can significantly differ with regard to ostial SB lesion severity, ostial SB lesion length, SB angle, and most importantly SB size and its corresponding myocardial territory. These anatomic elements are critical to technique selection, procedural success, and the risk of SB occlusion, yet it is not reflected in any of the above classification. A recent classification was proposed by Movahed (14) to account for these elements, but this classification is difficult to remember and to use in everyday practice. The implications of this issue is that the current bifurcation classifications schemes are not reliable indicators of the complexity of bifurcations included in the RCTs, and therefore it can be fairly stated that the degree of bifurcation complexity in these trials remains a “black box”!
How Do We Apply the Results of the RCTs in the Context of Patient-Centered Decision Making? The most effective approach to provide guidance regarding the use of the results of the RCTs for decision making in individual patients is to simulate the process of technical decision making in patients with coronary bifurcation lesions. Patients in Figure 4(A) and 4(B) have ischemia producing coronary bifurcation lesions that require PCI. How would an interventionalist make a decision as to which technique to use in each of these patients? Currently, physicians prescribe to one of the two following distinct approaches: 1. One approach would advocate the literal application of the results of the RCTs choosing the methodology that was used in these trials (i.e., choose one technique to treat all patients). Hence, they would adapt universal PS for all patients with bifurcation lesions irrespective of the specifics of the anatomy of each bifurcation. The assumption being made is that all patients with bifurcation lesions were well represented in these trials, and therefore they would have similar outcome to the patients enrolled in these trials! 2. The second approach would advocate patient-centered decision making and therefore would not choose one technique to treat all patients with bifurcation lesions but rather match the technique to the individual bifurcation anatomy guided by the available data as well as by personal experience. The assumption being made is that the results of the RCTs cannot be generalized to all patients encountered in clinical practice, because patients with “complex” bifurcations were not well represented in these trials. These two divergent approaches illustrate the gap between the methodology and findings of clinical research as well as the dynamics of patient-centered decision making. Who is right? Is there anyone wrong? An approach that would satisfy both perspectives is to determine which patients are well represented in the RCTs and which patients are not. Surely, no one can argue for the application of the results of the RCTs in patients who were not well represented in these trials! For the purpose of this discussion, we will address the largest RCTs published in peerreviewed journals (NORDIC, BBK, and CACTUS) (10–12). The BBC trial will not be discussed because the angiographic and morphologic information are not yet available. As shown in Table 3, patients included in these RCTs had focal lesions of moderate severity in the SB ostium. This means that patients with long and/or severe stenoses in the ostial SB were largely excluded, although these anatomic variables were not prespecified as exclusion criteria. This may indicate a natural bias to exclude patients with “high-risk” bifurcation anatomy from randomization. Furthermore, no data were provided in these trials regarding other important anatomic features such as the myocardial territory supplied by the SB, the angle of the SB, and the presence or absence of distal SB disease. Therefore, when one contemplates how to apply the evidencebased knowledge derived from these RCTs to an individual patient, one should first ask the question whether the patient was well represented in these trials or not! For example, let us use this process for decision making for patients in Figure 4(A) and 4(B). It is clear that the patient in Figure 4(A) is representative of patients included in the above RCTs and therefore PS
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(B) Figure 3 Case examples illustrating the limitations of the Medina classification. (A) Coronary angiography in two different patients with Medina class 0,1,1 bifurcation lesions: (a) LCX/OM1 bifurcation lesion and (b) LAD/2nd diagonal bifurcation lesion. Note the difference in SB lesion length between the two patients. (B) Coronary angiography in two different patients with Medina class 1,0,1 bifurcation lesions: (a) LAD/2nd diagonal bifurcation lesion and (b) LCX/OM1 bifurcation lesion. Note the difference in SB size. It is clear from these examples that the Medina classification is not a sufficient descriptor of bifurcation anatomy.
