Bifurcation Stenting - Ron Waksman - E-Book

Bifurcation Stenting E-Book

Ron Waksman

0,0
102,99 €

-100%
Sammeln Sie Punkte in unserem Gutscheinprogramm und kaufen Sie E-Books und Hörbücher mit bis zu 100% Rabatt.

Mehr erfahren.
Beschreibung

Here is expert guidance on one of the most vexing clinical challenges faced by interventional cardiologists. Written by global thought leaders in the area and edited by two internationally-recognized pioneers in interventional cardiology, Bifurcation Stenting covers all techniques, imaging modalities, and devices in current use, including VH-IVUS and OCT. It includes practical tips/tricks from leading experts and a section of challenging cases to further illustrate the material and help readers better understand the treatment of bifurcation lesions.

Sie lesen das E-Book in den Legimi-Apps auf:

Android
iOS
von Legimi
zertifizierten E-Readern

Seitenzahl: 519

Veröffentlichungsjahr: 2012

Bewertungen
0,0
0
0
0
0
0
Mehr Informationen
Mehr Informationen
Legimi prüft nicht, ob Rezensionen von Nutzern stammen, die den betreffenden Titel tatsächlich gekauft oder gelesen/gehört haben. Wir entfernen aber gefälschte Rezensionen.



Contents

Cover

Title Page

Copyright

Contributors

Foreword

Acknowledgements

Chapter 1: Classification of coronary artery bifurcation lesions

Coronary Bifurcation Classifications

Clinical Relevance of Bifurcation Lesion Type

Angiographic Description and Quantification of Bifurcation Lesions

Conclusions

References

Chapter 2: Provisional side branch stenting for the treatment of bifurcation lesions

Background

Basic Principles

Role of Bench Testing

Definition of a Coronary Bifurcation Lesion

Definition of Treatments

What is Provisional SB Stenting?

How to Perform Bifurcation Stenting Using the Provisional Approach

Role of IVUS

One or Two Guide Wires?

Should We Pre-Dilate the Lesion or Not?

Stenting Across

POT (Proximal Optimization Technique)

Outcome Analysis: When Should the SB be Treated?

Should kissing balloon inflation be performed after simple technique?

How to Carry out final Kissing Balloon Inflation Appropriately?

When and How Should the SB be Stented ?

Conclusion

References

Chapter 3: The Nordic experience

Introduction

The Nordic bifurcation studies

The Nordic Bifurcation Study (I)

The Nordic Bifurcation Stent Technique Study (II)

The Nordic-Baltic Bifurcation Study (III)

The Nordic Bifurcation Study (IV)

The Nordic-Baltic-British Left Main Revascularisation Study (NOBLE)

Patient Level Meta-Analysis Collaboration

Recommended Strategies for Treatment of Bifurcation Lesions

Future Studies from the Nordic PCI Study Group

Future Perspectives

References

Chapter 4: Crush and mini-crush

The Crush Technique

Variations of the Standard Crush Technique

Internal Crush Technique for “Provisional Crush” Approach

The Mini-Crush Technique

Comparison of the mini-crush and classical crush techniques

Clinical Studies with Crush Technique vs Single Stent Techniques

Clinical Studies with Minicrush Technique vs Single Stent Techniques

Conclusions

References

Chapter 5: Simultaneous kissing stent technique: A contemporary review

Introduction

Bifurcation Classification

Interventional Stenting Techniques for Bifurcations

Simultaneous Kissing Stents (SKS) and “V” Stenting Techniques

Clinical Studies

Lesion Preparation and Adjunct Pharmacotherapy

Conclusions and Future Directions

References

Chapter 6: Stenting for left main coronary artery bifurcation lesions

Introduction

Selection of Stenting Strategy

Periprocedural Preparation

Stenting Procedure

Conclusion

References

Chapter 7: Intravascular ultrasound and new imaging in bifurcation stenting

Introduction

IVUS-guided PCI and Predictors of Restenosis and Thrombosis

Role of IVUS in PCI for Bifurcating Lesions

Vascular Responses and Mechanisms of Restenosis

How to Evaluate Bifurcating Lesion by IVUS?

OCT Evaluation of Bifurcation Stenting

Conclusion

References

Chapter 8: Drug-eluting balloons and bifurcations, a new future for treatment?

Overview

Introduction

Technical Aspects

Animal Studies

Clinical Studies with DEB

Future Perspective

References

Chapter 9: Percutaneous coronary intervention for bifurcation lesions: Bench testing and the real world

Introduction

Testing of Mechanical Properties

Testing of Device Delivery

Evolution of Imaging Modalities and Phantom Construction

Micro-computed Tomography

Summary

References

Chapter 10: Coronary bifurcation stenting and stent thrombosis

Introduction

Pathophysiology

Stent Thrombosis

Conclusion

References

Chapter 11: Bifurcation angles during the cardiac cycle

Introduction

Bifurcation as the “Achilles' Heel” of PCI

Importance of 4D Imaging for Bifurcation

Development of Coronary Bifurcation 3D Imaging Preceding 4D Imaging

Novel Methodology of 4D Multidetector Computed Tomography (MDCT) Imaging

Conclusion

References

Chapter 12: OCT in coronary bifurcations

Introduction

Methodological Problems in the Study of Bifurcations

The Role of OCT

Minimal Methodological Requirements

Apposition

Strut Overlap Segments and Multilayer Segments

NASB (Non-Apposed Side-Branch Struts)

Scaffolding of the Carina and the Shoulder

Access to the Side Branch

Coverage

Advantages of Fourier-Domain Versus Time-Domain OCT

References

Chapter 13: Bifurcation quantitative coronary angiography

Pathophysiology of Bifurcation Disease

Classification of Bifurcation Lesions

Quantitative Coronary Angiography of Bifurcation Lesions

3-dimensional Angiography

Techniques of Bifurcation Stenting

Treatment with One Versus Two Stents

Dedicated Devices

Conclusions

References

Chapter 14: Evaluation of a dedicated everolimus coated side branch access (SBA) system

Introduction

Materials and Methods

Results

Discussion

Acknowledgements

References

Chapter 15: Devices: TriReme

Introduction

Anatomic Characterization of Coronary Bifurcations

Device Description

Procedure

Clinical Trials

Post-marketing Evaluation

Technical Considerations

Considerations and Future Directions

References

Chapter 16: Dedicated bifurcation stents: The petal stent

Introduction

Rationale for Dedicated Bifurcation Stenting System

Taxus Petal stent

Device Description

First-in-human Study

Conclusion

References

Chapter 17: The Sideguard Side branch stent

Challenges of bifurcation stenting

Approaching Bifurcation from the Side Branch First

Advantages of the Sideguard First Approach in the Treatment of Bifurcations

Early Experience: Animal Studies

Pivotal CE Clinical Trial

Conclusion

Future Developments

References

Chapter 18: XIENCETM side branch access system for the treatment of bifurcation lesions (XIENCE SBA)

References

Chapter 19: The spherical balloon: A new tool to optimize bifurcation treatment

Introduction

Plaque Distribution in Coronary Bifurcations

Review of the Provisional SB T-Stenting Technique

A New Tool: the Spherical Balloon

The Need of a Final Kissing Inflation

Conclusions

References

Chapter 20: Axxess stent

Overview of Bifurcation Lesions

Classification of Bifurcation Lesions

Outcomes of Patients Treated with PCI Using Drug-Eluting Stents

The Axxess Bifurcation DES Experience

Summary

References

Index

Color Plates

This edition first published 2012 © 2012 by Blackwell Publishing Ltd

Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell's publishing program has been merged with Wiley's global Scientific, Technical and Medical business to form Wiley-Blackwell.

