NIC Handbook of Interventional Cardiology [1 ed.] 9789386150066, 9789351528753

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NIC Handbook of

Interventional Cardiology

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NIC Handbook of

Interventional Cardiology

Editors Praveen Chandra MD DM FACC FESC FSCAI FAPSIC Chairman Division of Interventional Cardiology Medanta Medicity Gurgaon, Haryana, India

Rishi Sethi MD DM FACC FESC FSCAI MAMS FAPSIC Professor Department of Cardiology King George’s Medical University Lucknow, Uttar Pradesh, India

Balram Bhargava MD DM FRCP FACC FAHA FNASc Professor Department of Cardiology All-India Institute of Medical Sciences (AIIMS) New Delhi, India

Rakesh Yadav MD DM FCSI Professor Department of Cardiology All-India Institute of Medical Sciences (AIIMS) New Delhi, India

The Health Sciences Publisher New Delhi | London | Philadelphia | Panama

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Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: [email protected] Overseas Offices J.P. Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44-2031708910 Fax: +02-03-0086180 Email: [email protected]

Jaypee-Highlights Medical Publishers Inc City of Knowledge, Bld. 237, Clayton Panama City, Panama Phone: +1 507-301-0496 Fax: +1 507-301-0499 Email: [email protected]

Jaypee Medical Inc The Bourse 111 South Independence Mall East Suite 835, Philadelphia, PA 19106, USA Phone: +1 267-519-9789 Email: [email protected]

Jaypee Brothers Medical Publishers (P) Ltd 17/1-B Babar Road, Block-B, Shaymali Mohammadpur, Dhaka-1207 Bangladesh Mobile: +08801912003485 Email: [email protected]

Jaypee Brothers Medical Publishers (P) Ltd Bhotahity, Kathmandu, Nepal Phone: +977-9741283608 Email: [email protected] Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2015, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. 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. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected] NIC Handbook of Interventional Cardiology First Edition: 2015 ISBN 978-93-5152-875-3 Printed at

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Contributors AB Mehta

Dhruv Tyagi

Director of Cardiology Jaslok Hospital & Research Centre Mumbai, Maharashtra, India

GB Pant Institute & MAMC New Delhi, India

Adrian F Low National University Heart Centre, Singapore Associate Professor Yong Loo Lin School of Medicine National University of Singapore

Amitabh Arya

DS Chadha Professor, Department of Cardiology MH (CTC), AFMC Pune, Maharashtra, India

G Karthikeyan All India Institute of Medical Sciences (AIIMS) New Delhi, India

Department of Nuclear medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS) Lucknow, Uttar Pradesh, India

G Sengottuvelu

Anil Dhall

Goran Stankovic

Director Cardiovascular Sciences Sarvodaya Hospital & Research Centre Faridabad, Haryana, India

Anmol Sonawane Jr. Consultant, Cardiology Jaslok Hospital & Research Centre Mumbai, Maharashtra, India

Senior Consultant & Interventional Cardiologist Apollo Hospitals, Greams Lane Chennai, Tamil Nadu, India Medical faculty, University of Belgrade Belgrade, Serbia

Huay Cheem Tan Director National University Heart Centre Singapore (NUHCS) Singapore

Justin ER Davies

NH-RTIICS, Kolkata, West Bengal, India

Consultant Cardiologist Interventional Cardiology Hammersmith Hospital Imperial College London

Balram Bhargava

Poay Huan Loh

Professor Department of Cardiology All India Institute of Medical Sciences (AIIMS) New Delhi, India

National University Heart Centre Singapore (NUHCS) Singapore

Ayan Kar

Milorad Zivkovic

Glenmark Cardiac Center Mumbai, Maharashtra, India

Department of cardiology, Diagnostic and catheterization laboratories Clinical Center of Serbia

Debdatta Bhattacharyya

Nagendra Chauhan

Chief of Cathlab Services NH-RTIICS Kolkata, West Bengal, India

Consultant Medanta– The Medicity, Gurgaon, Haryana, India

Bharat Dalvi

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Niraj Gupta Consultant Medanta-The Medicity Gurgaon, Haryana, India

Education & Research Director Professor, Dept of Cardiology GB Pant Institute & MAMC New Delhi, India

Prasanta Kumar Pradhan

Sanjeev Kathuria

Department of Nuclear medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS) Lucknow, Uttar Pradesh, India

GB Pant Institute & MAMC New Delhi, India

Praveen Chandra Chairman Division of Interventional Cardiology Medanta– The Medicity, Gurgaon, Haryan, India

Prithwiraj Bhattacharya Fortis Hospital, Kolkata, West Bengal, India

R Ravindran Associate Consultant Apollo Hospitals, Greams Lane Chennai, Tamil Nadu, India

Rajeev Rathi Senior Consultant Interventional Cardiologist Max Super Specialty Hospital, Saket New Delhi, India

Sabyasachi Mitra Fortis Hospital Kolkata, West Bengal, India

Sameer I Dani

Sayan Sen NIHR Clinical Lecturer Interventional Cardiology Hammersmith Hospital Imperial College London

Shashwat Verma Department of Nuclear medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS) Lucknow, Uttar Pradesh, India

Shreepal Jain Glenmark Cardiac Center Mumbai, Maharashtra, India

SK Malani Professor and Head of Department (Cardiology) MH (CTC), AFMC, Pune, Maharashtra, India

Shuvanan Ray Fortis Hospital Kolkata, West Bengal, India

Subhendu Mohanty GB Pant Institute & MAMC New Delhi, India

Director, Department of Cardiology Apollo Hospital & Lifecare Hospital Ahmedabad, Gujarat, India

Takashi Matsukage

Sanjay Chugh

Vijay Trehan

Senior Consultant Department of Cardiology AHI (Artemis Health Institute) Gurgaon, Haryana, India

Sanjay Tyagi Director GB Pant Institute of Postgraduate Medical

Tokai University Hachioji Hospital 1838 Ishikawa Hachioji-city, Tokyo, Japan GB Pant Institute & MAMC New Delhi, India

VS Bedi Chairman Peripheral Vascular and Endovascular Surgery Sir Ganga Ram Hospital New Delhi, India

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Y Vijayachandra Reddy Senior Consultant & Interventional Cardiologist Apollo Main Hospitals Chennai, Tamil Nadu, India

Yashasvi Chugh Internal Medicine Jacobi Medical Center Albert

Einstein College of Medicine, New York, USA

Zlatko Mehmedbegovic Department of cardiology Diagnostic and catheterization laboratories Clinical Center of Serbia

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Preface “You cannot open a book without learning something”. The practice of interventional cardiology in India and around the world is presently undergoing rapid transformation. The number of procedures and the hospitals performing them are increasing exponentially. This is giving rise to a situation where most of the young interventional cardiologists feel a constant need for further learning under expert guidance. During various formal and informal meetings for CSI-NIC— 2015, a need was felt to publish a book that would be a useful for interventional cardiologists of India. It was decided that the target audience of this book would be young interventional cardiologists and the ethos of the book was to be a step-by-step guide to common procedures, problems and techniques. The plan was to have highly acclaimed experts in various fields of interventional cardiology to come together on one platform through this book, and share their enormous experience with their younger colleagues. We discouraged extensive discussions on indications, theory and trials and prayed that each chapter reflects the practical experience of the expert author, as he would wish to pass on to his fellow in training. The time was short and we had to do the planning, management and execution of the job in less than two months. It was solely the encouragement from the esteemed authors that made this task possible. Despite being legends in their fields and extremely busy individuals they agreed to contribute and finally submitted the chapters within the desired period. After days of some stress and hectic activities it is really gratifying to see this book take a final shape. I hope you will ignore the shortcomings, that are an integral part of all human endeavors. Praveen Chandra Rishi Sethi Balram Bhargava Rakesh Yadav

“Begin at the beginning”, the King said, very gravely, “and go on till you come to the end: then stop”. —Lewis Carroll, Alice in Wonderland

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From The Desk of Convener National Interventional Council The tremendous experiences and expertise in interventional developing is growing exponentially amongst us, has created a huge reservoir of knowledge which needs to be shared and preserved. As you are aware there is always a large gap in India on what we do and what we document and create as a legend to follow. On this background, this is a small effort to start writing up and create a document on tips and tricks, and actual day to day practical solution usable in cardiac cath lab in our day to day practice. This may not be the final document, written and read, but certainly will be a document in evolution, for India and made in India. A number of international experts—who are top experts in their respective fields—have also kindly contributed to our small effort. We will need the help of each and every Cardiologist of India to give valuable feedback and ideas for further improvement on this book. Please respond on my email: praveen.chandra@medanta. org. Till then enjoy reading The NIC Handbook of Interventional Cardiology. Praveen Chandra

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Acknowledgments On behalf of entire editorial team we wish to thank all people who have played key roles in the development of this book. Most important people we wish to thank are all the illustrious authors as they not only graciously accepted our invitation but also worked really hard on a very short notice to produce chapters that are phenomenal. Their contribution is deeply acknowledged. I also wish to thank the entire executive committee of “Cardiological Society of India” for their support and guidance. A Special thanks to Dr HK Chopra, Dr Santanu Guha, Dr PK Deb, and Dr Amal Banerjee for their guidance. Dr Nagendra and Dr Niraj from Medanta–The Medicity (Haryana), Dr Ramakrishnan from AIIMS (New Delhi) and Dr Safal from KG Medical University (Lucknow) were unsung soldiers who helped and supported us throughout the journey of this publication. The team from Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, India, especially Mr PN Venkatraman (Vice President International), and from editorial, Ms Madhvi Thakur, Ms Preeti Mehra, Mr Prabhjeet Singh and Mr Davender Pratap Singh were extremely helpful and always just a phone call away. Many friends spread across many cities extended a helping hand and need to be acknowledged—RP, Sreeram, Hiral, Niraj, Aakash, Tajinder, Jaspreet, Vishwas, Arpit, Rahul, Deepak and many more form a part of that team. Families are our constant support and cannot be thanked enough. Unfortunately however, they are learning to live with a lot of our love but little of our time. Rishi Sethi

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Cardiological Society of India Executive Committee Members: 2014-2015 President HK Chopra F-16, Kalkaji New Delhi, India

President Elect Santanu Guha 16, Subodh Park Scheme B Kolkata, West Bengal, India

Immediate Past President—CSI K Venugopal Narayaneeyam Kakkazhom Alapuzha, Kerala, India

General Secretary—CSI Mrinal Kanti Das

Editor —Indian Heart Journal Sundeep Mishra 425, Mount Kailash Tower No. 2, East of Kailash New Delhi, India

Associate Editor— Indian Heart Journal Ajay Kumar Sinha House No.75, Road No. 3A Magistrate Colony Ashiana Road Patna, Bihar, India

EC Members—CSI Pravin K Goel

Prof & Head Department of Cardiology, SGPGI Lucknow, Uttar Pradesh, India

7RC, Rukmani Parasmani 92/1, Moulana Abul Kalam Azad Sarani, Kolkata, West Bengal, India

Dhiman Kahali

Vice President—CSI

G Karthikeyan

Praveen Jain Life Line Hospital, Kanpur Road Jhansi, Uttar Pradesh, India

Harshwardhan Mohan Mardikar 31, Off Chitale Marg, behind Hitavada Press Dhantoli, Nagpur Maharashtra, India