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would be a safe and effective approach. On the other hand, patients in Figure 4(B) are not well represented in the RCTs, and PS may not be a safe and effective approach. WHAT IS THE COST OF INAPPROPRIATE GENERALIZABILITY OF THE RCTs TO ALL PATIENTS WITH BIFURCATION LESIONS? The primary reason why PCI of bifurcation lesions has been a challenge is the risk of SB occlusion (SBO) or compromise after treating the MV. Almost 25 years ago, Meier and colleagues (15) demonstrated that coronary angioplasty in coronary stenoses that involve a diseased SB results in SBO in 14% of patients. They also noted that CK-MB elevation (non–Q-wave MI in today’s terminology) occurred in 30% of these patients. These results were obtained in patients with small SBs because patients with large SBs were disqualified from undergoing PCI. These results were corroborated by Arora et al. (16) who evaluated 167 patients (181 bifurcations lesions) with SB occlusions during PCI of the MV. In this study, 14% of patients developed postprocedure myocardial infarction (MI) despite successful SB reopening in 16% of patients. Of course, one would be quick to note that antithrombotic therapy, PCI technology, and techniques have progressed so much that results are now much better. However, despite the significant aforementioned progress, SBO and/or compromise remains a problem particularly in patients with “at risk” bifurcations. In a study by Chaudhry et al. (17), 158 patients with bifurcation lesions with SBs ≥2 mm were treated with single stenting approach (MV stent). In this study, 16% of patients had SB compromise (TIMI flow 50% stenosis (Medina types: 1,1,1; 1,0,1; 0,1,1) [Fig. 4(C)]. Although the Movahed classification did address some of the deficiencies of prior classifications, it remains difficult to use (18). Therefore, although the existing bifurcation classifications provide a basic description of bifurcation anatomy, it does not provide sufficient anatomic information to standardize reporting in clinical trials or to guide technical decision making. This point is clearly illustrated
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, MB (Proximal)
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Medina type 1,0,0
Medina type 1,0,1
Medina type 1,1,0
Medina type 0,1,1
Medina type 0,1,0
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(C) Figure 4 (A) Current coronary bifurcation classifications. (B) Medina classification. (C) Examples of coronary bifurcation lesions according to each type of the Medina classification.
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(A)
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(A1)
(B1)
(C1)
Figure 5 “True” coronary bifurcation lesions involving the proximal LAD/Diagonal location. Note that all lesions (A,B,C) are classified as Medina type 1,1,1; however, with different complexity and outcome: A – bifurcation lesion with a severe focal stenosis involving the SB ostium successfully treated with provisional (SB) stenting approach (A1); B – bifurcation lesion with SB diffusely diseased unsuccessfully treated (SB occlusion) with provisional (SB) stenting approach (B1); C – bifurcation lesion with SB diffusely diseased successfully treated with double stenting technique (“mini-crush”), (C1).
in Figure 5 that shows bifurcation lesions that have similar Medina classification but clearly different levels of complexity that require different techniques to treat. What Are the Bifurcation Anatomic Characteristics That Affect the Frequency and Severity of SB Compromise? Historically, it has been suggested that SB compromise during PCI [Fig. 6(A)] is the result of snowplowing of plaque over the SB ostium or simply “plaque shift.” However, pathologic evaluation and IVUS studies have demonstrated that although atherosclerosis develops frequently at the bifurcation, it is often located opposite to the flow divider, that is, opposite the origin of the SB. This led to the proposition that SB compromise after MV stenting is due to “carina shift” rather than plaque shift. Nevertheless, some patients do have plaque accumulation at the SB ostium and these patients are at high risk for plaque shift [Fig. 6(B)] (6). Although angiographic SB compromise, even when it is >50% stenosis, is not always hemodynamically significant when assessed physiologically (1), it can result in periprocedural ischemia or myocardial infarction when there is compromised flow. In any event, irrespective of the mechanism that led to SB compromise in bifurcation PCI, there are several bifurcation anatomic features that affect the frequency and severity of this event. These features are not well represented in the current bifurcation classifications and are as follows.
SB Size and Its Correspondent Myocardial Territory Although the size of the SB and its correspondent myocardial territory are the most important factors that would determine the clinical consequences of SB compromise during bifurcation PCI, neither of these anatomic elements are represented in any of the coronary bifurcation classifications. Furthermore, the effect of the size of myocardial territory supplied by the SB on patient outcomes has been neither quantified nor considered in any of the studies addressing PCI of bifurcation lesions. Although the effect of SB vessel size on procedural and long-term outcome after bifurcation PCI is not as well defined as it relates to MV intervention, there are several studies that did address this issue. In general, the cutoff values for SB vessel diameters that determine inclusion or exclusion from a specific bifurcation study has been arbitrary chosen in both retrospective registries (19,20) and randomized controlled trials (RCTs) (Table 1) (21–26). Of note, regardless of the technical
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(B) Figure 6 (A)—(a) coronary bifurcation lesion with mild SB stenosis; (b) stent implantation in the MV; and (c) SB compromise after stent implantation in the MV. (B) An example of side branches that were occluded after angioplasty of the parent vessel in a patient with acute myocardial infarction. (a) A severe stenosis (arrowhead ) at the bifurcation of the middle segment of the left anterior descending artery (LAD) and the diagonal branch (Dx) is shown in a left anterior cranial view. (b) After deployment of a stent, the diagonal branch was occluded. (c and d) Preintervention intravascular ultrasound (IVUS) images showing diffuse plaque around the ostium of the Dx. Source: Adapted from Ref. 7.