Registered office: John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

Editorial offices: 9600 Garsington Road, Oxford, OX4 2DQ, UK

The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

111 River Street, Hoboken, NJ 07030-5774, USA

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell

The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988.

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, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.

Library of Congress Cataloging-in-Publication Data

Bifurcation stenting / edited by Ron Waksman and John A. Ormiston.

p.; cm.

Includes bibliographical references and index.

ISBN 978-1-4443-3462-3 (cloth)

1. Stents (Surgery) 2. Coronary heart disease–Surgery. I. Waksman, Ron. II. Ormiston, John A.

[DNLM: 1. Coronary Disease–surgery. 2. Stents. 3. Cardiac Surgical Procedures. 4. Coronary Angiography. WG 300]

RD598.35.S73B54 2012

617.4'12–dc23

2011018729

Contributors

Alexandre Abizaid, MD, PhD Chief of Coronary Interventions Instituto Dante Pazzanese de Cardiologia Chairman, Cardiovascular Research Center São Paulo, SP, Brazil Visiting Professor of Medicine Columbia University Medical Center New York, NY, USA

Pierfrancesco Agostoni, MD, PhD University Medical Center Utrecht Department of Interventional Cardiology Utrecht, The Netherlands

Remo Albiero, MD Director Cardiac Cath Lab Emodinamica, Istituto Clinico San Rocco Ome (Brescia), Italy

Giombattista Barrano, MD Postgraduate School of Cardiology University of Catania Catania, Italy

Anouar Belkacemi, MD University Medical Center Utrecht Department of Interventional Cardiology Utrecht, The Netherlands

Hiram G. Bezerra, MD, PhD Assistant Professor Medical Director Cardiovascular Imaging Core Laboratories Case Western Reserve University University Hospitals Case Medical Center Cleveland, OH, USA

Gary Binyamin, PhD Director of Science and Technology TriReme Medical, Inc. Pleasanton, CA, USA

Katrin Boeke-Purkis, BSc, CCIR Abbott Vascular Santa Clara, USA

Marco A. Costa, MD, PhD, FACC, FSCAI Professor of Medicine Director, Interventional Cardiovascular Center Director, Center for Research and Innovation Harrington-McLaughlin Heart and Vascular Institute University Hospitals, Case Western Reserve University Cleveland, OH, USA

Ricardo A. Costa, MD Department of Interventional Cardiology Instituto Dante Pazzanese de Cardiologia Director, Angiographic Core LaboratoryCardiovascular Research CenterSão Paulo, SP, Brazil

Luca Costanzo, MD Postgraduate School of Cardiology University of Catania Catania, Italy

Frederic de Vroey, MD Cardiac Investigation Unit Auckland City Hospital Auckland, New Zealand

Alfredo R. Galassi, MD, FACC, FESC, FSCAI Associate Professor of Cardiology Postgraduate School of Cardiology Head of the Catheterization Laboratory and Cardiovascular Interventional Unit Clinical Division of Cardiology Ferrarotto Hospital University of Catania Catania, Italy

Eberhard Grube, MD Professor of Cardiology University of Bonn Departement of Medicine II Bonn, Germany

Juan Luis Gutiérrez-Chico, MD, PhD, FESC Erasmus Medisch Centrum, Thoraxcentrum Interventional Cardiology Department Rotterdam, The Netherlands

Niels R. Holm, MD Research Fellow Department of Cardiology Aarhus University Hospital, Skejby Aarhus, Denmark

Gary M. Idelchik, MD Division of Interventional Cardiology Scottsdale Healthcare Hospitals Scottsdale, AZ, USA

Soo-Jin Kang, MD, PhD Assistant Professor of Medicine Asan Medical Center Seoul, Korea

Young-Hak Kim, MD, PhD Associate Professor of Internal Medicine University of Ulsan College of Medicine Asan Medical Center Seoul, Korea

Pieter H. Kitslaar, MSc Department of Cardiology Leiden University Medical Center Leiden, The Netherlands

Eitan Konstantino, PhD Chief Executive Officer TriReme Medical, Inc. Pleasanton, CA, USA

Alexandra J. Lansky, MD Associate Professor, Cardiovascular Medicine Director, Yale Cardiovascular Research Group Co-Director, Valve Program Yale University School of Medicine New Haven, CT, USA

Jens Flensted Lassen, MD, PhD, FESC Associate Professor of Cardiology Consultant, Invasive Cardiology Department of Cardiology B Aarhus University Hospital, Skejby Aarhus, Denmark

Thierry Lefèvre, MD, FESC, FSCAI Director of the Cardiac Catheterization Department at Institut Cardiovasculaire Paris Sud Hôpital Privé Jacques Cartier, Massy France

Victor Legrand, MD, PhD, FESC, FACC Professor of Clinical Medicine University of Liège, Liège, Belgium Director of Centre Intégré d'Interventions Transluminales CHU de Liège, Liège, Belgium

Jurgen Ligthart, BSc Department of Cardiology Erasmus Medisch Centrum, Thoraxcentrum Rotterdam, The Netherlands

Li Hui-Ling, MD, PhD Department of Cardiology Erasmus Medisch Centrum, Thoraxcentrum Rotterdam, The Netherlands

Yves Louvard, MD, FSCAI Institut Cardiovasculaire Paris Sud, Massy, France

Michael Maeng, MD, PhD Department of Cardiology Aarhus University Hospital, Skejby Aarhus, Denmark

Michael Mahmoudi, MD, PhD Division of Cardiology Washington Hospital Center Washington, DC, USA

Vivian G. Ng, MD Columbia University Medical Center New York, NY, USA

John A. Ormiston, MBChB Mercy Angiography Auckland, New Zealand

Seung-Jung Park, MD, PhD Professor of Internal Medicine University of Ulsan College of Medicine Asan Medical Center Seoul, Korea

Evelyn Regar, MD, PhD, FESC Associate Professor Interventional Cardiology Department Erasmus Medisch Centrum, Thoraxcentrum Rotterdam, The Netherlands

Johan H.C. Reiber, PhD Department of Cardiology Leiden University Medical Center Leiden, The Netherlands

David G. Rizik, MD, FACC, FSCAI Director of the Division of Heart & Vascular Medicine Scottsdale Healthcare Hospitals Scottsdale, AZ, USA

Patrick W. Serruys, MD, PhD, FESC, FACC Erasmus Medisch Centrum, Thoraxcentrum Interventional Cardiology Department Rotterdam, The Netherlands

Samin K. Sharma, MD, FACC Professor of Medicine Cardiology Catheterization Laboratory of the Cardiovascular Institute Mount Sinai Hospital New York, USA

John E. Shulze, BSEE, MBA Chief Technical Officer Biosensors International Morges, Switzerland

Oana Sorop, PhD Department of Cardiology Erasmus Medisch Centrum, Thoraxcentrum Rotterdam, The Netherlands

Pieter R. Stella, MD, PhD Professor of Cardiology Medical University Ho Chi Minh (VN) Associate Professor of Cardiology, UMCU Director Heart Catheterization Laboratories, UMCU Director Clinical Cardiovascular Research, UMCU University Medical Centre Utrecht The Netherlands