Kajal Ganguly DA-124, Sector – 1 Salt Lake, Kolkata, West Bengal, India

Treasurer—CSI Soumitra Kumar 58/1, Ballygunge Circular Road Flat - 52B, “SAPTAPARNI” Kolkata, West Bengal, India

294, Jodhpur Park, Kolkata, West Bengal, India C 014, Gemspark Apartments ERI Scheme, Mogappair West Chennai, Tamil Nadu, India

Brian Pinto 301 Monarch, 2nd Hasnabad Road, Santa-Cruz(W) Mumbai, Maharashtra, India

Satyanarayan Routray Qr. No. 3R-8, Doctors Flat Near Cancer Wing, SCB Medical College Cuttack, Odisha, India

Sanjay Tyagi F-4, Type V, Hudco Place Andrews Ganj Extension New Delhi, India

A Sreenivas Kumar Chief Cardiologist, Continental Hospitals, Gachibowli

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Financial Dist. Hyderabad Andhra Pradesh, India

Kane Ghanshyam Ramnath 8/1, Ornate House, 310, Veer Savarkar Road Dadar West Mumbai, Maharashtra, India

A Jabir Daressauaam, Mariathuruthu P.O.–Kottayam Kerala, India

BP Singh E-3/3, IGIMS Campus Sheikhpura Patna, Bihar, India

Rakesh Yadav E-25, AV Nagar August Kranti Marg New Delhi, India

Dr PK Asokan Anagha, Pottangadi Raghavan Road West Nadakkavu Calicut, Kerala, India

M Somasundaram D-161 Annanagar East Chennai Tamil Nadu, India

Rabindra Nath Chakraborty BE-407, Sector-1 Salt Lake City Kolkata, West Bengal, India

MS Ravi Old No. 71New 139 East Mada Church Street Royapuram Chennai, Tamil Nadu, India

Umesh Chandra Samal Yadav Bhawan, Nayatola Patna, Bihar, India

Joint Secretary—CSI Saumitra Ray 99/5/C, Ballygunge Place Kolkata, West Bengal, India

Assistant Secretary—CSI Arunangshu Ganguly 6/4, Pubali, Bidhan Nagar Sector-2A Durgapur, West Bengal, India

Past President—CSI BK Goyal Lotus House New Marine Lines Mumbai, Maharashtra, India

Co-opted Member (From Armed Forces) R Girish CSI Dept of Cardiology Command Hospital Lucknow Cant., Uttar Pradesh, India

Past President CSI PK Deb 1st Floor, 246, Bangur Avenue, Block ‘B’ Kolkata West Bengal, India

Convenor–Congenital Heart Disease Vijayalukshmi IB CSI Sub-Speciality Council 44V, Main, Vijayanagar II state Bengaluru, Karnataka, India

Convenor–Rheumatic Heart Disease Arati Lalchandani CSI Sub-Speciality Council 7/154, Swaroop Nagar Kanpur, Uttar Pradesh, India

Convener-Imaging

B Ramesh Babu

Sunita Maheshwari

7th Floor, Medwin Hospital Nampally Hyderabad, Andhra Pradesh, India

CSI Sub-Speciality Council Villa No. 19, Prestige Regent Place Whitefield Main Road Tuberhalli, Bengaluru, India

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Convenor—Hypertension Dr Gurpreet Singh Wander

CSI Sub-Speciality Council 95B, Kitchlu Nagar Ludhiana, Punjab, India

Convenor—Preventive Cardiology Geevar Zachariah A CSI Sub-Speciality Council “PANTHEON” Ramadevi Mandir Lane P.O. Punkunnam, Thrissur (Kerala), India

Convenor—Pacing & Electrophysiology C Narasimhan CSI Sub Speciality Council

Care Hospital, Nampally Hyderabad, Andhra Pradesh, India

Convenor–Echo Cardiography Nitin J Burkule CSI Sub-Speciality Council 42, Sharmishtha, Tarangan - I, Tower No. 2, Near Cadbury Co. Eastern Express Highway Thane (W), Maharashtra, India

Convenor—CSI—Heart Failure Council Umesh Chandra Samal CSI Sub Speciality Council Yadav Bhawan, Nayatola Patna, Bihar, India

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Table of Contents Chapter 1

Coronary Interventions: A Brief History

1

G Karthikeyan, Balram Bhargava

Chapter 2

Coronary Guidewires

6

Rajeev Rathi

Chapter 3

Guide Catheter Selection In Pci 15 Y Vijayachandra Reddy

Chapter 4

Tips and Tricks to Overcome Challenging Anatomies during Radial Approach

24

Sanjay Chugh, Yashasvi Chugh, Takashi Matsukage

Chapter 5

FFR Technique and Interpretation: Step-by-Step

42

Adrian F Low

Chapter 6

Pressure Wire… Beyond FFR

50

Sayan Sen, Justin Er Davies

Chapter 7

IVUS—Basics and Beyond for Lesion Assessment and Result Optimization

60

Debdatta Bhattacharyya, Ayan Kar

Chapter 8

Optical Coherence Tomographic Imaging in Cath-Lab— Basic Techniques and Interpretation

77

G Sengottuvelu, R Ravindran

Chapter 9

Bioresorbable Vascular Scaffolds: The 4th Revolution in Interventional Cardiology and the Holy Grail to Restore Freedom

92

Praveen Chandra, Niraj Gupta, Nagendra Chauhan

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Chapter 10

Thrombus Burden and No-Ref low

107

Poay Huan Loh, Huay Cheem Tan

Chapter 11

Technique and Role of Rotablation in Interventional Cardiology

134

AB Mehta, Anmol Sonawane

Chapter 12

Bifurcation Coronary Lesions—Def inition, Classif ication and Approaches to Bifurcation Management 159 Goran Stankovic, Zlatko Mehmedbegovic, Milorad Zivkovic

Chapter 13

Tips and Tricks: Lef t Main Pci 175 Shuvanan Ray, Prithwiraj Bhattacharjee, Sabyasachi Mitra

Chapter 14

Carotid Angioplasty—Step-By-Step

182

Anil Dhall, DS Chadha, SK Malani, VS Bedi

Chapter 15

Balloon Mitral Valvuloplasty

202

Sameer I Dani

Chapter 16

Step-by-Step Atrial Septal Defect Closure

221

Shreepal Jain, Bharat Dalvi

Chapter 17

Renal Stenting: Rationale and Techniques

242

Sanjay Tyagi, Subhendu Mohanty, Dhruv Tyagi

Chapter 18

Retrieval of Foreign Bodies During Cardiac Catheterization

258

Vijay Trehan, Sanjeev Kathuria

Chapter 19

Nuclear Cardiology: Basics and Beyond

270

Prasanta Kumar Pradhan, Shashwat Verma, Amitabh Arya

Index 295

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1 Coronary Interventions: A Brief History G Karthikeyan, Balram Bhargava

RIGHT, LEFT HEART AND CORONARY CATHETERIZATION The year 1929, arguably, marks the dawn of modern interventional cardiology. Standing on the shoulders of earlier visionaries, Werner Forsmann, a young surgical resident, inserted 65 cm of a ureteral catheter through basilic vein and documented its position in the right atrium by chest X-ray. Although he envisaged this as a procedure for intracardiac injection of drugs and for “central bloodletting”, it paved the way for accessing the right heart for pressure measurements, oximetry, angiography and interventional catheterization. In parallel, by 1947, polyethylene replaced rubber as the material for catheters and subsequently by a radiopaque variant in 1956. The other major advance which helped usher in the era of modern catheterization was the development of the image intensifier in the 1950s which allowed for the recording of cineangiograms as roll films (as opposed to single plate angiograms and series of “cut-films”). Catheterization of the left heart took a different route to progress. Perhaps because it is counterintuitive to traverse retrograde through the peripheral arteries into the left sided chambers, most initial attempts to catheterize the left heart involved direct puncture of the thoracic aorta, left atrium and left ventricle, often with disastrous results. Though Farinas had demonstrated that it was possible to access the left heart through the femoral arteries in 1941, it was not until Seldinger devised his simple, safe and elegant technique in 1953 that leftheart catheterization became mainstream in catheterization laboratories. The next great landmark in the evolution of interventions is the serendipitous catheterization of the right coronary by Mason Sones in 1958 during an ascending aortogram. Hitherto,

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direct contrast injection into the right coronaries was thought to be fatal. It is worth noting that Sones did not formally publish his work until he had carefully worked to improve the technique of coronary arteriography. Further refinements to the technique ensued over the subsequent years through the work of several people most notably, Judkins and Amplatz.

BALLOON ANGIOPLASTY Although Dotter was using balloon-tipped catheters for angiography since the early 50s, it was not until 1963 that he, again serendipitously, recognized their therapeutic value while inadvertently crossing an occluded iliac artery while performing an aortogram. Dotter and his fellow Judkins performed the first intentional dilatation of a popliteal artery in an 82-year-old woman with gangrene. Though this technique of relieving obstruction (subsequently called “Dottering”) had been practiced centuries ago for relieving urethral strictures (Egypt, 500 BC), it failed to gain popularity because of the need to introduce rigid, wide-bore catheters and the hazard to side branches due to the “snow-plough effect”. The next courageous step was taken by Andreas Gruentzig, an epidemiologist by training, who worked to reduce the bore of the catheters and used polyvinyl chloride for his balloons (which were less compliant than balloons made of latex). Gruentzig and Myler performed the first angioplasties retrogradely through the distal left anterior descending artery, in operating rooms after thoracotomy on patients who were undergoing coronary artery bypass grafting. Gruentzig performed the first coronary angioplasty on an awake patient in 1977 at Zurich and published the results of his first 5 patients in the Lancet. Of note, the subsequent cases also involved the left main in 1 patient and multiple vessels in another. Improvements to the technique and material (such as the introduction of the over-the-wire balloon by Simpson) followed. Gruentzig was planning a randomized trial of angioplasty compared to surgery at the time of his death in 1985 in a plane crash at the age of 46 (this was later funded as the Emory Angioplasty versus Surgery Trial).

ANGIOPLASTY BEYOND THE BALLOON The limitations of plain balloon dilatation were recognized early on, and Dotter and Judkins speculated in the early 60s that silastic or plastic stents could maintain vessel patency after dilatation. But the main focus of investigators remained the mechanical removal of atherosclerotic material in the years after coronary angioplasty. Simpson developed the first atherectomy device which received US FDA approval in 1991. Other techniques such as rotational and laser atherectomy followed. The idea of stents in coronary arteries received a fillip through the work of Sigwart and colleagues who deployed the first self-expanding (Wallstent) in human coronary arteries

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Coronary Interventions: A Brief History

3

in 1987. Subsequently balloon-mounted slotted tube stents (Palmaz-Shatz) and coil stents (Gianturco-Rubin) were developed. The early stents were approved for use primarily in the event of acute vessel closure after balloon angioplasty. Primary stenting at the time of angioplasty was recognized to reduce restenosis only after the completion of the STRESS and Benestent trials (Table 1).