83%
3%
18.8%
• Flow limiting dissection, and/or • Residual stenosis ≥75% If after KB, SB with: • <TIMI 3, and/or • >70% stenosis at ostium, and/or • Threatened vessel closure, and/or • Dissection more than type A
31.2%
• Residual stenosis ≥50%, and/or • Dissection type B or worse, and/or • TIMI flow ≤2
4.3%
• TIMI flow = 0, after SB dilatation
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NA
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86% (16)
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CACTUS (24)
Any bifurcation lesion type according to Lefevre ` classification (16)
Significant stenosis in both MV and SB originb (diffuse SB lesion was excluded)
True bifurcation lesionsb
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• • • • • • • • • • • • • • • •
De novo bifurcation lesions Non-left main location TIMI flow ≥1 Vessel size 2.5–3.5 mm Lesion length ≤24 mma De novo bifurcation lesions Non-left main location MV: ≥2.5 mm SB: ≥2.25 mm De novo bifurcation lesion LM location allowed in a right dominant system MV: ≥2.5 mm SB: ≥2.0 mm De novo bifurcation lesions Non-left main location TIMI flow ≥1 (in both branches) MV: 2.5–3.5 mm SB: 2.25–3.5 mm Lesion length ≤28 mma De novo bifurcation lesions Non-left main location MV: 2.5–4.0 mm SB: ≥2.25 mm De novo bifurcation lesions Non-left main location MV: ≥2.5 mm SB: ≥2.25 mm
Criteria for SB stenting if:
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Pan et al. (22)
• • • • • • • • • • •
Lesion type
Cross-over (from single to double stenting)
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Angiographic Criteria in Randomized Clinical Trials with DES in Bifurcations
Randomized series with DES
Table 1
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Figure 7 Relationship between reference vessel diameter and SB restenosis rates in DES bifurcation series.
approach in treatment of bifurcations, smaller SBs appear to have increased risk of restenosis, even with DES (Fig. 7). More importantly, SB diameter also affects the risk of SB occlusion during bifurcation PCI, where even smaller SBs may be clinically relevant (2–5). A study by Arora et al. (2) reported a series of 167 patients including 181 bifurcations lesions presenting with SB occlusions during PCI of the MV. In this analysis, all SBs with diameter >1.00 mm in non-LM location were included, while lesions where the SB was protected with a wire or was treated with PCI were excluded. In this study, 14% of patients developed postprocedure MI (new Q-wave MI and/or three times increase in total CPK with elevated MB fraction within 24 hours post-PTCA) despite successful SB reopening in 16% of patients. In a study by Chaudhry et al. (5), 158 patients with bifurcation lesions with SBs ≥2.00 mm were treated with single stenting approach (MV stent). In this study, 16% of patients had SB compromise (TIMI flow 5 times the upper normal limit). Independent predictors of SB “compromise” were eccentric lesion morphology in the MV (OR, 2.92; 95% CI, 1.11, 7.63; p = 0.03), smaller SB vessel diameter (OR, 0.21; 95% CI, 0.06, 0.77; p = 0.02), and SB% diameter stenosis (OR, 1.02; 95% CI, 1.00, 1.04; p = 0.047).