Joseph M. Sweeny, MD Assistant Professor of Medicine CardiologyCatheterization Laboratory of the Cardiovascular Institute Mount Sinai Hospital New York, USA

Satoko Tahara, MD, PhD Research fellow Cardiovascular Imaging Core Laboratories University Hospitals Case Medical Center Harrington-McLaughlin Heart & Vascular Institute Cleveland, OH, USA

Leif Thuesen, MD, DMSci Director PCI Research Unit Department of Cardiology Aarhus University Hospital, Skejby Denmark

Salvatore Davide Tomasello, MD, PhD Department of Cardiology Morriggia-Pelascini Hospital, Italia Hospital Gravedona, Como, Italy

Brett Trauthen, MS Chief Scientific Officer Devax Inc. Irvine, CA, USA

Heleen M.M. van Beusekom, PhD Department of CardiologyErasmus Medisch Centrum, Thoraxcentrum Rotterdam, The Netherlands

Willem J. van der Giessen, MD, PhD Professor of Cardiology Erasmus Medisch Centrum, Thoraxcentrum Rotterdam Interuniversity Cardiology Institute of the Netherlands ICIN-KNAW The Netherlands

Robert Jan M. van Geuns, MD, PhD, FESC Associate Professor of Cardiology Erasmus Medisch Centrum, Thoraxcentrum Interventional Cardiology Department Rotterdam, The Netherlands

Stefan Verheye, MD, PhD Interventional Cardiology Antwerp Cardiovascular Center ZNA Middelheim Antwerp, Belgium

Michiel Voskuil, MD, PhD University Medical Center Utrecht,Department of Interventional CardiologyUtrecht, The Netherlands

Ron Waksman, MD Division of Cardiology Washington Hospital Center Washington, DC, USA

Bruce Webber, MHSc Mercy Angiography Auckland, New Zealand

Mark Webster, MBChB Mercy Angiography Auckland, New Zealand

Foreword

Marie Claude Morice, MD

Institut Cardiovasculiare Paris Sud, Hôpital Privé Jacques Cartier, Massy, France

The coronary arteries can be compared to tree trunks in that they produce branches: it would, therefore, be preposterous to treat a trunk without taking into account its branches.

The coronary network is a succession of bifurcations branching off into gradually narrower segments in an uneven pattern.

For a long time, the percutaneous treatment of diseased coronary bifurcations was voluntarily left aside because most interventional cardiologists were daunted by the anticipated inherent complexity of the procedures. Indeed, the tubular configuration and constant diameters of balloon-catheters and stents seemed to preclude any successful attempt at tackling and efficiently navigating the coronary bifurcation anatomy.

However, in view of the significant incidence of coronary bifurcation disease documented in 15–20% of patients undergoing PCI and with the support of increasingly enhanced technology, several teams gradually decided to overcome this obstacle and work towards a better understanding of the flow pattern, anatomical variations and physical principles governing coronary bifurcations. They endeavored to put into perspective the intricacies of bifurcation anatomy and the pattern of atheroma build-up in branching coronary segments.

Their efforts resulted in classifications of bifurcation types and potential customized treatments.

Increasingly subtle, refined and complex techniques were devised in order to adapt our tubular stents to diseased vessel segments with a proximal diameter larger than their distal extremity, and to access branches from the middle of tubular stents.

Of the multiple strategies suggested by diligent and very imaginative minds, experience showed that the implantation of a single stent was associated with a better outcome in lesions amenable to this strategy. This is why provisional stenting has become the standard treatment.

Several dedicated stents were designed by creative engineers but very few of these devices made their way from bench to bedside. The ones that did are presented here.

All specificities and technical strategies implemented in the treatment of the most important of all coronary bifurcations, the left main, are thoroughly addressed in this book.

Each chapter is written by the most prominent expert in the subject involved.

This impressive collaborative work provides an exhaustive account of all potential issues and concerns that may be raised by the treatment of coronary bifurcations.

There is no doubt that the reader will find here an invaluable source of information, which is based on the experience of seasoned specialists who share their findings with the interventional cardiology community in order to provide state-of-the-art therapeutic approaches and optimal care to our patients.

Acknowledgements

Chapter 2

The authors thank Catherine Dupic for assistance in manuscript preparation.

Chapter 3

Participating centres (Nordic-Baltic Bifurcation Studies I-III):

Finland: Oulu University Hospital, Tampere University Hospital, Turku University Hospital, Kajaani Central Hospital, Rovaniemi Central Hospital, Kemi Central Hospital, Kuopio University Hospital, Helsinki University, Hospital, Satakunta Central Hospital, Pori

Denmark: Aarhus University Hospital, Skejby, Odense University Hospital, Aalborg University Hospital, Gentofte University Hospital, Rigshospitalet, Copenhagen

Sweden: Örebro Central Hospital, Falun Hospital, Uppsala University Hospital

Norway: The Feiring Clinic, Feiring, University Hospital of Tromsoe, Oslo University Hospital, Rikshospitalet, Ullevaal University Hospital, Oslo, St. Olav Hospital, Trondheim, Haukeland University Hospital, Bergen

Latvia: Paul Stradins Clinical Hospital, Riga

Chapter 14

The work for this chapter was supported by a grant from Abbott Vascular Inc.

Chapter 17

The author would like to thank Mark Paquin for his time and contribution in preparing this chapter.

Chapter 1

Classification of Coronary Artery Bifurcation Lesions

Victor Legrand, MD, PhD, FACC, FESC

Centre Intégré d'Interventions Transluminales, CHU de Liège, Liège, Belgium

Bifurcation lesions constitute 12–15% of the lesions treated with percutaneous coronary intervention (PCI) [1–3]. They represent a distinct lesion subset associated with an increased risk of procedure-related complications and were recognized early in the development of PCI [3, 4]. Consequently, this stenosis morphology was considered to represent a moderately increased risk (type B) if side branches were protectable by a guidewire and high risk (type C) if they could not be protected, in the AHA/ACC Task Force classification [5].

Technical improvements, including development of dedicated stents and the use of drug-eluting stents, together with better medical management and treatment strategy have considerably reduced the risk of acute complications, restenosis and late stent thrombosis [6]. These advances were gained mostly from clinical experience, which showed that the likelihood of side branch occlusion depends on the relative position of the plaque to the bifurcation and whether the side branch originates from the primary lesion in the main vessel, as well as its degree of angulations [7]. These observations underlined the need for a comprehensive classification scheme to guide the treatment strategy. Classification of coronary artery bifurcation lesions is also of paramount importance to permit accurate comparisons of techniques, results and outcomes in homogeneous lesion groups.

A fundamental challenge in assessing bifurcation is to consider simultaneously lesion length and severity of the main vessel and the side branch, knowing that both vessels are not in the same plane and that angulations must be viewed in a three-dimensional space. Additionally, some morphologic considerations may be added, including the extent of calcification, the presence of coronary ectasia and irregularities, plaque ulceration and thrombus [8, 9]. Therefore, it is not surprising that many classifications have been proposed to describe this complex anatomical subset. Moreover, these inherent lesion complexity and imaging challenges also represent pitfalls and limitations for conventional quantitative angiographic analysis.

In order to guide interventional cardiologists, we reviewed the coronary artery bifurcation classifications that have been proposed and the challenges for a representative design of a coronary bifurcation. To achieve consistency in the reporting of bifurcation analyses we propose a simple comprehensive and universal approach that could help to better select a particular technique and define the risks of PCI.