CORONARY STENTS The use of stents brought to the fore two major problems: (1) stent thrombosis and (2) in-stent restenosis. Much of the focus in interventional cardiology has since then been on combating these two adverse consequences. Studies in the 90s recognized the central role of the platelet in causing stent thrombosis and established the need for dual antiplatelet therapy with aspirin and a P2Y12 inhibitor. The earliest P2Y12 inhibitor (Ticlopidine) has since been replaced by newer, more potent agents which afford greater protection against stent thrombosis, but also increase the risk of bleeding in some patients. Concurrently, changes in stent design (such as thinner struts) and deployment strategies (high-pressure deployment) have been applied to reduce the risk of restenosis and stent thrombosis. The recognition that in-stent restenosis is caused by injury-induced proliferation of local smooth muscle cells prompted the use of systemic, and later, local delivery of anti-proliferative agents at the site of injury. The development of the technology for stable stent coatings, with the desired antiproliferative agent which can be reliably delivered after stent implantation, is arguably the greatest recent advance in the prevention of restenosis. Validation of this strategy came in the year 2001 with the publication of the results of the Cypher trial of the sirolimus eluting stainless steel stent which showed near-zero restenosis rates. Paclitaxel eluting stainless steel stents followed soon. Putative reactions to the polymer vehicle for stable local drug delivery through stents and the delayed endothelialization as a result of the antiproliferative drug brought on the scourge of late stent thrombosis. While restenosis has been considered rather benign and has been referred to as the “mouse that roared”, stent thrombosis is often fatal. The occurrence of late stent thrombosis spurred the development of stents with biodegradable polymers, thinner strut platforms of alternative metal alloys, newer antiproliferative agents, and regimens of prolonged dual antiplatelet therapy. Newer generations of drug eluting stents are not only much more deliverable than their stainless steel predecessors, but also newer platforms, polymers and drugs have reduced the risk of stent thrombosis and restenosis to very low levels. One solution to the prevention of late stent thrombosis was the biodegradable stent: if there is no stent, there is no risk of thrombosis. The absence of a stent also may theoretically

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Table 1: Coronary angioplasty after Gruentzig*

Stents

Acute and subacute vessel closure, restenosis Stent thrombosis, in-stent restenosis

30–50

20–30

Neoatherosclerosis, bleeding due to prolonged dual antiplatelet therapy

left radial artery (LRA) > right ulnar artery (RUA) > left ulnar artery (LUA). yy However, in the following cases, ulnar access was preferred over radial: (i) Anomalous origin of radial artery from the brachial artery. (ii) Bifurcation of the brachial artery proximal to the antecubital fossa.

Figure 2: Site of radial artery puncture

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(iii) Presence of a radial loop. (iv) Bilaterally small radial arteries. Sheath- sizing protocol (Fig. 3): yy For all our interventions, we have commonly used 5F sheath and catheters for access artery (AcA) diameter more than or equal to 1.6 mm, 6F through AcA diameter more than or equal to 1.8 mm; 7F sheath for AcA diameter more than or equal to 2.2 mm. yy Until 2012, transfemoral access was used by us if a patient’s bilateral radial artery and ulnar artery diameters were: (i) Less than or equal to 1.5mm: not meeting protocol for coronary angiogram (CA) / PCIs using 5F. (ii) Less than 1.7 mm, if 6F had to be used for PCI. (iii) Less than 2.1 mm, if 7F had to be used for PCI.

Challenge 5: Overcoming the Challenge of Small Arteries yy For radial artery diameter less than 1.5 mm, since 2012, we began to use compression of the other artery (COOA), a technique to enhance the size of the access artery (Figs. 4A to C).23 This enabled us to use even 1.4 mm arteries for 5F access with enhanced success. Thus aiding in reducing puncture failures in small (1.7 mm), the crossovers (procedure failure) and access artery occlusions were 3.9% versus 0.9% and 2.8% versus 0.8% respectively (p 5 mm), or there is an unfavorable extreme angulation of the side branch take off.22,23 Since previous pathologic studies and in vivo IVUS evaluation demonstrated that atherosclerosis occurs predominantly at lateral walls of bifurcation while carina (flow divider) involvement by atherosclerosis is extremely unusual, main branch stenting results in carina displacement/shift.9 For that reason, if side branch was not predilated, guidewire will cross the stent strut exactly at the carina level (carina cell) after main branch stenting. However, recent randomized study showed that side branch predilatation may improve angiographic result of provisional stenting.24 Next step after main branch predilatation is stent implantation across the side branch, leaving the side branch wire in place (jailed wire) (Fig. 4C). If the angiographic results in main branch and side branch are satisfactory the procedure is complete and jailed wire can be removed.23 Different criteria have been used in randomized trials for acceptable result in the side branch following main branch stenting. There was still a debate regarding the use of routine FKIs, with general agreement that in the absence of an angiographically tight lesion at the ostium of the side branch, kissing balloon inflations (KBIs) may not be routinely required.11 However, when

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a tight lesion (> 75%) is present in the side branch after main vessel stenting, it is known that a KBI will reduce its functional significance.25 Therefore, two appropriate strategies are either to use a pressure wire to interrogate the significance of the side branch lesion or simply to do KBIs on all angiographically significant ostial side branch lesions in the knowledge that this reduces the proportion that remain physiologically significant, coupled with the information from the NORDIC III trial, that there appears to be no penalty for doing so.11 If the result at side branch ostium is not satisfactory or if FKI is performed systematically, the side branch is rewired with the MV wire (wire exchange) or a third wire is used for side branch wiring before removing jailed wire. In provisional technique wire cross through the distal strut following main branch stenting is strongly suggested because it creates better side branch scaffolding than proximal crossing.26 In order to optimize side branch access through the “carina strut”, the proximal optimization technique (POT technique) has been proposed, and relates to a method of expanding the stent at the carina, using a short oversized balloon.2 The jailed wire in the side branch should always be left in place as a marker until complete recrossing has been done. In addition, jailed wire modifies favorably the angle between both branches and keeps the side branch open. In case of difficulty in advancing the wire into the side branch, beside POT, wire reshaping, the use of a hydrophilic polymer-coated or a stiffer wire with improved torque, or even an adjustable microcatheter may help to overcome the technical issues.27 Stent selection for treating the main branch of bifurcation lesions is crucial and primary stent should be sized according to the distal main vessel diameter.11 After recrossing the side branch, balloon dilation of the side branch ostium and FKI should be performed (Figs. 4H and I). FKI is proposed if the side branch is dilated through the main branch stent struts to correct main branch stent distortion and expansion, and provide better scaffolding of the side branch ostium and facilitate future access to the side branch.26,28 Recently, Foin et al.29 proposed sequential balloon inflation, beginning with side branch, instead of simultaneous inflations in order to achieve better side branch opening and main branch and side branch scaffolding. It consists in inflating the side branch at 12 atm first, then the main branch at 12 atm while deflating the side branch at 4 atm. By this approach, final elliptical deformation is reduced and side branch access is optimized by reduced ostial area stenosis, compared to simultaneous FKI.30 Based on these results, a 2-step inflation, beginning by the side branch is recommended. The elliptical deformation, which has been associated with a greater amount of thrombus, can also be corrected after KBI by a final POT as also described by Foin.31

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Figures 4A to I: Provisional stenting technique. (A) Baseline angiogram showing bifurcation lesion LAD-D1, with diffuse disease of the ostial/ proximal segment of the side branch; (B) both branches wired (thin arrows); (C) stent positioning in the main branch across the side branch (thick white arrow); (D) angiographic result after main branch stenting; (E) optimization of the proximal segment of bifurcation with short noncompliant balloon (“POT” technique, white arrow); (F) result after proximal optimization; (G) side branch rewiring (white thin arrow), through the most distal strut; (H) kissing balloon inflation (main branch white arrow, side branch black arrow); (I) final angiographic result.

A Second Stent in the Side Branch Following Provisional Approach12 If the result remains unsatisfactory after FKI [> 75% residual stenosis, dissection, thrombolysis in myocardial infarction (TIMI) flow grade < 3 in a side branch ≥ 2.5 mm or FFR < 0.75]25,32 side branch stenting should be performed. According to randomized trials, a second stent in the side branch may be necessary in 2–51% of cases.14-16,33,34 FFR or new imaging techniques, such as OCT, could be of value in the evaluation of side branch result after balloon dilation. When the side branch stenting is needed, the T-stenting technique is most frequently used (Figs. 5A to F).35 It usually consists in positioning a stent at the ostium of the side branch without protrusion in the main branch. Some operators leave a balloon in the main branch to help precise positioning and sometimes inflate balloon at low pressure in order to help side branch stent positioning. In bifurcations with angles close to 90°C, T-stenting provides complete coverage of the side branch ostium.

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Figures 5A to F: T-stenting technique. (A) Baseline angiogram showing bifurcation lesion LAD-D1, with critical narrowing of the proximal segment of side branch; (B) result after main branch stenting; (C) proximal optimization technique (POT, thin white arrows); (D) side branch dissection; (E) side branch stent positioning (black thick arrow), stent markers depicted with white stars; (F) final angiographic result.

The T and small protrusion technique is a modification of the T-stenting technique and is based on an intentional minimal protrusion of the side branch stent within the main branch (Figs. 6A to I).19 The advantages of the TAP-stenting technique are: compatibility with 6 F guiding catheters, full coverage of side branch ostium and facilitation of FKI.12 The main drawback is related with the creation of a single layer stent struts neocarina of variable length.12 Final kissing inflation is performed to complete procedure. If bifurcation angle is smaller, some operators prefer using the culotte technique in order to improve side branch ostial scaffolding. The culotte technique leads to full coverage of the bifurcation at the expense of an excess of metal covering of the proximal end. The procedure starts with main branch stenting as in original description,20 although the first stent can be deployed across the most angulated branch, which is usually the side branch, (technique named inverted culotte technique and described below in a two-stent techniques as intention to treat).2,36 Another technique which was developed with the intent to minimize any possible stent gap between the main branch and side branch stents is a reverse or internal crush.37 In this technique, first stent is implanted in the main branch and balloon dilatation with kissing inflation toward the side branch is performed. Second stent is inserted in the side branch and pulled-back to protrude few mm inside the main branch stent.

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Figures 6A to I: T and small protrusion (TAP) technique. (A) Baseline angiography showing LAD-D1 bifurcation lesion; (B) stent positioning in the main branch across the side branch (thick white arrow); (C) control angiogram after main branch stenting; (D) opening stent cell toward the side branch after rewiring (thin black arrow); (E) control angiogram; (F) positioning of the side branch (diagonal) stent (thick black arrow) with small protrusion into LAD with balloon in the main branch (thin white arrow); (G) side branch stenting (thick black arrow); (H) final kissing; (I) final angiographic result.

The reverse crush can be performed utilizing a 6 F guiding catheter since protruding segment of the side branch stent is crushed with the balloon in the main branch. After that side branch is rewired, and high-pressure balloon inflation is performed and procedure ended by FKI.

Two Stents as an “Intention to Treat”12 A meta-analysis of randomized studies demonstrated that a provisional one-stent approach was comparable to two-stent approach in terms of mortality, repeat revascularization and quality of life,38,39 while one-stent technique was superior in terms of reduced risk of periprocedural myocardial infarction and stent thrombosis.40,41 Large caliber true bifurcations with significant ostial side branch length disease are currently considered by most experts to require a systematic two-stent strategy, but evidence to support this approach is lacking.11 When two-stent strategy is planned, the size and territory of distribution of the side branch and the angle between the

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main branch and the side branch needs to be considered. Side branches with ostial disease extending > 5–10 mm from the carina, are likely to require a two-stent strategy as well as the side branches whose access is particularly challenging.11 Importantly, wider-angle bifurcations are unfavorable for two-stent strategies because of the relative inability of stents to conform uniformly to the vessel wall in regions of acute angulation, even with optimal techniques. The most frequently applied two-stent techniques are culotte, mini crush or double kissing crush (DK-crush) and V and simultaneous kissing stent technique.