SB Lesion Severity and Length Although the Medina classification makes a distinction between SBs with > or 50%, where the risk of SB occlusion was 14% to 27%. Furukawa et al. demonstrated that the risk of SB deterioration (final TIMI flow ≤2) during bifurcation PCI is significantly more common in SBs with an ostial stenosis ≥50% compared to an ostial stenosis 70 degrees: (a, b) proximal LAD/Diagonal bifurcation with obtuse “distal” angle measured 112 degrees; (c, d) mid-LAD/Diagonal bifurcation with distal angle measured 89 degrees. (Continued on page 28 )
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(a)
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(C) Figure 9 (Continued)
T-stenting is used. In these bifurcations the operator is often required to allow the SB stent to protrude into the MV to ensure appropriate SB ostium coverage. This typically would not be an issue in T-shaped bifurcations where stent positioning can be ensured without significant protrusion into the MV. Although the bifurcation angle clearly affects the procedural performance of various double stenting techniques, its effect on clinical outcome need more study. Dzavik et al. (27) reported that a bifurcation angle more than 50 degrees is an independent predictor of major adverse cardiac event (MACE) in patients treated with a crush stent strategy. In this study, 133 patients treated with crush stenting at a single institution had angiographic assessment including measurement of the distal bifurcation angle. The mean distal bifurcation angle was 51.1 ± 15.3 degrees, and patients were divided into two groups on the basis of the median bifurcation angle (50 degrees). At one year, MACE-free survival was significantly lower in patients with wider angle (76.2% vs. 93.8%; p = 0.005), including a nonsignificant trend towards high TLR (12.3% vs. 3.1%; p = 0.096). In this study, only 90 of 133 cases underwent final kissing-balloon (FKB) inflation, and both FKB and distal angle ≥50 degrees were identified as significant independent predictors for MACE (HR, 0.22; 95% CI, 0.08–0.56; p = 0.002; and HR, 5.72; 95% CI, 1.83, 17.96; p = 0.003; respectively). Importantly, a significant association between bifurcation angle and FKB for the occurrence of MACE was found (p < 0.0001). Whether these results reflect the primary role of bifurcation angles in determining the outcome or other associated factors (such as FKB) is unclear, more studies are needed to settle this issue.
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IMAGING OF CORONARY BIFURCTION LESIONS Quantitative Coronary Angiography (QCA) Accurate analysis of coronary lesions is entirely dependent on the quality of the angiographic image acquisition including adequate projections to ensure optimal visualization. Previous studies have attempted to identify the most favorable viewing angles that provide optimal diagnostic value in terms of assessing stenosis severity, and minimizing vessel foreshortening and overlap (31). However, such studies did not include bifurcations. Angiographic assessment of coronary bifurcation lesions is often difficult and incomplete because of vessel overlap, limited (and inaccurate) visualization of the lesion (especially the SB ostium), and the requirement for multiple views. Current recommended views for optimal bifurcation lesion visualization are based on heuristic experience and have not been scientifically studied. Optimal visualization of the SB ostium remains the most critical issue with obvious implications for lesion complexity assessment and technical decision making, especially for stent positioning when using double stenting techniques, as relatively high incidence of incomplete SB ostium coverage has been reported, which has been also associated with restenosis at this location. As with non-bifurcation lesions when using angiography to image bifurcations one should choose the views with best visualization of the target lesion including the most orthogonal view of the SB ostium with particular attention to avoid vessel overlap and foreshortening. Current standard image acquisition protocol for angiographic analysis in non-bifurcated lesions require at least two orthogonal views >30 degrees apart. Although optimal visualization of the bifurcation carina and the SB ostium is sometimes achieved in one single projection, which may be found in nonstandard views, two or more projections are often required. Table 2 displays angiographic views commonly utilized for optimal visualization of bifurcation lesions [Fig. 10(A) to 10(I)]. Historically, QCA analysis of bifurcation lesions lacked standarized methodology, and several pitfalls were identified when standard QCA packages (designed for standard QCA analysis) were adopted for bifurcation analysis. The major challenge in performing QCA in bifurcations is to determine the reference diameter at all distinct locations within the bifurcation segment; incorrect reference determination will lead to either overestimation or underestimation of the stenosis severity. Inconsistencies in QCA methods and reporting (including not reporting the exact restenosis location) have occasionally precluded the understanding of the differences between bifurcation studies (Table 3). Although there were significant differences in baseline angiographic characteristics, which could partially explain differences in outcomes among trials