Coronary Bifurcation Classifications

According to American College of Cardiology/American Heart Association (ACC/AHA) task force classification [5] a bifurcation lesion is “a lesion located in a bifurcation point with a side branch >2 mm in diameter”. The lesion being defined as >50% diameter stenosis in the proximal and/or distal parent vessel and/or a >50% diameter stenosis in the ostium of the contiguous side branch. A less restrictive definition could be “any lesion located in a bifurcation point”. Conversely, a more clinically oriented definition could be a “lesion located in a bifurcation point with a side branch that you don't want to lose”. The position of a contiguous stenosis, relative to the bifurcation point is important. Should it be within the 2 mm of the bifurcation point or is a bifurcation lesion any side branch covered by an inflated balloon or covered by a stent? Differences in interpretation of these basic definitions may have important implications in treatment strategy and results as well as in comparisons between different studies and registries.

In order to clarify the definition of a coronary artery bifurcation lesion, the European Bifurcation Club proposed that a bifurcation lesion is “a coronary artery narrowing occurring adjacent to, and/or involving, the origin of a significant side branch”. A significant side branch is a branch that you do not want to lose in the global context of a particular patient (symptoms, location of ischemia, viability, collateralizing vessel, left ventricular function, and so forth) [8]. Treatment of the bifurcation also implies balloon inflation or stent coverage above the ostium of the side branch. Using this definition, the clinical viewpoint is preponderant. It corresponds to what is the most relevant for the patient regardless of the size of the vessel and taking into consideration the physiological role of the side branch rather than its anatomical feature.

Classification of bifurcation lesions have been attempted since 1994. Since then, six major classification systems have been proposed [1, 10–14]. A schematic representation of the published classification systems is given on Figure 1.1. Some of these classifications were proposed before the advent of stents and drug-eluting stents [10, 11]. These early classifications were not adapted for the contemporary interventional techniques and their rationale was based on results achieved using balloon only, thus not taking into consideration the use of stent(s) and newer treatment strategies such as kissing or crushing. With the use of stent(s), it appeared soon that not only localization of the plaque, but also angulations between branches had an impact on the results and hence may influence the technique used [1, 12–14]. All classification systems are based on the presence or absence of a stenosis in each of the three segments that constitute the bifurcation: the main branch proximal to the bifurcation, the main branch distal to the bifurcation and the side branch.

Figure 1.1 Schematic representation of reported classifications of bifurcation lesions according to their morphology. Lefevre classification also takes into consideration side branch angulations (Y- or T-shape). Description of Mohaved classification is given in the text.

The Sanborn classification [10] describes five types of lesions, it omits situations where the stenosis involves proximal and distal main branch without involvement of side branch, as well as situations without distal main branch stenosis. Balloon dilatation of these lesions usually yielded similar results of non bifurcated lesions, indeed. No description of the bifurcation angle is proposed.

The Safian classification [11] addresses all the possible combinations. Risk of complications or failure is greater in type I lesions followed by type II lesions. Treatment of type III and IV lesions leads to excellent outcomes indistinguishable from low-risk procedures.

The Duke classification [12] is similar to the Safian classification. Lesions involving simultaneously distal main branch and side branch are not described, however. Like the Sanborn and Safian schemes, it ignores the bifurcation angle. This classification first considers stenoses without ostial side branch narrowing (lesions involving the main vessel only: type A, B or C). Lesions involving the side branch are referred to as type D, E or F.

The Lefevre classification [1] considers lesions involving a side branch ≥2.2 mm and take into consideration angulations of the bifurcation as well as the location of the plaque. T-shape lesions refer to bifurcation angle >70°, these lesions are generally perfectly treated using T-stenting, when needed. Conversely, in Y-shape lesions (<70° angle), the risk of a snow-plow effect seems higher and treatment strategy is usually more complex. Types 1, 2 and 4 lesions are similar to Sanborn type I and III, Safian type IA, IB and IIIA and Duke type D, C classifications. These lesions carry the highest risk of side branch occlusion after stent implantation, particularly when angulations is <70°. In a series of 366 patients treated with stenting, in-hospital major adverse cardiac events were noted respectively in 4.0%, 4.5% and 4.2% of type 1, type 2 and type 4 lesions, versus 2.7% in type 3 and 0% in types 4 A,B lesions [1].

The Medina classification [13] takes the advantage to be the simplest to memorize, even though it provides all the information contained in the others. It consists in recording any narrowing ≥50% in each of the three arterial segments of the bifurcation in the following order: proximal main vessel, distal main vessel and side branch. Presence of a narrowing is coded 1 and absence of a significant stenosis 0. These three figures are separated by commas. This straightforward classification doesn't mentioned bifurcation angle. It has been suggested that the Medina classification should also contain information on lesion length, especially for the side branch, or presence of calcification, in addition to angulations (Y- or T-shape). However, adding these variables would negate the simplicity of the Medina classification. The only parameter that is currently being debated is the lesion length in the side branch, which could have a significant impact on the technique used [6].

A different classification scheme was proposed by Movahed [14] in an attempt to propose a simple algorithm for lesion-specific techniques [15]. The lesion classification begins with the prefix B (for bifurcation) to which four suffixes are added to obtain the final description of the lesion. The first suffix deals with the characteristics of the proximal segment: C = close to bifurcation, N = non-significant side branch, S = small proximal segment, L = large proximal segment (defined as more than two-thirds of the sum of diameters of both branch vessels). The second suffix describes the involvement of bifurcation branches: 1M =only main branch ostium diseased, 1S = only side branch ostium diseased, 2 = both main and side branch ostia diseased. The third suffix describes the angulations of the bifurcation: V = angle <70°, T = angle ≥70°. If the lesion is heavily calcified or involves the left main, a fourth suffix can be added: CA = calcified, LM = left main involvement. Lack of consensus regarding the (evolving) treatment strategy of bifurcation lesions limits the widespread utilization of this classification.

Following the second European Bifurcation Club meeting, a consensus emerged to recommend the Medina classification as the “gold standard”. Despite limitations underlined above, this binary classification is easy to memorize and to implement in general practice as well as in case record forms. Adding information on angulations, lesion length on side branch, presence of calcification, TIMI flow and vessel size would give a complete description and may be valuable for specific clinical evaluations. For current routine practice and registries, the Medina classification takes advantage to be easily understood and applied by all interventional cardiologists, however.

In some situations, it is not easy to distinguish between the distal main vessel and the side branch when both vessels have the same diameter. The choice may be subjective, but we consider that the side branch is the vessel with the shortest lesion as in most bifurcation stenosis, side branch lesion length is usually short.

Clinical Relevance of Bifurcation Lesion Type

Based on recent trials, the five most common Medina classes were (1,1,1), (1,1,0), (0,1,0), (0,1,1) and (1,0,0). These five patterns account for more than 90% of the bifurcations (Table 1.1).

Table 1.1 Medina class frequency of occurrence.

Some bifurcation patterns carry a high risk of snow plow effect or plaque shift. The term “true bifurcation”, introduced for many years, refers to lesion types associated with the highest risk of acute complications. These are lesions involving both the main vessel and the side branch. Treatment of theses bifurcation lesions often needs complex stenting strategies with use of two or more stents, and/or dedicated stents. Based on Table 1.1, “true” bifurcation lesions account for 63% of bifurcated lesions. The definition of “complex” or “true” bifurcation according to the different classifications is given in Table 1.2 (see also Figure 1.1).