Inverted Culotte Technique12 The procedure starts with predilatation of both branches (Figs. 7B and C) and stent implantation across the most angulated branch, usually the side branch (Fig. 7D).2,36 The main branch is then rewired through the struts of the side branch stent, dilated and POT technique performed (Fig. 7E). A second stent is advanced and expanded into the main branch, followed by POT (Fig. 7F). Procedure is completed by final kissing inflation (Fig. 7H). Important limitation of culotte technique is dependence on maximal stent cell diameter.11 For this reason open cells stents are preferable. Other disadvantage of the technique is that rewiring both branches through the stent struts can be difficult and time consuming.12 This technique is suitable for a narrow angle bifurcation with similar size of both branches.12 Disadvantages are that, like the crush, the culotte technique leads to a high concentration of metal with a double-stent layer at the carina and in the proximal part of the bifurcation.12 To reduce excess of metal component, minimal overlap of main branch and side branch stent strut in proximal main branch segment is suggested.

The Mini-crush Technique12 The classical crush technique42 consists in partial deployment of the side branch stent in the main branch, which is crushed by the main branch stent after removal of the side branch wire. The main disadvantage of this technique is that it requires a 7 F guiding catheter. In order to use a 6 F guiding catheter a “balloon mini crush” technique43 is suggested (Figs. 8A to I). After predila-tation of main branch and side branch, balloon is inserted in the main branch and stent in the side branch, positioned by pulling the side branch stent into the main branch for about 2–3 mm. The stent in the side branch is deployed and balloon and wire removed into the guiding catheter (Fig. 8B). An angiogram is taken to verify that stent is fully expanded and there is no distal dissection. Main branch balloon is then inflated to crush protruding struts. After that stent is inserted in the main branch and fully deployed at high pressure (Fig. 8E). Side branch is then rewired and procedure completed by FKI. Clinical outcome of crush technique is improved by FKI,44 which is now strongly recommended and some operators

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Figures 7A to I: Culotte stenting technique. (A) Baseline angiography showing LAD-D1 true bifurcation lesion; (B) predilatation of the main branch (thin white arrow); (C) predilatation of the side branch (thin black arrow); (D) positioning of the diagonal stent across main branch (thick black arrow); (E) opening stent cell toward main branch after rewiring (thin white arrow); (F) positioning and implantation of the main branch stent (thick white arrow); (G) control angiogram; (H) final kissing inflation; (I) final result.

prefer to inflate a high-pressure balloon toward the side branch before performing KBI.34 The main disadvantage of crush technique is that the performance of the FKI makes the procedure more laborious, due to the need to recross multiple struts with a wire and a balloon.11 Several other crush technique variants are proposed, such as mini-crush, step-crush or DK-crush.45 As compared with the original description42 the “mini-crush” approach has minimal pullback of the side branch stent into the main branch, so that the proximal marker of the side branch stent is positioned in the main branch at a distance of 1–2 mm proximally to the carina of the bifurcation.46 The DK-crush technique differs from the classical crush technique because the part of the side branch stent protruding into the main branch is first crushed with a balloon in the main branch and then first KBI is performed. Second kissing inflation is performed after main branch stenting.47 The main advantage of the crush technique is that immediate patency of both branches is assured, which is particularly important when the side branch is large or diffi-

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Figures 8A to I: Balloon crush stenting technique. (A) Baseline angiography showing LAD-D1 bifurcation lesion, with occluded diagonal branch; (B) side branch stent deployment (white thick arrow), main branch balloon (thin black arrow); (C) main branch balloon inflation, side branch stent crushed (thin black arrow); (D) control angiogram after side branch stent crush; (E) main branch stent inflated (thick black arrow); (F) control angiogram; (G) side branch balloon (sequential) dilatation (thin white arrow); (H) final kissing inflation; (I) final angiographic result.

cult to wire.12 The main disadvantage is that the performance of the FKI makes the procedure more laborious, due to the need to recross multiple struts with a wire and a balloon.12

The V and the Simultaneous Kissing Stent (SKS) Techniques12 The V-stenting and the SKS techniques are performed by simultaneous implantation of two stents.48,49 Both branches are wired and fully predilated. One stent is advanced in the side branch, the other one in the main branch. Both stents are pulled back and once the position of the stents is confirmed and proximal stent markers are overlapped, the stents are deployed with simultaneous inflation and deflation.12 The size of the balloon and of the stents is chosen according to the diameter of daughter vessels (1:1). Stent length is selected to cover the length of diseased segments. The main advantage of the V and SKS technique is that the operator will never lose access to any of the two branches.12 In addition, when a FKI is performed there is no need to recross through the stent struts. Main disadvantage

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Table 1: Main characteristics of two-stent techniques12 T/TAP

Culotte

SKS

Mini-crush

Guiding Catheter (F)

6

6

7

7*

Provisional side branch stenting

Yes

Possible

No

No

Number of steps

5

7

1

3 (6 if DKC)

Bifurcation angle < 70°

Not ideal

Suitable

Suitable

Ideal

Bifurcation angle > 70°

Ideal

Not ideal

Not ideal

Not ideal

Similar diameters main branch and side branch

Suitable

Ideal

Ideal

Suitable

Small side branch

Suitable

Not ideal

Not ideal

Ideal

*: 6 Fr could be used for balloon “step-crush”. DKC: Double kissing crush; TAP: “T and small protrusion”

of these two techniques is metallic neocarina created in the proximal main branch, which may increase the risk of restenosis or stent thrombosis.2 Lesions most suitable for this technique are very proximal lesions, such as bifurcation of a short left main coronary artery (LMCA), with ostium free of disease. Ideally, the angle between the two branches should be less than 70°. The V-stenting technique is also suitable for other bifurcations, provided that vessel proximal to bifurcation is free of disease and there is no need to deploy additional stent more proximally.12 Principal characteristics of the most frequently used twostent techniques are presented in Table 1.12

Dedicated Bifurcation Stents Dedicated bifurcation stents may potentially overcome limitations of conventional stents in bifurcations (side branch protection, multiple layers, distortion, side branch access, crossing through side of the stent, gaps in scaffolding).11,12 However, although efforts to produce dedicated bifurcation stent delivery systems are strongly encouraged and research fostered, none of the currently available systems can at the moment challenge the results offered by the provisional T-stent strategy in the majority of bifurcation lesions.

CONCLUSION Selection of appropriate strategy for individual bifurcation lesion and optimal procedural result ensure satisfactory early and long-term clinical outcome. Provisional strategy remains the gold standard technique for most bifurcation lesions since routine two-vessel stenting does not improve either angiographic or clinical outcomes. However, further studies

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are required to determine which bifurcation lesions may particularly benefit from planned upfront two-stent strategy.

REFERENCES 1. Louvard Y, Lefevre T, Morice MC. Percutaneous coronary intervention for bifurcation coronary disease. Heart. 2004;90:713-22. 2. Stankovic G, Darremont O, Ferenc M, Hildick-Smith D, Louvard Y, Albiero R, et al. Percutaneous coronary intervention for bifurcation lesions: 2008 consensus document from the fourth meeting of the European Bifurcation Club. EuroIntervention. 2009;5:39-49. 3. Louvard Y, Thomas M, Dzavik V, Hildick-Smith D, Galassi AR, Pan M, et al. Classification of coronary artery bifurcation lesions and treatments: time for a consensus! Catheter Cardiovasc Interv. 2008;71:175-83. 4. Movahed MR, Stinis CT. A new proposed simplified classification of coronary artery bifurcation lesions and bifurcation interventional techniques. J Invasive Cardiol. 2006;18:199-204. 5. Movahed MR. Coronary artery bifurcation lesion classifications, interventional techniques and clinical outcome. Expert Rev Cardiovasc Ther. 2008;6:261-74. 6. Y-Hassan S, Lindroos MC, Sylven C. A Novel Descriptive, Intelligible and Ordered (DINO) classification of coronary bifurcation lesions. Review of current classifications. Circ J. 2011;75:299-305. 7. Medina A, Suarez de Lezo J, Pan M. [A new classification of coronary bifurcation lesions]. Rev Esp Cardiol. 2006;59:183. 8. Nakazawa G, Yazdani SK, Finn AV, Vorpahl M, Kolodgie FD, Virmani R. Pathological findings at bifurcation lesions: the impact of flow distribution on atherosclerosis and arterial healing after stent implantation. J Am Coll Cardiol. 2010;55:1679-87. 9. Oviedo C, Maehara A, Mintz GS, Araki H, Choi SY, Tsujita K, et al. Intravascular ultrasound classification of plaque distribution in left main coronary artery bifurcations: where is the plaque really located? Circ Cardiovasc Interv. 2010;3:105-12. 10. Koo BK, Waseda K, Kang HJ, Kim HS, Nam CW, Hur SH, et al. Anatomic and functional evaluation of bifurcation lesions undergoing percutaneous coronary intervention. Circ Cardiovasc Interv. 2010;3:113-9. 11. Hildick-Smith D, Lassen JF, Albiero R, Lefevre T, Darremont O, Pan M, et al. Consensus from the 5th European Bifurcation Club meeting. EuroIntervention. 2010;6:34-8. 12. Colombo A, Stankovic G. Bifurcations and branch vessel stenting. In: Eric J. Topol, Teirstein P (Eds). Textbook of Interventional Cardiology, 6th edition. Philadelphia: Saunders Elsevier; 2012. pp. 270-87. 13. Colombo A, Bramucci E, Sacca S, , Violini R, Lettieri C, Zanini R, et al. Randomized study of the crush technique versus provisional sidebranch stenting in true coronary bifurcations: the CACTUS (Coronary Bifurcations: Application of the Crushing Technique Using SirolimusEluting Stents) Study. Circulation. 2009;119:71-8. 14. Colombo A, Moses JW, Morice MC, Ludwig J, Holmes DR Jr, Spanos V, et al. Randomized study to evaluate sirolimus-eluting stents implanted at coronary bifurcation lesions. Circulation. 2004;109:1244-9. 15. Ferenc M, Gick M, Kienzle RP, Bestehorn HP, Werner KD, Comberg T, et al. Randomized trial on routine vs. provisional T-stenting in the treatment of de novo coronary bifurcation lesions. Eur Heart J. 2008;29:2859-67. 16. Pan M, de Lezo JS, Medina A, Romero M, Segura J, Pavlovic D, et al. Rapamycin-eluting stents for the treatment of bifurcated coronary lesions: a randomized comparison of a simple versus complex strategy. Am Heart J. 2004;148:857-64.