such as Nordic vs. CACTUS (CACTUS included smaller vessels with more severe obstruction), it is clear that a standardized methodology was needed in order to allow consistent comparisons of bifurcations trials. The consensus panel of the European Bifurcation Group provides several recommendations for bifurcation imaging acquisition, analysis, and reporting (Table 4) (29). In this algorithm, the three segments of the bifurcation are independently analyzed including a predefined subsegmental analysis on the basis of the areas of interest depending on the technique and/or device used during PCI (Fig. 11). Because of vessel tapering in bifurcation lesions, pre-, post-, and follow-up MLD may vary according to location, thus creating systematic under- or overestimation. Therefore, MLD and percent diameter stenosis postprocedure and at follow-up should be calculated at each subsegment, and the interpolated reference diameter generated at each predefined area of interest should be used at each study point (final and follow-up). Importantly, in patients with restenosis, location of recurrence would be documented. Currently, there are two dedicated commercial softwares for bifurcation QCA analysis: the Medis Medical Imaging Systems bifurcation application (QAngio XA V 7.2, Leiden, the Netherlands) and the CAAS 5 (Pie Medical Bifurcation Imaging software, Maastricht, the Netherlands). Angiography-based three-dimensional (3-D) vessel reconstruction systems are another development that may enhance visualization of coronary vessel anatomy. In bifurcation lesions, 3-D reconstructed images reduce vessel overlap and provide accurate measurements of bifurcation angles and degree of SB ostial involvement (Fig. 12). A preliminary study by Dvir et al. reported a series of 18 patients with serial pre- and postprocedure 3-D reconstruction analysis of bifurcation lesions treated with PCI and stenting. In this study, the authors used the CardiOp-BTM 3-D reconstruction system (CardiOp-BTM , Paieon Medical Inc., Rosh Ha’ayin,
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Recommended Angiographic Projections for Optimize Viewing of Coronary Bifurcations
Target bifurcation
Location
Common views
Proximal
a. RAO 25–35◦ /Cranial 30–45◦ b. Cranial 35–45◦ c. LAO 25–35◦ /Cranial 30–45◦ for LAD/Diagonalis: d. LAO 30–45◦ /Caudal 30–45◦ e. RAO 20–30◦ /Caudal 20–40◦
Mid/distal
a. RAO 25–35◦ /Cranial 30–45◦ b. Cranial 35–45◦ c. LAO 25–35◦ /Cranial 30–45◦
Proximal
a. RAO 20–30◦ /Caudal 20–40◦ b. LAO 30–45◦ /Caudal 30–45◦ c. LAO 25–35◦ /Cranial 30–45◦
Mid
a. AP 0◦ b. RAO 20–30◦ /Caudal 20–40◦ c. LAO 30–45◦ /Caudal 30–45◦
Distal
a. AP 0◦ b. RAO 20–30◦ /Caudal 20–40◦ c. Cranial 35–45◦
Ramus
Proximal
a. RAO 20–30◦ /Caudal 20–40◦ b. LAO 30–45◦ /Caudal 30–45◦ c. LAO 25–35◦ /Cranial 30–45◦
RCA
Mid (i.e., RCA/AM)
a. LAO >30◦ b. Cranial 20–40◦ c. RAO 25–45◦
Distal (i.e., PDA/PLSA)
a. LAO 30–45◦ b. LAO 20–45◦ /Cranial 20–40◦ c. Cranial 20–40◦
Distal (i.e., LAD/LCx)
a. AP 0◦ b. RAO 20–30◦ /Caudal 20–40◦ c. LAO 30–45◦ /Caudal 30–45◦
LAD/Diagonal
LCx/OM
LM
Abbreviations: AM, acute marginal; AP, antero-posterior; LAD, left anterior descending; LAO, left anterior oblique; LCx, left circumflex; LM, left main; OM, obtuse marginal; PDA, postero descending artery; PLSA, postero-lateral side artery; RAO, right anterior oblique; RCA, right coronary artery.
Israel) (32). This study showed significant reduction in the distal bifurcation angle from preto postprocedure (71 ± 17 degrees vs. 58 ± 18 degrees; p < 0.001), primarily when double stenting techniques were used. A previous study also suggested that angle changes from preto post-stent implantation predict late adverse events (28). Reasons for this observation are not clear, and the existing data are insufficient to make any actionable recommendations in this regard. Although standardizing methods of reporting of angiographic analyses of bifurcation interventions and development of new angiography-based imaging systems are welcome developments, it is critically important to remember that angiography, at its best, is limited in terms of providing accurate anatomic information at baseline and postprocedure. Therefore, there should always be a healthy degree of skepticism regarding insights provided by angiography and aim to confirm these observations with other imaging modalities.
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(B) Figure 10 Series of orthogonal views demonstrating optimized views for coronary bifurcations at different locations: (A) Proximal LAD bifurcation: poorly visualized in a (RA0 23◦ /CAU 20◦ ) and b (LA0 35◦ /CAU 33◦ ); best visualization achieved in cranial views, c (RA0 10◦ /CRA 38◦ ) and d (LA0 35◦ /CR 35◦ ). (B) Proximal LAD/Diagonalis bifurcation: not optimal assessment of bifurcation lesion, angle and SB ostium in a (RA0 29◦ /CAU 22◦ ), b (RA0 13◦ /CAU 41◦ ), C (LA0 48◦ /CAU 30◦ ); best visualization achieved in d (LAO 8◦ /CAU 36◦ ) and e (LA0 43◦ /CAU 29◦ ). (Continued on pages 32–34)
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Figure 10 (Continued) (C) Mid-LAD bifurcation: SB ostium best assessed in a (RA0 3◦ /CRA 39◦ ) and b (LA0 43◦ /CRA 32◦ ); poorly assessed in c (RA0 24◦ /CAU 20◦ ) and d (LA0 28◦ /CAU 42◦ ). (D) Distal LAD bifurcation: poorly assessed in a (RA0 20◦ /CAU 16◦ ) and d (LA0 36◦ /CAU 39◦ ); lesion best visualized in b (RA0 2◦ /CAU 42◦ ) and d (LA0 34◦ /CRA 32◦ ).