Table 1.2 “Complex” or “true” bifurcation lesions according to classifications systems.

Side branch occlusion which was initially thought to be related to plaque shift is mostly related to carina shift. Recent MDCT [21] and IVUS [22] studies have reported that the carina was almost always spared of plaque growth, whereas plaque burden was almost always being present in the proximal vessel. Recognizing that the carina is free of plaque has major implications on interpretation of lesion classification and stenting technique.

Angiographic Description and Quantification of Bifurcation Lesions

Classification of coronary bifurcation lesions based on visual evaluation offers the advantage of simplicity, but lacks precision in terms of vessels sizes, angulations and lesion dimensions. These limitations may be overcome by angiographic quantification. Quantitative coronary angiography (QCA) of single lesions is often used to objectively evaluate lesions type and severity. However, because of the fractal nature of coronary bifurcations, lesion shape and complex three-dimensional geometry, QCA assessment of coronary bifurcation lesions is problematic.

Using standard QCA systems, the bifurcation main vessel is considered as a single segment with a single reference diameter function assuming progressive vessel tapering. This is not in line with the fractal geometry and the structure-function scaling laws that govern a coronary tree [23]. It has been shown, indeed, that the coronary tree is an object of fractal geometry governs by the Murray's law [24]. Therefore, the relation between the proximal main vessel (PMV), the distal main vessel (DMV) and side branch (SB) is governed by the following equation: PMV = 0.67(DMV + SB). Current available QCA systems do not use this formula, which leads to an underestimation of the true dimensions of the proximal main vessel or to an underestimation of plaque burden.

Another fundamental challenge in QCA assessment of bifurcations is in acquiring the entire bifurcation lesion without significant foreshortening, geometrical distortion or vessel/side branch overlap. Because of its complex geometry, bifurcation lesion should be assessed in the two best single views. Identification of the projection which displays the widest bifurcation angle is important. Because the PMV is not always in the same plane as the DMV or the SB, this parameter is highly dependent on image acquisition.

Beside reference diameters and vessels angulations and other important morphologic considerations include lesion length on each segment, ostial SB location, extent of coronary calcification, presence of coronary ectasia and irregularity, plaque ulceration, presence of thrombus and flow characteristics, all of which have been shown to have prognostic significance in procedural and long-term outcomes [25, 26].

Based on the above mentioned considerations and recommendations of the European Bifurcation Group [9], QCA software with specific algorithm dedicated for bifurcation analysis are currently developed and validated (CAAS 5 Pie Medical Bifurcation Imaging, Maastricht, the Netherlands). Use of dedicated QCA software together with a standard angiographic report of bifurcation analysis will soon provide an objective tool to describe a specific lesion classification and will help to determine treatment strategy as well as to evaluate procedural results. In addition to the visual assessment of lesions morphology, dedicated QCA software should now be recommended for future trials and device comparisons.

Conclusions

Percutaneous coronary angioplasty of coronary artery bifurcation lesions was soon recognized to be associated with an increased risk of procedure-related complications and recurrent ischemia. This observation lead to the development of lesion type classifications, aiming to identify the riskier situations as well as to select the most effective treatment strategy. Since the end of the 1990s, technical evolution of percutaneous techniques and regular use of drug-eluting stents in these situations have dramatically improved both immediate and late results. As such, the role of a classification code is to describe, in a simple and easily understandable manner, the lesions' characteristics in order to allow comparisons between trials and techniques used. Consequently, the Medina classification is now accepted as the universal scheme for the visual assessment of coronary bifurcation lesions. Adding information on angulations and lesion length in the side branch could further improve the information, however.

This classification does not replace QCA measurements, which remain indispensable for an accurate evaluation of plaque morphology and vessels' dimensions. Recent advances and standardization in angiographic analysis software will allow an even more comprehensive assessment of this complex anatomic subset.

References

1. Lefèvre T, Louvard Y, Morice MC, Dumas P, Loubetre C, Benslimane A, Premchand RK, Guillard N, Piéchaud JF. Stenting of bifurcation lesions: Classification, treatment and results. Cathet Cardiovasc Intervent 2000; 49: 274–83.

2. Thomas M, Hildick-Smith D, Louvard Y, Albiero R, Darremeont O, Stankovic G, Pan M, Legrand V, De Bruyne B, Lefèvre T. Percutaneous coronary intervention for bifurcation disease. A consensus view from the first meeting of the European Bifurcation Club. EuroInterv 2006; 2: 149–53.

3. Meier B, Gruentzig AR, King S.B. 3rd, Douglas JS Jr, Hollman J, Ischinger T, Aueron F, Galan K. Risk of side branch occlusion during coronary angioplasty. Am J Cardiol 1984; 53: 10–14.

4. Al Suwaidi J, Berger PB, Rihal CS, Garratt KN, Bell MR, Ting HH, Bresnahn JF, Grill DE, Holmes Jr. DR. Immediate and long term outcome of intracoronary stent implantation for true bifurcation lesions. J Am Coll Cardiol 2000; 35: 929–36.

5. Ryan TJ, Faxon DP, Gunnar R.M. et al. Guidelines for percutaneous transluminal angioplasty: a report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Angioplasty). Circulation 1998; 78: 486–502.

6. Stankovic G, Darremont O, Ferenc M, Hildick-Smith D, Lassen JF, Louvard Y, Albiero R, Pan M, Lef èvre T. Percutaneous coronary intervention for bifurcation lesions: 2008 consensus document from the fourth meeting of the European Bifurcation Club. EuroInterv 2009; 5: 39–49.

7. Legrand V, Thomas M, Zelisko M, De Bruyne B, reifart N, Steigen T, Hildick-Smith D, Albiero R, Darremont O, Stankovic G, Pan M, Lassen JF, Louvard Y, Lef èvre T. Percutaneous coronary intervention of bifurcation lesions: state-of-the-art. Insights from the second meeting of the European Bifurcation Club. EuroInterv 2007; 3: 44–9.

8. Louvard Y, Thomas M, Dzavik V, Hildick-Smith D, Galassi AR, Pan M, Burzotta F, Zelizko M, Dudek D, Ludman P, Sheiban I, Lassen JF, Darremont O, Kastrati A, Ludwig J, Iakovou I, Brunel P, Lansky A, Meerkin D, Legrand V, Brunel P, Medina A, Lef èvre T. Classification of coronary artery bifurcation lesions and treatments: Time for a consensus! Catheter Cardiovasc Interv 2008; 71: 175–83.

9. Lansky A, Tuinenburg J, Costa M, Maeng M, Koning G, Popma J, Cristea E, Gavit L, Costa R, Rares A, Van Es GA, Lefevre T, Reiber H, Louvard Y, Morice MC. Quantitative angiographic methods for bifurcation lesions: A consensus statement from the European Bifurcation Group. Catheter Cardiovasc Interv 2009; 73: 258–66.

10. Spokojny AM, Sanborn TM. Stategic approaches in coronary intervention. Baltimore, MD, Williams and Wilkins, 1996: 288.

11. Popma JJ, Leon MB, Topol EJ. Atlas of interventional cardiology. Philadelphia, PA, W.B. Saunders, 1994: 77.

12. Freed M, Grines C, Safian RD. Bifurcation stenosis. In Freed M, Grines C, Safian RD, eds. The New Manual of interventional Cardiology. Birmingham, MI, Physician Press, 1996: 233–43.