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NIC Handbook of Interventional Cardiology 17. Ormiston JA, Webster MW, Ruygrok PN, Stewart JT, White HD, Scott DS. Stent deformation following simulated side-branch dilatation: a comparison of five stent designs. Catheter Cardiovasc Interv. 1999;47:258-64. 18. Lefevre T, Louvard Y, Morice MC, Loubeyre C, Piechaud JF, Dumas P. Stenting of bifurcation lesions: a rational approach. J Interv Cardiol. 2001;14:573-85. 19. Burzotta F, Gwon HC, Hahn JY, Romagnoli E, Choi JH, Trani C, et al. Modified T-stenting with intentional protrusion of the side-branch stent within the main vessel stent to ensure ostial coverage and facilitate final kissing balloon: the T-stenting and small protrusion technique (TAP-stenting). Report of bench testing and first clinical Italian-Korean two-centre experience. Catheter Cardiovasc Interv. 2007;70:75-82. 20. Chevalier B, Glatt B, Royer T, Guyon P. Placement of coronary stents in bifurcation lesions by the “culotte” technique. Am J Cardiol. 1998;82:943-9. 21. Porto I, van Gaal W, Banning A. “Crush” and “reverse crush” technique to treat a complex left main stenosis. Heart. 2006;92:1021. 22. Pan M, Suarez de Lezo J, Medina A, Romero M, Delgado A, Segura J, et al. Drug-eluting stents for the treatment of bifurcation lesions: a randomized comparison between paclitaxel and sirolimus stents. Am Heart J. 2007;153:15 e1-7. 23. Pan M, Suarez de Lezo J, Medina A, Romero M, Segura J, Ramírez A, et al. A stepwise strategy for the stent treatment of bifurcated coronary lesions. Catheter Cardiovasc Interv. 2002;55:50-7. 24. Pan M, Medina A, Romero M, Ojeda S, Martin P, Suarez de Lezo J, et al. Assessment of side branch predilation before a provisional T-stent strategy for bifurcation lesions. A randomized trial. Am Heart J. 2014;168:374-80. 25. Koo BK, Park KW, Kang HJ, Cho YS, Chung WY, Youn TJ, et al. Physiological evaluation of the provisional side-branch intervention strategy for bifurcation lesions using fractional flow reserve. Eur Heart J. 2008;29:726-32. 26. Ormiston JA, Webster MW, El Jack S, Ruygrok PN, Stewart JT, Scott D, et al. Drug-eluting stents for coronary bifurcations: bench testing of provisional side-branch strategies. Catheter Cardiovasc Interv. 2006;67:49-55. 27. Burzotta F, De Vita M, Sgueglia G, Todaro D, Trani C. How to solve difficult side branch access? EuroIntervention. 2010;6 Suppl J:J72-80. 28. Brunel P, Lefevre T, Darremont O, Louvard Y. Provisional T-stenting and kissing balloon in the treatment of coronary bifurcation lesions: results of the French multicenter “TULIPE” study. Catheter Cardiovasc Interv. 2006;68:67-73. 29. Foin N, Torii R, Mortier P, De Beule M, Viceconte N, Chan PH, et al. Kissing balloon or sequential dilation of the side branch and main vessel for provisional stenting of bifurcations: lessons from microcomputed tomography and computational simulations. JACC Cardiovasc Interv. 2012;5:47-56. 30. Mortier P, Hikichi Y, Foin N, De Santis G, Segers P, Verhegghe B, et al. Provisional stenting of coronary bifurcations: insights into final kissing balloon post-dilation and stent design by computational modeling. JACC Cardiovasc Interv. 2014;7:325-33. 31. Foin N, Mattesini A, Ghione M, Dall’ara G, Sen S, Nijjer S, et al. Tools & techniques clinical: optimising stenting strategy in bifurcation lesions with insights from in vitro bifurcation models. EuroIntervention. 2013;9:885-7. 32. Koo BK, Kang HJ, Youn TJ, Chae IH, Choi DJ, Kim HS, et al. Physiologic assessment of jailed side branch lesions using fractional flow reserve. J Am Coll Cardiol. 2005;46:633-7.

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33. Steigen TK, Maeng M, Wiseth R, Erglis A, Kumsars I, Narbute I, et al. Randomized study on simple versus complex stenting of coronary artery bifurcation lesions: the Nordic bifurcation study. Circulation. 2006;114:1955-61. 34. Colombo A, Bramucci E, Sacca S, Violini R, Lettieri C, Zanini R, et al. Randomized study of the crush technique versus provisional sidebranch stenting in true coronary bifurcations: The CACTUS (Coronary Bifurcations: Application of the Crushing Technique Using SirolimusEluting Stents) study. Circulation. 2009;119:71-8. 35. Verheye S, Agostoni P, Dubois CL, Dens J, Ormiston J, Worthley S, et al. 9-month clinical, angiographic, and intravascular ultrasound results of a prospective evaluation of the axxess self-expanding biolimus a9eluting stent in coronary bifurcation lesions: the DIVERGE (DrugEluting Stent Intervention for Treating Side Branches Effectively) study. J Am Coll Cardiol. 2009;53:1031-9. 36. Kaplan S, Barlis P, Dimopoulos K, La Manna A, Goktekin O, Galassi A, et al. Culotte versus T-stenting in bifurcation lesions: immediate clinical and angiographic results and midterm clinical follow-up. Am Heart J. 2007;154:336-43. 37. Hussain F. Provisional reverse “mini-crush” technique for bifurcation angioplasty. J Invasive Cardiol. 2008;20:E154-7. 38. Behan MW, Holm NR, Curzen NP, Erglis A, Stables RH, de Belder AJ, et al. Simple or complex stenting for bifurcation coronary lesions : a patient-level pooled-analysis of the Nordic Bifurcation Study and the British Bifurcation Coronary Study. Circ Cardiovasc Interv. 2011;4:57-64. 39. Sirker A, Sohal M, Oldroyd K, Curzen N, Stables R, de Belder A, et al. The impact of coronary bifurcation stenting strategy on health-related functional status: a quality-of-life analysis from the BBC One (British Bifurcation Coronary; Old, New, and Evolving Strategies) study. JACC Cardiovasc Interv. 2013;6:139-45. 40. Zimarino M, Corazzini A, Ricci F, Di Nicola M, De Caterina R. Late thrombosis after double versus single drug-eluting stent in the treatment of  coronary bifurcations: a meta-analysis of randomized and observational studies. JACC Cardiovasc Interv. 2013;6:687-95. 41. Maeng M, Holm NR, Erglis A, Kumsars I, Niemelä M, Kervinen K, et al. Long-term results after simple versus complex stenting of coronary artery bifurcation lesions: Nordic Bifurcation Study 5-year follow-up Results. J Am Coll Cardiol. 2013;62:30-4. 42. Colombo A, Stankovic G, Orlic D, , Corvaja N, Liistro F, Airoldi F, et al. Modified T-stenting technique with crushing for bifurcation lesions: immediate results and 30-day outcome. Catheter Cardiovasc Interv. 2003;60:145-51. 43. Lim PO, Dzavik V. Balloon crush: treatment of bifurcation lesions using the crush stenting technique as adapted for transradial approach of percutaneous coronary intervention. Catheter Cardiovasc Interv. 2004;63:412-6. 44. Ge L, Airoldi F, Iakovou I, Cosgrave J, Michev I, Sangiorgi GM, et al. Clinical and angiographic outcome after implantation of drugeluting stents in bifurcation lesions with the crush stent technique: importance of final kissing balloon post-dilation. J Am Coll Cardiol. 2005;46:613-20. 45. Ormiston JA, Webster MWI, Webber B, Stewart JT, Ruygrok PN, Hatrick RI. The “crush” technique for coronary artery bifurcation stenting: insights from micro-computed tomographic imaging of bench deployments. JACC Cardiovasc Interv. 2008;1:351-7. 46. Galassi AR, Colombo A, Buchbinder M, Grasso C, Tomasello SD, Ussia GP, et al. Long-term outcomes of bifurcation lesions after implantation of drug-eluting stents with the “mini-crush technique”. Catheter Cardiovasc Interv. 2007;69:976-83. 47. Chen SL, Zhang JJ, Ye F, Chen YD, Patel T, Kawajiri K, et al. Study comparing the double kissing (DK) crush with classical crush for the

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13 Tips and Tricks: Lef t Main Pci Shuvanan Ray, Prithwiraj Bhattacharjee, Sabyasachi Mitra

Percutaneous coronary intervention (PCI) of unprotected left main stem is always a challenge since its beginning in the hands of the master Dr. Andreas Gruentzig. In the initial period it always remained a contraindication for elective PCI. After the introduction of stents, particularly the drug eluting stents, PCI is currently associated with short and medium time survival rates similar to coronary artery bypass grafting. As a result, left main coronary artery (LMCA) disease is not considered per se as a contraindication for PCI; rather it is grouped as ClassIIa (Ostial and shaft) and Class-IIb (Bifurcation) indications in current guidelines. The ostial and mid shaft lesions not involving the bifurcation have excellent results with PCI which is comparable to coronary artery bypass grafting, but majority of the LMCA lesions are located in the distal bifurcation for which we still do not have a unified and ideal stenting approach, moreover in such patients results are very much dependent on patient selection and proper technique.

WHY LMCA STENTING IS SO SPECIAL? Left main coronary artery stenting is different from other bifurcation stenting because: yy It involves 75–95% myocardium at jeopardy yy Less room for error during the procedure yy Both branches are main branches yy Less likely to accept suboptimal results. The success of LMCA intervention depends on the anatomy of the artery and its branching, the lesion characteristics as well as patient factors (e.g. LV function) presence of significant disease in other arteries adversely affect the immediate and long-term result.

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Figure 1: Relative distribution of left main coronary artery lesions according to site

Flow Chart 1: Technique selection for distal left main bifurcation lesions

Anatomical Factors Anatomically the LMCA lesion can be classified as ostial, shaft and distal bifurcation lesions, but from intervention perspective the lesion can be classified as distal and non-distal lesions, of them about 66% is distal lesion and the rest is nondistal lesion (Fig. 1). Non-distal lesions are quite straight forward for angioplasty and stenting whereas distal lesions are usually complex and inhomogeneous. The success of PCI in distal lesion depends on the size of the SB (usually the LCX), lesion in the side branch (whether SB is free or diseased, and if diseased, whether the disease is involving only the ostium or extending >5 mm of the ostium), angle of the SB. The distal angle is the most important parameter to select strategy where two stents are planned for intervention, for example, almost all bifurcation techniques can be adopted for an angle less than 90 degree, but when it is more than 90 degree, only T/DK Crush technique can be an answer to the problem (Flow Chart 1).

Selecting the Patient for PCI Numerous patients throughout the world are currently undergoing Drug Eluting Stent for UPLM. Nevertheless it should be emphasized that it is still Class-IIa/IIb for PCI in all

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available guidelines. Before selecting a patient for intervention it must be established that left main disease exists (e.g. if an ostial disease is evident only in cranial angulations) in such situations where left main disease appears doubtful, intravascular ultrasound (IVUS) is the ideal method for confirming the presence of significant left main coronary artery (LMCA) disease. Commonly used IVUS threshold for significant LM disease is a minimal luminal area of 6.0 mm. Informed consent is essential for UPLM stenting. Patients who are not candidates for surgery because of comorbidities or poor distal targets are the least controversial but patients who are acceptable candidates for coronary artery bypass graft (CABG) are extremely challenging to consent. A heart team approach is mandatory. One sub-group is whom DES might wisely be avoided are patients who have heavily calcified left main, ostial LAD and/or LCX and otherwise good candidates for coronary artery bypass grafting. A non-angiographic visualization device is probably essential during UPLM intervention. Pre- and post-procedural IVUS or optical coherence tomography is helpful for judging the degree of calcification, stent diameter selection, final stent expansion and stent apposition and confirming stent edge dissection. A circulatory assist device like intra-aortic balloon pump/impella/tandem heart is rarely needed in UPLM intervention, but may be essential in acute left main occlusion, hypotension, poor left ventricular function and/or totally occluded right coronary artery, or if the LMCA, LAD or LCX are significantly calcified and require rotational atherectomy before stenting.