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Figure 10 (Continued) (E). Proximal LCx bifurcation: bifurcation and SB ostium not visualized in a (RA0 18◦ /CRA 43◦ ) and b (LAO 35◦ /CRA 37◦ ); best visualization in c (RA0 20◦ /CAU 25◦ ) and d (LA0 36◦ /CAU 31◦ ). (F) Ramus bifurcation: a-–bifurcation not visualized (LAO 36◦ /CAU 32◦ ); b-–best visualization of bifurcation lesion and SB ostium (RAO 25◦ /CAU 27◦ ). Distal LCx (i.e., OM) bifurcation: c-–bifurcation not visualized (LAO 50◦ /CAU 29◦ ); D-–best visualization of bifurcation lesion and SB ostium (RAO 30◦ /CAU 25◦ ). (Continued )
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(a)
(c)
(G)
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(H)
(a)
(b)
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(I)
Figure 10 (Continued) (G) Mid-RCA bifurcation: SB ostium poorly visualized in a (RA0 33◦ /CAU 6◦ ) and b (LAO 85◦ /CAU 5◦ ), best visualized in c (LAO 58◦ /CRA 2◦ ). (H) Distal RCA bifurcation (i.e., RCA-PDA/PLSA): a (LAO 22◦ /CAU 2◦ ); SB ostium best visualized in b (LAO 12◦ /CRA 19◦ ). (I) LM bifurcation: SB ostium not visualized in a (RAO 20◦ /CAU 22◦ ) and b (LAO 85◦ /CAU 5◦ ), best visualized in c (LAO 38◦ /CAU 35◦ ).
− −
− −
−
2.19 − − − − −
0.61 −
− −
2.75 − − 10 − −
0.93 64
− −
2.66 − − 9 − −
0.85 65
− 2.5
− −
2.73 − − 13.0 − −
0.89 65.9
8.99 2.39
15.38 2.71 − − 0.93 − − 65.9 − −
− −
2.82 − − 5.9 − −
0.66 72.2
12.35 2.36
18.62 2.87 − − 0.88 − − 69.4 − −
− −
2.47 − − 14.4 − −
1.23 43.4
5.4 2.21
14.4 2.78 − − 1.01 − − 64.4 − −
− −
2.69 − − 13.9 − −
1.27 41.5
4.7 2.22
16.6 2.93 − − 0.94 − − 67.7 − −
SES‡‡ 68
− −
− 2.86 2.34 − 11 13
− −
− 3.04 2.50 − 7 11
1.22 47
6.4∗∗ 2.6∗∗
6.0∗∗ 2.6∗∗ 1.21 46
17.5∗∗ 3.3∗∗ 3.00 2.63 − 1.62 1.32 − 46 50
Double SES 206
18.0∗∗ 3.3∗∗ 2.93 2.41 − 1.43 1.18 − 40 52
Single SES 207
− −
2.75 − − 9 − −
1.00 60
7 2.42
19 3.0 − − 0.84 − − 72 − −
Single SES 103
− −
2.76 − − 8 − −
1.15 56
7 2.36
20 3.0 − − 0.80 − − 73 − −
Single PES 102
Pan et al. (2007)55
− 1.66
2.56 − − 14.7 − −
1.14 49.7
7.20 2.28
16.25 2.68 − − 0.90 − − 68.2 − −
“MiniCrush” SES/ PES 52
Galassi et al.77
− 1.1
2.58 − − 13 − −
0.83 61
5.7 2.16
14.7 2.74 − − 0.83 − − 69 − −
Single SES 177
− 1.47
2.71 − − 12 − −
0.84 63
5.9 2.30
15.8 2.85 − − 0.90 − − 68 − −
Double SES 173
CACTUS30
1.54 1.53
− 3.17 2.74 − 3.0 9.3
1.11 54.4
9.9 2.38
20.9 3.08 − − − 1.63 1.20 − 47.3 54.9
Double SES 101
(Continued )
1.69 1.48
− 3.22 2.77 − 2.5 7.6
1.13 53.1
10.4 2.39
21.7 3.08 − − − 1.53 1.28 − 50.3 53.4
Single SES 101
BBK31
7in×10in
2.66 − − 11.5 − −
0.88 56.8
1.14 46.2
− 2.5
− 1.99
− 2.9 − − 0.76 − − 74 − −
BMS‡‡ 58
NORDIC29
Specs: 7x10 tight
2.65 − − 11.7 − −
5.5 2.1
5.1 2.1
− 3.0 − − 0.74 − − 77 − −
− 2.64 − − 0.64 − − − − −
“Crush” SES 120
“Crush” Double Single Double SES/ SES SES SES PES 65 50 41 241