13. Medina A, Suarez de Lezo J, Pan M. A new classification of coronary bifurcation lesions. Rev Esp Cardiol 2006; 59: 183–4.

14. Mohaved MR, Stinis CT. A new proposed simplified classification of coronary artery bifurcation lesions and bifurcation interventional techniques. J Invasive Cardiol 2006; 18: 199–204.

15. Mohaved MR. Coronary artery bifurcation lesion classifications, interventional techniques and clinical outcome. Expert Rev Cardiovasc Ther 2008; 6: 261–74.

16. Hildick-Smith D, de Belder AJ, Cooter N, Curzen NP, Clayton TC, Oldroyd KG, Bennett L, Holberg S, Cotton JM, Glennon P.E. et al. Randomized trial of simple versus complex drug-eluting stenting for bifurcation lesions: the British Bifurcation Coronary Study: old, new and evolving strategies. Circulation 2010; 121: 1235–43.

17. Frangos C, Noble S, Piazza N, Asgar A, Fortier A, Doucet S, Bonan R. Impact of bifurcation lesions on angiographic characteristics and procedural success in primary percutaneous coronary intervention for ST elevation myocardial infarction. EuroInterv 2010; in press.

18. Collins N, Seidelin PH, Daly P, Ivanov J, Barolet A, Mackie K, Bui S, Schwartz L, Dzavik V. Long-term outcomes after percutaneous coronary intervention of bifurcation narrowings. Am J Cardiol 2008; 102: 404–410.

19. Enrico B, Suranyi P, Thilo C, Bonomo L, Costello P, Schoepf UJ. Coronary artery plaque formation at CT angiography: morphological analysis and relationship to hemodynamics. Eur Radiol 2009; 19: 837–44.

20. Van Mieghem CA, Thury A, Meijboom WB, Cademartiri F, Mollet NR, Weustink AC, Sianos G, de Jaegere PP, Serruys PW, de Feyter P. Detection and characterization of coronary bifurcation lesions with 64-slice computed tomography coronary angiography. Eur Heart J 2007; 28: 1968–76.

21. van der Giessen AG, Wentzel JJ, Meijboom WB, Mollet NR, van der Steen AF, van de Vosse FN, de Feyter PJ, Gijsen FJ. Plaque and shear stress distribution in human coronary bifurcations: a multislice computed tomographic study. EuroInterv 2009; 4: 654–61.

22. Oviedo C, Maehara A, Mintz GS, Araki H, Choi SY, Tsujita K, Kubo T, Doi H, Templin B, Lansky A.J. et al. Intravascular ultrasound classification of plaque distribution in left main coronary artery bifurcations: Where is the plaque really located? Circ Cardiovasc Interv 2010; 2: 105–12.

23. Kassab GS. Scaling laws of vascular trees: Of form and function. Am J Physiol Heart Circ Physiol 2006; 290: 894–903.

24. Zhou Y, Kassab GS, Molloi S. On the design of the coronary arterial tree: A generalization of Murray's law. Phys Med Biol 1999; 44: 2929–45.

25. Ellis SG, Vandormael MG, Cowley M, et al. Coronary morphologic and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease. Implication for patient selection. Circulation 1990; 82: 1193–202.

26. Dzavik VKR, Ivanov J, Ing DJ, Bui S, Mackie K, Ramsamujih R, Barolet A, Schwartz L, Seidelin PH. Predictors of long term outcome after crush stenting of coronary bifurcation lesions: importance of bifurcation angle. Am Heart J 2006; 152: 762–9.

Chapter 2

Provisional Side Branch Stenting for the Treatment of Bifurcation Lesions

Thierry Lefèvre, MD, FESC, FSCAI and Yves Louvard, MD, FSCAI

Institut Cardiovasculaire Paris Sud, Massy, France

Background

The treatment of coronary bifurcation lesions forms an integral part of the history of coronary angioplasty [1–4] and kissing balloon inflation was strongly recommended as early as the 1980s. In those days, the two angioplasty balloons were positioned using two separate guiding catheters.

A few studies were carried out on the use of directional or rotational atherectomy and showed relatively disappointing results [5, 6]. The advent of stenting resulted in the creativity of interventional cardiologists being challenged. For this reason, many stent implantation techniques were described during the 1990s [7–18]. Among these strategies, the single-stent technique, that is stenting of the main branch (MB) with provisional SB stenting (Figure 2.1), was associated with the most acceptable outcome [19–25].

Figure 2.1 Repeat intervention rate after bifurcation stenting with BMS and DES.

The development of the DES technology at the dawn of the third millennium brought about a very significant reduction in the risk of restenosis [26] and repeat intervention [27] as shown in Figure 2.2. As a result, surgery for patients with bifurcation lesions in large coronary vessels became obsolete. Simultaneously, the decreased risk of restenosis led certain teams to re-implement techniques that had been discredited in the BMS era [28] and carry out new ‘very metallic’ strategies [29–34].

Figure 2.2 Repeat intervention rate with DES using provisional techniques versus complex techniques.

Six randomized studies [35–40] as well as various meta-analyses [41–47] comparing dual-stent techniques with provisional SB stenting have demonstrated that complex strategies do not confer any benefit; in addition, they are associated with an increase in the risk of myocardial infarction and probably also in stent thrombosis (Figure 2.3).

Figure 2.3 Risk of stent thrombosis associated with DES using provisional techniques versus complex techniques.

Circumstances in which dual-stent strategies are required as a primary option, such as difficult access or long SB lesions are the subject of controversy, as is the choice of the optimal technique in such cases [48]. Implantation of stents dedicated to the treatment of bifurcation lesions, using the provisional SB stenting strategy in a reproducible manner with permanent access to both branches, seems to be associated with satisfactory results. However, there is no formal evidence as yet that these stents are instrumental in simplifying the procedure and improving procedural success

It is important to keep in mind that the main objective is not only to achieve a good mid-term outcome with a low risk of repeat intervention, but also to avoid jeopardizing the SB with potential non Q-wave-myocardial infarction, or compromising the MB by focusing on the achievement of a perfect result in the SB.

Basic Principles

Considerable progress has been achieved since the turn of the millennium in the understanding of fundamental aspects of coronary bifurcations in terms of flow pattern, shear stress on the vessel wall, anatomo-pathology and stent assessment in bench tests. Knowledge of these aspects is fundamental for managing coronary bifurcation treatment.

Ramifications of the coronary tree, as all ramifications in nature, follow the rule of minimum energy cost in providing the underlying myocardium with the amount of blood required [49, 50]. Coronary ramification follows a self-similarity fractal geometry pattern of iterative, asymmetric bifurcations [51–53]. There are three segments in a bifurcation (and not two as previously thought), each of which has its own reference diameter. The relation between the diameter of the proximal segment of the MB and the two distal segments is governed by the classic Murray's law (Dprox3 = Ddist3 + Dside3), the exponent being probably closer to 2.3. This complex formula [54] was recently simplified by Finet [55]: Dprox = (Ddist + Dside) × 0.678 (Figure 2.4). Consequently, the reference diameter of a coronary artery from its ostium to its distal segment does not taper following a linear pattern, but by steps, following the formation of a bifurcation branch. Therefore, the diameter of a coronary vessel is constant between two bifurcations. This makes all conventional quantitative coronary angiography computer programs obsolete, at least in the vicinity of bifurcations. They have been replaced by dedicated software in compliance with a consensus of the European Bifurcation Club [56].