THE TECHNIQUE Non-distal UPLM Intervention Usually Judkins’ left guide catheter, because of its less aggressive cannulation, is preferred. Always a bigger size is selected (≥7F) so that catheter does not suck in easily. The procedure is quite straight forward but we have to remember: yy Prepare the bed carefully before stenting yy The oscillation of the guide catheter, particularly in elderly atherosclerotic aorta with high differential blood pressure, increases the risk of stent malposition (hangout or ostial missing). Troubleshooting: ƒƒTo place the guidewire deeply into the LAD and try to obtain a distal loop, so that the guide catheter can be withdrawn easily, exposing the true ostium of the artery ƒƒPutting a second wire in the aortic sinus preventing selective cannulation of the ostium by the guiding catheter, in order to locate the LMCA origin precisely ƒƒDevices like Ostial-pro and Square One are occasionally required

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yy In short LMCA, another wire in LCX should be parked and jailed during stent implantation to ensure the distal point reference.

Distal UPLM Intervention This is really challenging and a strategy should be made beforehand by careful inspection of the angiography. There are basically two modes of treatment for distal UPLM intervention. (1) Provisional stenting: Where main branch is stented and side branch stenting is optional—this is actually a one stent affair. Plaques with Medina class 1,1,0 or 1,0,0 (plaque located in MB alone) should be stented with this technique. (2) Elective double stenting: When LMCA bifurcation stenosis involved both MB and SB (LCx), particularly when the myocardial territory supplied by the SB is large (SB≥2.5 mm) and the angle between MB and SB is wide, elective double stenting is considered as a strategy before taking up the case. Two very important issues should be remembered during distal UPLM intervention: (1) Guide catheter backup is essential in distal UPLM intervention and large bore (≥7F) extra backup catheter (XB, EBU, Voda) should be preferred. (2) Bed preparation is also very essential before stenting. Plaque modification (cutting balloon, scoring balloon, rotational atherectomy) is often required for bed preparation before stenting, so that stent under-expansion and malapposition can be excluded during the procedure.

One Stent Strategy Few important points: yy Wire both branches yy Choose MB stent according to the distal diameter yy Always do a proximal optimization of the stent by a 0.5 mm larger, short NC balloon, before exchanging the wires yy Final kissing balloon inflation is not mandatory. It is done only when the ostium of the SB become truly narrowed after MB stenting.

Two Stent Strategy There are many innovative techniques using two stents for UPLM bifurcation. For simplification and ready use one should classify them into two broad headings: (1) Main branch first (2) Side branch first. Remember: Finish the job always with a final kissing balloon inflation 1. Main branch first: Should be adopted when SB lesion is not very tight, it is only at the ostium and the angle between

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the MB and SB less than 90 degree. Procedure is almost like one stent strategy but after exchanging wire between MB and SB, the SB ostium should be opened using an NC balloon trans-strut at high pressure. Then an appropriate sized stent is placed in SB and an NC balloon (equal to MB stent) is placed in MB in such a fashion that the SB stent is slightly inside the struts of MB stent. SB stent is then deployed at nominal pressure and followed by final kissing balloon inflation at a moderate pressure (12–16 atm). 2. Side branch first: Again there are many strategies but basically most popular are one or either of the crush stenting techniques and Cullotte stenting techniques. Crush stenting: Here the side branch stent is crushed by the main branch balloon or stent. From proper crush which used more length (5 mm) of the SB stent into MB to crush, people now has shifted either to Mini-Crush or DK-Crush where 2–3 mm of the SB stent is placed inside the MB.

Technique of Mini-Crush/DK-Crush After preparation of the bed in both MB and SB: yy Place an appropriate sized stent in SB, touching either a balloon (in DK-Crush) or proper sized stent in MB, so that 2–3 mm of stent is inside the MB yy Deploy the SB stent at nominal pressure yy Remove the balloon and wire from SB yy Crush the SB stent by MB balloon or stent yy Cross trans-strut by another wire and enter SB with a proper sized NC balloon yy Do FKB by using a proper sized NC balloon in MB and SB in moderate pressure. yy There are few additional steps in DK-Crush: yy After crushing the SB stent by a proper sized NC balloon in MB, cross to SB and do the first kissing balloon inflation using two NC balloons at moderate pressure yy Then remove balloon and wire from SB and put a proper sized stent in MB yy Cross trans-strut into SB again and dilate the SB ostium by NC balloon at high pressure yy FKB using proper sized NC balloons in MB & SB at moderate pressure.

Cullotte Stenting This can be used in all bifurcation lesions (1:1:1) where the angle is less than 90 degree and when there is not much discrepancy between the mother vessel and the daughter vessels. Steps of Cullotte stenting are same to other techniques till wiring and lesion preparation. yy Then the SB stent is placed from MB to the most angulated branch and deployed at nominal pressure.

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yy The balloon is removed and the wire is placed into the straighter branch through the stent and the jailed wire is removed. yy The branch ostium across the stent is then dilated by an NC balloon at moderate pressure. yy Another stent is placed trans-strut from mother to the straighter branch, deployed at nominal pressure. yy Proximal optimization of the mother vessel stent done with a 0.5 mm larger short NC balloon at high pressure and another wire is placed trans-strut into the more angulated branch. yy FKB done with two NC balloons of the size of the daughter branches at moderate pressure.

Take Home Message: UPLM Intervention yy Heart team approach and proper counseling and consent. yy Planning of strategy after angiographic and non-angiographic visualizations (IVUS/OCT). yy Use best drug eluting stents—2nd and 3rd generation ones. yy Optimal LM stent technique: ƒƒLow threshold for hemodynamic support ƒƒFinish the job with IVUS/OCT guidance ƒƒOptimal pharmacotherapy during and after the procedure.

SUGGESTED READINGS 1. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. 2. Boudriot E, Thiele H, Walther T, Liebetrau C, Boeckstegers P, Pohl T, et al. Randomized comparison of percutaneous coronary intervention with sirolimus-eluting stents versus coronary artery bypass grafting in unprotected left main stem stenosis. J Am Coll Cardiol. 2011;57(5): 538-45. 3. Chen SL, Zhang Y, Xu B, Ye F, Zhang J, Tian N, et al. Five-year clinical follow-up of unprotected left main bifurcation lesion stenting: one-stent versus two-stent techniques versus double-kissing crush technique. EuroIntervention. 2012;8(7):803-14. 4. de la Torre Hernandez JM, Hernandez FH, Alfonso F, Rumoroso JR, Lopez-Palop R, Sadaba M, et al. Prospective application of pre-defined intravascular ultrasound criteria for assessment of intermediate left main coronary artery lesions: results from the multicenter LITRO study. J Am Coll Cardiol. 2011;58(4):351-8. 5. Lee SW, Kim SH, Kim SO, Han S, Kim YH, Park DW, et al. Comparative long-term efficacy and safety of drug-eluting stent versus coronary artery bypass grafting in ostial left main coronary artery disease: analysis of the MAIN-COMPARE registry. Catheter Cardiovasc Interv. 2012;80(2):206-12. 6. Mehilli J, Richardt G, Valgimigli M, Schulz S, Singh A, Abdel-Wahab M, et al. Zotarolimus-versus everolimus-eluting stents for unprotected left main coronary artery disease. J Am Coll Cardiol. 2013;62(22):2075-82. 7. Mehilli J, Kastrati A, Byrne RA, Bruskina O, Iijima R, Schulz S, et al. Paclitaxel-versus sirolimus-eluting stents for unprotected left main coronary artery disease. J Am Coll Cardiol. 2009;53(19):1760-8.

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8. Ng W, Lundstrom R, McNulty E. Impact of stenting technique and bifurcation anatomy on long-term outcomes of PCI for distal unprotected left main coronary disease. J Invasive Cardiol. 2013;25(1):23-7. 9. Park SJ, Kim YH, Park DW, Yun SC, Ahn JM, Song HG, et al. Randomized trial of stents versus bypass surgery for left main coronary artery disease. N Engl J Med. 2011;364(18):1718-27. 10. The European Association for Cardio-Thoracic Surgery (EACTS), The task force on myocardial revascularization of the European Society of Cardiology (ESC), Wijns W, Kolh P, Danchin N, Di Mario C, et al. Guidelines on myocardial revascularization. Eur Heart J. 2010;31(20):2501-55.

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14 Carotid Angioplasty— Step-By-Step Anil Dhall, DS Chadha, SK Malani, VS Bedi

INTRODUCTION Carotid artery occlusive disease is responsible for up to 25% of stroke. Prevalence of carotid stenosis increases from approximately 0.5% at 60 years of age to approximately 10% at age 80 years. Carotid endarterectomy (CAE) has been thoroughly evaluated by many clinical trials. Several clinical and anatomic features are considered high risk for surgical intervention necessitating need to develop carotid artery stenosis (CAS) (Table 1).

INDICATIONS The indications for carotid intervention include: yy A symptomatic patient with an angiographic stenosis of more than 50%; that is, a lesion-related neurological event in the preceding 6 months.

Table 1: Clinical situations where carotid endarterectomy is complex or is contraindicated. Hostile or difficult necks: –Tracheostomy –Laryngeal paralysis –Restenosis –Cervical X-ray therapy –Carotid stenosis induced by X-ray therapy –Major arthrosis –Small and large neck with high bifurcation“buffalo neck” –Carotid bypass stenosis Highly located lesions Angiodysplasia Lesions at the common carotid level and on the aortic arch

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yy An asymptomatic patient with an angiographic stenosis of more than 70%, symptoms are relevant for risk of major stroke after hemispheric transient ischemic attacks (TIAs). Recurrence risk of TIA/stroke follows a relation to severity of stenosis, although this issue has been challenged recently (Fig. 1).

STRATEGY To attain good results the multifactorial CAS strategy involves: 1. A “tailored-approach” in the application of endovascular technologies and techniques to a specific-patient with a specific-lesion and vascular anatomy. 2. The choice of stent, embolic protection device (EPD), guiding-catheter and sheath is strongly dependent on an in-depth knowledge of neuro-assessment, carotid plaque characteristics, vascular anatomy and technical features of a vast array of endovascular materials. Following the patient assessment, this information should be integrated to predict the embolic-risk of revascularization. 3. Experience with a wide range of devices allows the operator the flexibility to choose the most appropriate tools and techniques for the safe application of CAS.

EVALUATION The evaluation of carotid plaque profile should describe.

Degree Stenosis and Vessel Dimensions yy Length/bulk of disease and the morphologic features that predict lesion complexity such as degree of calcification and embolization-potential (“vulnerable plaque”).

Figure 1: What is the risk of stroke in asymptomatic patients?

Source: Risk of stroke in asymptomatic patients with carotid artery stenosis. (NEJM 315(14);860-5

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yy Long, irregular or ulcerated lesions (Figs. 2A and B) and clinically unstable plaques (recurrent TIAs) define a high-risk disease subset. Plaques characterized by a large lipid pool covered by a thin fibrous cap are more prone to perioperative embolization as compared to fibrous plaques.