SCANDSTENT53
11:8
Final Parent Vessel MLD, mm Proximal stent Distal stent % DS Proximal stent Distal stent Acute gain, mm Proximal stent Distal stent
10.8 2.6 − − 0.99 − − 61.7 − −
12.2 2.6 − − 0.92 − − 64.7 − −
Moussa et al.36
Pan et al. (2004)28
Hoye et al.52
Tanabe et al.26
April 9, 2010
Baseline Parent Vessel Lesion length, mm RD, mm Proximal vessel Distal vessel MLD, mm Proximal vessel Distal vessel % DS Proximal vessel Distal vessel Side Branch Lesion length, mm Reference diameter, mm MLD, mm % DS
Double SES 63
Colombo et al.27
QCA Parameters Reported in DES Bifurcations Trials
IHBK063-Moussa
Stenting Technique Single and Device SES Number of Lesions 23
Studies
Table 3
c02 Char Count=
2.35 − − 17.3 − − 0.28
− −
1.59 29.4 0.50
− −
1.42 32.0 0.37
2.11 14.4 −
2.51 − − 13.1 − − 0.14
1.69 23.5 −
1.49 31.0 0.31
1.78 28 −
− −
2.50 − − 18 − − −
1.95 21 −
1.73 30 −
− −
2.30 − − 23 − − −
2.15 12 −
1.85 30.7 0.41
− −
2.43 − − 22.9 − − 0.30
2.26 15.5 −
− − 1.70 28.0 0.03
− − −
2.35 − − 20.7 − − 0.99
1.77 24.5 −
− −
− − − − − − −
2.20 10.8 −
BMS‡‡ 58
1.19 45.1 0.56
− −
1.68 − − 42.5 − − 0.12
1.73 26.1 −
SES‡‡ 68
1.52 31 −0.04
0.00 0.04
− 2.86 2.29 − 11 15 −
1.50 34 −
Single SES 207
1.86 24 0.20
0.10 0.10
− 2.94 2.38 − 10 15 −
2.05 16 −
Double SES 206
NORDIC29
1.74 29 0.20
− −
2.45 − − 20 − − 0.31
2.03 17 −
Single SES 103
1.58 33 0.36
− −
2.10 − − 29 − − 0.60
1.97 17 −
Single PES 102
Pan et al. (2007)55
1.63 28.4 0.35
− −
1.99 − − 29.8 − − 0.30
2.16 14.6 1.02
“MiniCrush” SES/ PES 52
Galassi et al.77
1.52 31 0.13
− −
2.19 − − 25 − − 0.06
1.65 27 0.81
Single SES 177
1.66 30 0.29
− −
2.24 − − 25 − − 0.14
1.94 16 1.41
Double SES 173
CACTUS30
1.93 18.3 0.03
−0.01 0.01
− 3.23 2.77 − 3.0 9.9 −
1.97 16.6 0.84
Single SES 101
1.98 23.4 0.32
−0.02 0.08
− 3.16 2.65 − 3.6 12.5 −
2.30 9.6 1.19
Double SES 101
BBK31
7in×10in
− −
2.07 − − 22.9 − − 0.12
1.80 − −
“Crush” SES 120
“Crush” Double Single Double SES/ SES SES SES PES 65 50 41 241
SCANDSTENT53
Specs: 7x10 tight
Angiographic FU Parent Vessel MLD, mm Proximal stent Distal stent % DS Proximal stent Distal stent Late lumen loss, mm Proximal stent Distal stent Side Branch MLD, mm % DS Late lumen loss, mm
Side Branch MLD, mm % DS Acute gain, mm
Double SES 63
Moussa et al.36
Pan et al. (2004)28
Hoye et al.52
Tanabe et al.26
11:8
Stenting Technique Single and Device SES Number of Lesions 23
Colombo et al.27
April 9, 2010
Studies
QCA Parameters Reported in DES Bifurcations Trials (Continued )
IHBK063-Moussa
Table 3
c02 Char Count=
− − −
− −
−
−
−
−
−
−
−
−
72 (34/47) −
−
−
−
−
77 (10/13) 77 (10/13) 0 (0/13)
0 (0/4) 0 (0/4)
−
100 (4/4) −
11.3 (13/115)# 3.5 (4/115) 8.7 (10/115)
−
−
−
−
−
−
−
−
−
−
−
−
−
−
−
43.4
14.8
−
28.3
−
4.9
−
100 (29/29)†† 38 (11/29)††
−