Figure 2.4 Drawing of bifurcations. Right panel: former representation. Left panel: representation of bifurcations taking into the account Murray's law.

Coronary bifurcation flow has specific characteristics. In the vicinity of the carina (flow divider), as on the outside of curves, the flow is rapid (diastole), linear and generates intense friction (wall shear stress, WSS) on the vessel wall resulting in anti-atherogenic molecular, histological and functional modifications [57, 58]. Opposite the carina, as on the inside of curves, there is a re-circulating, oscillating flow generating low and pro-atherogenic WSS.

Anatomopathologists have underlined the fact that the carina is generally atheroma-free and that atheroma develops in low WSS areas in segments opposite the flow divider in the vicinity of bifurcations [58]. The formation of atheroma alters the flow pattern (distal to the atherosclerotic plaque) and the distal and circumferential expansion of the plaque [59] may reach as far as the carina.

Measurement of the fractional flow reserve (FFR) shed light on the issue of ostial SB stenosis following MB stenting. Although such a lesion may often appear to be angiographically tight, it is in fact seldom significant from a physiological point of view (FFR <0.80). As demonstrated in the article by Koo [61], only 28% of >75% SB stenoses (QCA) are physiologically significant lesions. The reason for this discrepancy between angiographic images and flow has not been thoroughly accounted for: lesion of the SB ostium related to the carina shift phenomenon reshaping a circular ostium into a “slit”, which is angiographically visualized from the worst possible angle, phenomenon of slow flow and turbulences hampering adequate contrast filling of the ostium and border effect artifact.

Role of Bench Testing

The assessment of stents in bench tests has been essential in improving the comprehension of bifurcation stenting [62, 65]. The initial bench tests did not comply with Murray's law and stent deployment was filmed inadequately. The tests currently used comply with the laws of branching and stent deployment is digitally recorded either in a micro CT [66] or by rotational acquisition in a cath-lab. The more elaborate bench tests are perfused.

The first benefit of bench testing was to show the distortion generated in the MB stent by the opening of a strut towards the SB, resulting in the projection of struts into the SB ostium and attraction of opposite struts in the main lumen. Various stenting techniques have been simulated in benches, allowing an accurate description of the inherent advantages and disadvantages of each technique as well as a reproduction of complication instances.

Digital simulation is likely to replace bench testing in the near future. Indeed, it is now possible to acquire images of a bifurcation lesion via rotational angiography or 3D reconstruction from orthogonal views of a patient.

The “finite elements” technique allows the reconstruction of a bifurcation by attributing to each element the technical characteristics of the vessel and plaque. It is also possible to reproduce copies of commercially available stents, with their physical properties and simulate their deployment by balloon inflation or the opening of a strut [67].

Definition of a Coronary Bifurcation Lesion

After years of fruitful discussion, the EBC finally reached a consensus: a bifurcation lesion is “a coronary artery narrowing occurring adjacent to, and/or involving the origin of a significant SB”. A significant SB is a branch that you do not want to lose in the global context of a particular patient. The prognostic value of an SB occlusion depends on many factors such as size, length, viability of the myocardium perfused by the branch, the collateralizing role of the SB, ventricular function and finally the threshold value defined by the interventional cardiologist himself. Although, biomarker elevation has been correlated with prognosis, including mortality, the level from which biomarker elevation is likely to influence the outcome is still debated.

Given the relationship between the diameter of a branch and the amount of perfused myocardium, and between the size of the artery and the area under the biomarker curve (when the artery is occluded), it should be possible to determine the minimum diameter at which SB occlusion may influence the outcome, thus providing a more objective definition of “a significant side branch”.

Many bifurcation lesion classifications have been proposed [68], most of which need to be memorized, except for the classification established by Medina [69], which has become widely accepted. The EBC suggested that the bifurcations be individually identified using the same codification as the Medina classification, namely 1 (lesion ≥ 50%) or 0 in the proximal MB segment, 1 or 0 in the distal SB segment and 1 or 0 in the SB, separated by a coma. Medina classification forms can be filled in after visual assessment or using dedicated QCA software. The three segments of a bifurcation generate three angles: A (approach), between the proximal MB and SB; B (between), between the two distal branches; and C between the proximal and distal MB segments. As Biplane QCA does not provide reliable measurements of these angles, 3D QCA is required.

Angle A defines the difficulty in accessing the SB. This angle, when small, can be significantly increased by the insertion of a guide wire [70]. A small angle B predicts the occurrence of SB occlusion after MB stenting [71].

Definition of Treatments

Many techniques have been described in the literature. The MADS classification [68], adopted by the EBC in 2007 is an open classification based on two principles: a definition of “generic” techniques according to the final positioning and aspect of stents at the end of the procedure, and strategic techniques, according to the position of the first stent deployed in the bifurcation.

Variations of generic techniques can subsequently be described according to the manner in which guides and balloons are used.

What is Provisional SB Stenting?

This strategy was designed to meet the main objectives of bifurcation lesion treatment focusing on the MB whilst ensuring patency of the SB. This strategy consists in deploying a stent from the proximal segment to the distal segment of the MB. In some instances, due to technical (angles), or anatomical reasons (location of the tightest stenosis), or for reasons of myocardial viability, the stent is deployed from the proximal segment of the MB to the SB (inverted provisional).

The advantages of this strategy lie mainly in the “open” nature of this approach, the purpose of which is to perform an optimal treatment of the MB and coronary bifurcation with a single stent whenever possible. When necessary, a second stent can be deployed in the SB using the T or Culotte implantation technique. This procedure can be easily carried out with a 6 F guiding catheter in the majority of cases.

The drawbacks of this technique are, on the one hand, the difficulty in ensuring permanent access to the SB, and on the other hand, potential problems in re-crossing the stent struts towards the SB or even in implanting a second stent in the SB after stenting the MB.

The relative simplicity of the provisional approach requiring a single stent in 80–90% of cases [72] and resulting in similar outcome compared with more complex strategies as demonstrated in randomized studies [35–47], has made this strategy the gold standard of bifurcation treatment even for the left main coronary artery as illustrated by the Syntax data [73]. Indeed, in the treatment of the distal left main, the Syntax study showed that the provisional approach was associated with a lower MACE risk compared to systematic dual-stenting strategies.

How to Perform Bifurcation Stenting Using the Provisional Approach

Coronary angiography allows an appropriate selection of stents to be made and provides the diameter and length of lesions located in the coronary bifurcation. Given the tri-dimensional structure of bifurcations, it is impossible to obtain a plane image of the three bifurcation segments without avoiding the foreshortening effect. Consequently, it is necessary to record several views from various angles in order to obtain a comprehensive picture of the lesion characteristics, to carry out the technical procedure appropriately and assess the procedural outcome.

The SB ostium poses the most frequent technical problems and is associated with poor outcome and occurrence of restenosis. This site is rarely visualized adequately from two orthogonal views and may be explored from a single angle called “the working view”. This view allows the visualization of branch division as well as the measurement of angles and assessment of the degree of ostial SB stenosis. This is generally an RAO or LAO view with caudal inclination for the left main coronary artery, an anterior-posterior projection with marked cranial angulation for LAD-diagonal bifurcations, a slight RAO or LAO projection with caudal angulation for circumflex-proximal marginal bifurcations or cranial angulation for dominant distal circumflex coronary arteries and an antero-posterior projection with cranial angulation for distal right coronary arteries.