The Assessment of Vascular Profile Includes Defining: yy Configuration of the aortic arch yy Arch embologenic-risk in terms of burden of irregular, ulcerated and calcified atheroma yy Angulations and tortuosity, coiling and kinking of supraaortic trunks yy Level of carotid bifurcation and its anatomy regarding angle of take-off of the internal carotid artery (ICA), tortuosity at lesion-site and vessel dimensions yy Intracranial segment of the ICA and ipsilateral/contralateral cerebral circulation to determine collateral flow including circle of Willis and identify abnormal flow patterns.

Neuroprotection Systems Embolization occurs in all percutaneous cardiovascular interventions; however, it acquires more significance in the neurovascular territory. Carotid lesions contain friable ulcerated plaque and thrombotic material that can embolize during endovascular or open surgery. Embolic particles are classified as either macroemboli (>100 μm) or microemboli (70%) rate was 2.7%.

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15 Balloon Mitral Valvuloplasty Sameer I Dani

INTRODUCTION Mitral stenosis is a progressive disease that leads to heart failure and is finally fatal unless mechanical intervention enlarges the mitral valve orifice to permit adequate cardiac output at a tolerable left atrial pressure. Starting over 50 years ago, a variety of surgical techniques were developed; first closed commissurotomy followed by open commissurotomy after the introduction of the cardiopulmonary bypass. Balloon mitral valvuloplasty (BMV) was introduced in 1984 by the Japanese surgeon Inoue, who developed the procedure as a logical extension of surgical closed commissurotomy. Since then, BMV has emerged as the treatment of choice for severe pliable rheumatic mitral stenosis.

RHEUMATIC HEART VALVE DISEASE— STILL AN EPIDEMIC IN ASIA The decrease in incidence of rheumatic heart disease in developed countries had already begun in 1910, and it is now below 1 per 100,000. On the other hand, the occurrence rate of rheumatic heart disease in developing countries remains substantial. Because the decline in the prevalence of rheumatic fever in industrialized nations started even before the era of penicillin and thus was related to improved living standards, the continued prevalence of rheumatic heart disease in undeveloped or developing countries is related not only to the limited availability of penicillin but also to their socioeconomic status (i.e. overpopulation, overcrowding, poverty and poor access to medical care). According to the annual report by the World Heart Federation few years back, an estimated 12 million people were affected by rheumatic fever and rheumatic heart disease

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worldwide, and high incidence rates were reported in the Southern Pacific Islands. Several studies were conducted on the prevalence of rheumatic heart disease, reporting 0.14/1,000 in Japan, 1.86/1,000 in China, 0.5/1,000 in Korea, 4.54/1,000 in India, and 1.3/1,000 in Bangladesh.

RHEUMATIC MITRAL STENOSIS If the mitral valve (MV) orifice area exceeds 1.5 cm2, patients are generally asymptomatic at rest. The clinical exacerbation of mitral stenosis occurring with pregnancy or complications such as atrial fibrillation or embolic events confers a poor prognosis if no intervention is performed to correct the mitral stenosis. Commissural fusion is the requisite lesion for percutaneous balloon mitral valvuloplasty (PBMV) to be effective (Figs. 1A to D). Thus, the effectiveness of BMV is related to the etiology of mitral stenosis. Rheumatic fever (RF), the major cause of mitral stenosis, results in commissural fusion of the mitral valve, which leads to narrowing of the valve orifice and valve

A

B

C

D

Figures 1A to D: Example of a typical rheumatic mitral stenosis. (A) Leaflet thickening at the edges is shown in a parasternal long axis transthoracic view. (B) The immobility of the posterior leaflet and the doming of the anterior leaflet as typical morphological characteristics of rheumatic mitral valve disease are shown in a 3-dimensional transesophageal image. The 3-dimensional transesophageal images [(C) left atrial aspect] and [(D) left ventricular aspect] show the fusion of both commissures (red arrows) {AML: Anterior mitral leaflet; PML: Posterior mitral leaflet}. Source: JACC Cardiovascular Interventions. 2013;6(11):1191-205.

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obstruction. In degenerative mitral stenosis, generally seen in the elderly or in patients with severe renal disease and secondary hyperparathyroidism, advanced mitral annular calcification is the main lesion and commissural fusion is not present. Other rare causes of mitral stenosis include congenital mitral stenosis, inflammatory diseases, infiltrative diseases, carcinoid heart disease and drug-induced mitral stenosis. As with degenerative mitral stenosis, commissural fusion is rare in these cases; most commonly, the leaflets are thickened and restricted, and, thus, these cases are generally not well suited for BMV.

ECHOCARDIOGRAPHIC EVALUATION Echocardiography is the mainstay of the noninvasive evaluation of mitral stenosis. The transthoracic echocardiography provides an evaluation of the valvular apparatus, mitral valve area (MVA), left atria dimension and associated valve lesions. Doppler echo provides hemodynamic evaluation including mean mitral gradient, MVA, assessment of concomitant tricuspid regurgitation (TR) and estimation of pulmonary artery pressure. Transesophageal echocardiography (TEE) should be performed before BMV for patients with atrial

Table 1: Wilkins score Grade

Subvalvular thickening

Mobility

Thickening

Calcification

1

Highly mobile with only leaflet tips restricted

Leaflets near normal in thickness (4–5 mm)

A single area of increased echo brightness

Minimal thickening just below the mitral leaflets

2

Leaflet mid portions and base portions have normal mobility

Mid leaflets normal, considerable thickening of margins (5–8 mm)

Scattered areas of brightness confined to leaflet margins

Thickening of chordal structures extending to one of the chordal length

3

Valve continues to move forward in diastole, mainly from the base

Thickening extending through the entire leaflets (5–8 mm)

Brightness extending into the mid portions of the leaflets

Thickening extended to distal third of the chords

4

No or minimal forward movement of the leaflets in diastole

Considerable thickening of all leaflet tissue (>8–10 mm)

Extensive brightness throughout much of the leaflet tissue

Extensive thickening and shortening of all chordal structures extending down to the papillary muscle

Source: Circulation. 2009;119:e211-9.

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fibrillation or prior history of systemic embolism or very obese patient where the left atrium was not properly visualized. In cases of moderate or severe mitral stenosis, one has to assess the anatomy of the mitral valve meticulously with regard to the feasibility and safety of BMV. As shown in Table 1, the most widely used echocardiographic parameter is the Wilkins’ score, which takes into consideration the anatomy of the leaflet, the commissures and the subvalvular apparatus. The scoring system assigns a point value from 1 to 4 for each of (1) valve calcification, (2) leaflet mobility, (3) leaflet thickening and (4) subvalvular apparatus degeneration. A mitral valve with a score less than 8 to 9 with no more than moderate mitral regurgi-tation is deemed the best candidate for PBMV. In patients with a score more than 9 to 10, especially with more than moderate mitral regurgitation, surgical therapy should be advised except in cases with serious comorbidities.

ASSESSMENT OF MITRAL STENOSIS SEVERITY The severity of mitral stenosis should not be defined by a single value but rather be assessed by a multimodality approach that determines valve areas, mean Doppler gradients, and pulmonary pressures (Table 2). Mitral valve area can be assessed by planimetry using either 2D or 3D imaging, pressure half-time (PHT), the continuity equation and the proximal isovelocity surface area (PISA) method.

CONTRAINDICATIONS TO PERCUTANEOUS BALLOON MITRAL VALVULOPLASTY Contraindications to BMV are elicited below. In addition to these, a mitral stenosis with no commissural fusion should be considered as a relative contraindication, as previously described. BMV should be considered first-line therapy in most cases of severe mitral stenosis without obvious contraindications. yy Persistent left atrial or left atrial appendage thrombus yy More than moderate mitral regurgitation yy Massive or bicommissural calcification yy Severe concomitant aortic valve disease yy Severe organic tricuspid stenosis or severe functional regurgitation with enlarged annulus yy Severe concomitant coronary artery disease requiring bypass surgery.

MECHANISM OF BALLOON MITRAL VALVULOPLASTY The mechanism of successful BMV is splitting of the fused commissures toward the mitral annulus, resulting in commi-

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Table 2: Quantification of mitral stenosis severity using various methods Method

Mild MS

Pressure half-time

Valve area in cm2 Mild, >1.5; moderate, 1-15; severe, 1.5 cm2, mitral regurgitation 60 years) where LV restrictive physiology is suspected, temporary balloon occlusion is performed to assess its effect on PAWP/LVEDP. If the pressures increase by above 5 mm Hg, one needs to consider using a fenestrated device in order to avoid acute pulmonary edema.

SELECTING DEVICE SIZE The device size is selected based on the size of the defect. There are two methods to determine the defect size. (1) TTE/TEE/ICE measuremen10 where the defect is directly measured on 2-D images in multiple views (as described above).

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(2) Balloon sizing: There are two ways to size the defect by balloon. One is the “Stop-flow” technique and other is the “Waist” measurement technique. yy Stop-flow technique: The sizing balloon is placed across the ASD and inflated till there is stoppage of flow across the defect on color flow Doppler imaging. The maximum width of the balloon is then measured on TTE/TEE/ICE as well as fluoroscopy. yy Waist measurement technique: The sizing balloon is placed across the ASD and inflated till there is a waist formation noted along both the margins of the balloon on fluoroscopy. This waist is then measured on fluoroscopy We use TEE imaging (without balloon sizing) to determine the size of the device to be used. Defect size is measured in three planes (0, 40 and 90 degrees) and the maximum diameter is noted. Twenty percent more than the maximum diameter is the size of the device used for that defect. Some groups using balloon sizing, tend to use the device of the same diameter as the balloon size of the defect while the others tend to oversize the device by 2 mm or in case of large defects with complete absence of aortic rim upsize the device even up to 4 mm. In short, there is no definite rule for selecting the device size and most of the operators evolve their own way based on their experience.