57 (4/7) 0 (0/7) 57 (4/7) 43 (3/7) 0 (0/7)
22.5 (34/151) 4.6 (7/151) 19.2 (29/151)
94 (17/18)†† 33 (6/18)††
−
13 (1/8)†† 38 (3/8)†† 40 (4/8)†† 25 (2/8)††
−
16.0 (25/156) 5.1 (8/156) 11.5 (18/156)
100 (4/4)†† 100 (4/4)†† −
67 (2/3)†† 33 (1/3)†† 33 (1/3)†† 33 (1/3)†† 0 (0/3)††
9.4 (5/53) 5.7 (3/53) 7.5 (4/53)
100 (10/10)†† 100 (10/10)†† −
73 (8/11)†† 27 (3/11)†† 46 (5/11)†† 27 (3/11)†† 0 (0/11)††
28.6 (16/56) 10.7 (6/56) 8.9 (10/56)
−
−
−
−
−
−
−
−
12.2 (6/49) 2.0 (1/49)
−
−
−
−
−
−
−
−
−
6.7 (10/150) 14.7 (22/150)
−
−
−
−
−
−
−
−
−
4.6 (7/152) 13.2 (20/152)
−
−
−
−
−
−
−
−
−
12.5 (12/96) 7.3 (7/96) 9.4 (9/96)
−
−
−
−
−
−
−
−
13.5 (13/96) 3.1 (3/96) 12.5 (12/96)
7in×10in
Percentage of overall population with angiographic follow-up. † Defined as ostium 5 mm plus balloon-treated area in the side branch. ‡ Number of lesions with angiographic success at index procedure and angiographic follow-up (angiographic success defined as attainment of 4.0 mm2 . The lesions were
(a)
(c)
LAD
(b)
(d)
(A) Figure 13 Examples of IVUS cross-sectional images assessing coronary bifurcations. (A)—(a, b) Angiograms demonstrating proximal LAD/Diagonal bifurcation lesion: SB ostium involvement not visualized in (a), better assessed in (b). (c) SB ostium (pullback from SB) demonstrating significant amount of plaque located opposite to the flow divider. (d) Distal reference of the SB. (B)—(a) angiogram demonstrating proximal LAD/Diagonal bifurcation lesion: Note that the MV has moderate stenosis by angiography. (b) MV proximal reference (IVUS). (c) MV minimum lumen area with large plaque burden (IVUS). (d) MV distal reference (IVUS). (e) SB ostium (IVUS). (f) SB distal reference (IVUS). (C) LAD/Diagonal bifurcation post-double stenting implant (“crush” technique). (a, b) Final angiograms demonstrating optimal angiographic result. (c) SB distal reference. (d) SB ostium minimum stent area with significant stent underexpansion compared to distal reference. (Continued on pages 41 and 42 )
c02
IHBK063-Moussa
April 9, 2010
11:8
Specs: 7x10 tight
7in×10in
Char Count=
CORONARY ARTERY BIFURCATION LESIONS
41
analyzed at three cross-section locations: (a) proximal rim of the ostium (first frame proximal to the SB take-off); (b) in-bifurcation (frame with the larger SB ostial diameter); and (c) distal rim of the SB ostium (first frame distal to the SB take-off) (Fig. 16). The authors predefined the following characteristics for identifying high-risk plaque morphology: (a) fibroatheroma (FA)-–the presence of more than 10% confluent necrotic core covered by a fibrous cap thicker than 65 m; (b) calcified FA (CaFA)-–FA with more than 10% of confluent dense calcium; (c) IVUS-VH/OCT-derived thin capped FA (TCFA)-–more than 10% confluent necrotic core at the lumen covered by a fibrous cap