Role of IVUS

The benefit of IVUS in the treatment of bifurcation lesions is still being evaluated with a randomized study (BLAST) comparing angiography-guided with IVUS-guided coronary bifurcation PCI. IVUS is currently recommended as a guidance tool for complex treatments especially in the left main coronary artery.

One or Two Guide Wires?

Systematic insertion of a guide wire in the SB at the beginning of the procedure is a sign that the operator considers the lesion to be a bifurcation stenosis. There are several advantages associated with the initial insertion of a guide wire in each branch. In addition to ensuring patency of the branch post dilatation, which has never been demonstrated, the wire modifies angle A, thus facilitating guide wire exchange as well as balloon and stent advancement [70]. Furthermore, in cases of occlusion, the guide wire is a good marker of the SB and may be rarely used as a “bail-out” strategy in order to re-open the SB with a small balloon advanced outside the stent. Cases of guide rupture have been associated with the use of “jailed” hydrophilic wires or when the radio-opaque distal segment of a wire is “jailed”. When treating a coronary bifurcation (a branch that we do not want to lose) our strategy is to begin the procedure with systematic insertion of two guide wires. In the TULIP multicenter study [74], use of only one wire when starting the procedure was a predictor of SB treatment failure and repeat intervention at 6 months.

Should We Pre-Dilate the Lesion or Not?

Kissing pre-dilatation is not recommended due to the risk of extensive dissection in unstented segments. Predilatation of the MB may be left to the discretion of the operator according to the type of lesion. However, predilatation of the SB remains a subject of controversy. Our opinion is that it is preferable not to predilate the SB for two reasons. Firstly, the occurrence of dissection inherent in the enlargement of the lumen of the SB ostium may hinder or prevent access to the SB through the struts of the MB stent, and secondly, the enlargement of the SB lumen increases the likelihood that access to the SB may also be possible through a proximal strut, although access through a distal strut is the only possibility for projecting struts in the SB (Figure 2.5). Certain teams choose to dilate the SB, but generally complete the procedure by stent deployment in the MB without final kissing inflation [37].

Figure 2.5 Potentially untoward effects of SB predilatation. Top of figure: SB predilatation followed by stenting of the MB and result after kissing balloon inflation according to whether or not the proximal strut has been opened towards the SB. Bottom of figure: no SB predilatation.

Stenting Across

Selection of the MB stent is an important step. Although DES allow a reduction in the risk of restenosis and repeat intervention compared with BMS, acceptable rates of restenosis may be obtained with BMS when using only one stent. Stent selection should be made according to the maximal expansion ability of the stent allowing stent apposition on the MB wall and on the SB ostium. The size of the stent struts is also an important criterion for the most proximal bifurcations. Stents with uneven struts should be avoided.

The choice of stent diameter for implantation in the MB is crucial. When excessively large (commensurate with the proximal segment), it may significantly increase the risk of SB occlusion by causing the carina to shift (Figure 2.6). Selection of the stent diameter should be made according to the diameter of the main distal segment in compliance with Murray's law. In such cases, the drawback is the inadequate apposition of the stent on the proximal segment, especially when the difference between the diameter of the proximal and distal segments is large (i.e. when the SB is large).

Figure 2.6 Risk of SB occlusion according to the MB sent diameter. Top of figure: stent selection according to the proximal MB reference. Bottom of figure: stent selection according to the distal MB reference.

POT (Proximal Optimization Technique)

This technique provides a solution to the problem of under-deployment of the proximal part of the MB stent. It involves the post-dilatation of the proximal segment of the stent in order to match the diameter of the main proximal segment of the bifurcation. It is carried out by inflating a short balloon along the whole length of the proximal segment. As a result, the original anatomical configuration of the bifurcation is restored in compliance with the branching law (Figure 2.7). It changes also the orientation of the SB ostium, facilitating the insertion of a guide-wire, balloon and, if necessary, a stent in the SB (Figure 2.8), as well as the projection of struts in the SB ostium.

Figure 2.7 Representation of the proximal optimization technique (POT).

Figure 2.8 Drawing of carina modification brought about by MB stenting. Top: carina modification caused by excessive stent size. Bottom: stent of appropriate size.

POT is especially useful in large SBs with a marked difference in the diameter of the proximal and distal main segments, which increases the need for implantation of a second stent in the SB. This technique is not useful in small SB which do not require stenting and which are only protected by the presence of a guide wire.

Outcome Analysis: When Should the SB be Treated?

Angiographic assessment of the procedural outcome in the SB ostium is not easy. The degree of angiographic stenosis is higher than when assessment is made by IVUS or FFR. In the case of > 75% residual SB stenosis by angiography, FFR analysis shows that only a minority of lesions are < 0.80 [61]. The reasons for this poor angiographic performance are the non-circular shape of the SB ostium and the edge effect generated by angiography. The use of FFR for outcome evaluation in the SB may prove a valid approach.

Should kissing balloon inflation be performed after simple technique?

When POT has not been previously performed, balloon inflation in the SB ostium tends to cause stent distortion in the MB and attraction of the struts opposite the SB in the MB lumen. Kissing balloon inflation (KB) allows SB treatment and apposition of the MB stent struts on the SB ostium, which, when inadequately apposed, generate flow disruption. It also enables correction of stent distortion and correction of inadequate apposition in the MB. However, KB increases procedural complexity and may result in stent ovalization, proximal dissection when balloons are inadequately positioned and even suboptimal deployment of the proximal stent segment. Although final KB is recommended after dual stenting, it remains a controversial issue in the case of single stent implantation. The one-year follow-up results of the NORDIC III trial should provide an answer to this unresolved problem.

The pending issue is not whether KB is the right strategy, but when the SB should be treated. In cases of angiographic slow flow in the SB combined with EKG signs of ischemia and chest pain, SB treatment is unanimously considered as necessary. In large SBs, a poor procedural outcome may result in the occurrence of symptoms and residual ischemia. Absence of cell opening towards the SB may cause serious difficulties in treating restenosis or de novo distal disease. Consequently, although this is not standard practice, it is preferable to systematically open the stent towards the SB when performing PCI of the distal left main.

How to Carry out final Kissing Balloon Inflation Appropriately?

First of all, it is fundamental to insert a free wire in the SB through the struts of the MB stent and, if possible, in the strut closest to the carina. In order to achieve this, we exchange guide-wires in most cases, although a third wire may also be used. The MB wire, pre-shaped into a long form and secured by the stent, is pulled towards the SB ostium. When guide wire advancement proves difficult, utilization of POT, reshaping of the guide wire, use of a hydrophilic or a more rigid wire with improved torque, or even an orientable micro-catheter (Venture, Saint-Jude) may help overcome the technical issues.

In cases of persisting difficulties, advancement and subsequent inflation of a very small balloon over the jailed wire may restore flow in the SB and enable the crossing of MB stent struts, or even in extreme cases, implementation of the inverted Crush strategy. In the presence of a large SB, strut projection outside the stent profile by means of balloon inflation may be carried out during MB stent implantation.

Following insertion of a free wire in the SB, the jailed wire must be withdrawn proximal to the stent. During this maneuver, the guiding catheter must be closely monitored in order to avoid deep intubation which might cause proximal dissection. In rare occurrences where the guide wire cannot be easily withdrawn, the use and potential inflation of a small balloon may prove efficient.

Once released, the wire, having previously been made into a short and angulated form, should be advanced in the MB if possible with a loop whilst avoiding advancement outside the stent.