COMMONLY USED DEVICES The Amplatzer Septal Occluder device (St. Jude, Plymouth, MN, USA) is a self-expandable double-disk device made of a nitinol (55% nickel; 45% titanium) wire mesh (Figs. 5A to C). The ASO device is constructed from a 0.004–0.0075 inch nitinol wire that is tightly woven into two flat disks. There is a 3–4 mm connecting waist between the two disks, corresponding to the thickness of the atrial septum. The devices are available in sizes ranging from 4 mm to 40 mm with an increment of 1 mm up to 20 mm and thereafter with an increment of 2 mm. The size of the device corresponds to the diameter of the waist connecting the left and the right atrial disk. The left atrial disk extends for 14–16 mm beyond the waist while the right atrial disk tends to extend for 8–10 mm. Both the disks as well as the waist have a sheet of polyester to promote thrombosis. The GORE® HELEX® Septal Occluder (W.L: Gore & Associates, Flagstaff, Arizona) is a soft and compliant, non self-centering device made from a single length nitinol wire shaped into a left and right atrial disk covered by a polytetrafluoroethylene (ePTFE) membrane. The ePTFE is treated with a hydrophilic coating to facilitate echocardiographic imaging of the occluder during implantation. When fully deployed, the occluder assumes a double disk configuration that bridges the septal defect to prevent shunting of blood between the right and left atria

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A

B

C

Figures 5A to C: (A) Gore Helex device. (B) Occlutech Figulla Flex II device. (C) Amplatzer septal occluder

(Figs. 5A to C). The GORE® HELEX® Septal Occluder received FDA clearance in 2006. The GORE® Septal Occluder, a new device, is the result of an extended development and improvement of the GORE® HELEX® Septal Occluder. The wire frame is formed from five wires shaped into the right and left atrial disks, the eyelets, and the lock loop. The five-wire design provides conformability, allowing each individual wire within a right or left atrial disk to conform to the heart anatomy. Device release is a two staged process, firstly locking of the device by the lock loop and then removal of the retrieval cord. A 2:1 ratio between the device size and the defect size “balloon-stretched diameter” is used for optimal results, and the device diameter is not allowed to exceed 90% of the measured septal length. The device is available in sizes of 15, 20, 25, 30 and 35 mm.11 Advantages of Gore occluders: yy No reported incidence of device erosion or cardiac perforation yy Even after locking the device in position after optimal position is confirmed, it can still be retrieved with the help of retrieval cord attached to the right atrial disk yy The GORE® Septal Occluder is a non-self centering device having a narrow mid portion that makes it suitable for closure of multifenestrated defects yy The device can easily be seen on fluoroscopy and echocardiography. Disadvantages of Gore occluders: yy Defects larger than 18 mm cannot be closed with this device. yy Wire frame fracture has been reported with the GORE® HELEX® Septal Occluder, especially the larger sizes, occurring in 6.4–8.0% of patients after 1 year.12 yy In the United States multicentre study of the GORE® HELEX® Septal Occluder, used in 143 patients for closure of ASDs there was a rate of residual leaks of 25.7% at 12 months.13 However, majority of residual shunts were small and clinically insignificant. yy There is a fixed right angle between the tip of the delivery catheter and the device. In some cases, especially in children, this can distort the anatomy and orientation of

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the atrial septum and make it difficult to decide whether the occluder position is optimal. With release of the device there is significant repositioning when the force from the delivery system is taken away from the septum. yy The Occlutech Figulla Flex II (Occlutech GmbH, Jena, Germany) is a self-expanding nitinol wire mesh, very similar to the Amplatzer device in shape, but with a different design that eliminates the left atrial microscrew (Figs 5A to C).14 The device, developed using a unique patented braiding technique, consists of a nitinol wire mesh to create a smooth and flexible outer layer. Two retention disks allow for a single central pin on the right atrial side. Two polyethylene terephthalate (PET) patches assure complete closure after implantation. Available sizes range between 6 and 39 mm with an increment of 3 mm. Additional larger sizes can be made available on placing a prior order. These devices are also available with a company made fenestration of 6–8 mm diameter for those with severe PHT or those having restrictive LV physiology. Advantages of Occlutech Figulla Flex II: yy There is a 50% reduction of meshwork material on the left atrial side along with elimination of the left atrial disc microscrew, minimizing both the risk of thrombus formation and damaging the distal wall of the left atrium during implantation. yy The delivery cable mechanism is different and allows pivoting of the device (up to 50°), which facilitates positioning across the septum, an advantageous feature especially in large defects and in those with less significant rims. yy The device is fully recapturable and repositionable. Disadvantages of Occlutech Figulla Flex II: yy It has a much larger profile as compared to ASO thereby making its use difficult in smaller children.

PREPARATION OF THE DELIVERY SHEATH AND DEVICE: The following description about device preparation and delivery is in context of the Amplatzer septal occluder or other similar devices. The various parts of the Amplatzer occluder delivery system are shown in Figures. 6A to F. The sheath size recommended by the manufacturer depends on the size of the device. Our practice is to use a sheath 1r more than the recommended size excepting in children weighing less than 15 kg in whom we use the same size as per the manufacturer’s recommendations.

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VARIOUS TECHNIQUES OF DEVICE DELIVERY Loading the Device: All the components of the delivery system are thoroughly flushed and wiped from outside with heparinized saline solution. It is necessary to load the device after gently messaging it in heparinized saline so as to get rid of the air that might have been trapped in the Dacron patches. The loader Figure 6A is connected to the hemostasis valve with the extension tube and the stopcock Figure 6B. The delivery cable is then passed through the loader. The device is then screwed onto the delivery cable by anticlockwise screwing movements. It is always a good habit to double check that the device is screwed onto the cable securely. The ASO is then slenderized within the loader by using underwater technique followed by thorough flushing to get rid of the air within the system.

Routine Deployment Technique The defect is crossed with a right coronary artery catheter and the tip is positioned in the left superior pulmonary vein (LSPV) (Fig. 7A). A floppy tip Amplatz superstiffTM guide wire (Boston Scientific, Marlborough, MA, USA) is then positioned in the LSPV (Fig. 7B). Over this wire, an Amplatzer TorqVueTM 45° delivery sheath (St. Jude, Plymouth, MN, USA) is passed and placed at the mouth of the LSPV. The delivery sheath is then gradually advanced over the dilator into the LSPV (Fig. 8A). After confirming the position on TEE, the dilator and wire are removed (Fig. 8B). It is essential to allow back bleeding of the sheath to prevent air embolism. If the patient is under general anesthesia with positive pressure ventilation, one can just

Figures 6A to F: Amplatzer delivery system. (A) Loader—used to introduce the Amplatzer Septal Occluder into the delivery sheath. (B) Hemostasis valve with extension tube and stopcock—allows flushing the delivery system and controls back-bleeding. (C) Delivery sheath—provides a pathway through which a device is delivered. (D) Dilator—used to ease penetration of skin and the subcutaneous tissue. (E) Delivery cable—the device is screwed onto the distal tip of the delivery cable, which allows for placement (and if necessary, retrieval) of the device. (F) Plastic vise—attached to the delivery cable, serving as a “handle” for detaching (unscrewing) the delivery cable from a device

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remove the dilator to allow back bleed. However, if the patient is breathing spontaneously, it is better to back bleed by holding the sheath below the level of the heart in a saline bowl. This helps in preventing inadvertent sucking of the air into the sheath resulting in air embolism. The loader containing the device is now attached to the sheath and the delivery cable is pushed to advance the device. The cable is pushed till the left atrial disk is extruded out of the sheath into the left atrium) (Fig. 9A). The position of the disk is confirmed on TEE (Fig. 9B). Once the left atrium disk is delivered, the entire assembly is pulled back till the disk hitches against the interatrial septum. Once this is confirmed, the delivery sheath is “peeled” back over the loading cable to allow release of the waist and the right atrial disk and thus deploying the device (Figs. 10A and B). Position of the device as well as adequate capture of all margins and separation from the AV valves is confirmed on TEE (Figs. 11A to C). Adequate separation of the two disks is also confirmed on fluoroscopy in left anterior oblique view (Fig. 12A). The device is then released by anticlockwise rotations of the delivery

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Figures 7A and B: (A) Crossing the defect with a right coronary artery catheter. The catheter tip is positioned in the left superior pulmonary vein (LSPV). (B) A floppy tip Amplatz superstiffTM guidewire (Boston Scientific, Marlborough, MA, USA) being placed in the LSPV

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Figures 8A and B: (A) Delivery sheath being advanced over the dilator into the mouth of LSPV. (B) The delivery sheath positioned in the left atrium just outside the LSPV

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cable. Final position of the device is again confirmed on TEE and fluoroscopy (Fig. 12B) before removing the vascular sheaths The above-described “routine technique” of device deployment is likely to fail in the following conditions: yy Large ASDs in children with small left atrium yy Large defects (requiring ASO > 30 mm) in adults yy ASDs with floppy rims yy Defects with just adequate (4–5 mm) rims yy ASDs with malaligned rims yy Patients having ASD with cardiac malpositions or associated spinal deformities. There seem to be two major underlying mechanisms for the failure of the routine technique: (1) Inability to accommodate the left atrial disk: commonly encountered in children with large ASD and small left atrium (Figs. 13A and B). (2) Inability to align the left atrial disk with the plane of the IAS: seen in the remaining subsets of patients. The first problem can be overcome by a group of techniques labeled as left atrial disk engagement disengagement technique (LADEDT).15 In this group of techniques the basic principle is

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Figures 9A and B: (A) Left atrial disk of the ASO being extruded in the left atrium. (B) Corresponding TEE loop showing left atrial disk in the left atrium

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Figures 10A and B: (A) Delivery sheath “peeled” back over the loading cable to allow release of the waist and the right atrial disk and deployment of device. (B) Corresponding TEE loop depicting deployment of the ASO across the defect

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Figures 11A to C: TEE loops at 0 (A), 45 (B) and 90 degrees (C) confirming adequate capture of all margins before releasing the device from the loading cable

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Figures 12A and B: (A) Well separated disks of the ASO in LAO view confirming a well-positioned device. (B) Final position of the device in anteroposterior projection—Fluoroscopic “Fingerprinting” of the device

to engage the left atrial disk within the left or right pulmonary veins or even within the left atrial appendage till such time the waist and RA disk can be delivered. In doing so, the RA disk aligns itself with the IAS from the right atrial aspect followed by disengagement of the left atrium disk either spontaneously or with the use of maneuvers (Figs. 14A to D). If the left atrium disk does not disengage spontaneously, there is a tendency to pull on the loading cable to disengage the disk. In doing so, the RA disk loses its alignment with the IAS and the left atrium disk tends to fall through the defect in the left atrium. In order to avoid this, we have used a contrarian technique of pushing on the cable rather than pulling, to disengage the left atrium disk (Figs. 14C and D). This creates a secondary torque on the left atrium disk resulting in its

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Figures 13A and B: (A1 and A2) and (B1 and B2) TEE loops depicting a large ASD in a small child. The left atrium is relatively smaller compared to the right atrium. (B2) TEE depicting the left atrial disk lying perpendicular to the atrial septum due to inability to accommodate the disk in the left atrium

disengagement from the site of engagement (pulmonary vein or left atrium appendage) while maintaining the alignment of the right atrial disk with the interatrial septum. The second problem of alignment of the left atrium disk with the plane of the IAS can be overcome by: 1. Changing the mode of delivery 2. Changing the delivery sheath 3. Using an additional support (1) Changing the mode of delivery: Here the left atrium disk is deployed from just outside the RSPV rather than doing it from just outside the LSPV. This occasionally helps in aligning the left atrium disk. (2) Changing the delivery sheath: Changing the delivery sheath to a Hausdorf sheath (Cook, Bloomington, IN) (Fig. 15A), a specially designed long sheath with two posterior curves at its end, can allow for a better alignment of the left atrial disk parallel to the septum.16 In addition, a “Sidecutting” sheath (Fig. 15B)—a modified Mullins sheath with the creation of a bevel at the inner curvature, also allows a more parallel alignment of the left atrial disk to the interatrial septum.17 More recently, a tip deflecting sheath (FuStar, Lifetech) has been introduced with an aim to improve the alignment. (3) Using an additional support: Additional support, to prevent prolapse of the left atrium disk, can be provided by use of a long dilator or balloons. Wahab technique (dilator assisted technique)18 (Fig. 16): In this technique, following deployment of the left atrial disk, a long dilator is advanced into the left atrium, holding the anterosuperior part of the left atrial disk to prevent it from prolapsing across the ASD.

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Figures 14A to D: (A) The left atrial disk of an ASO being delivered inside the left superior pulmonary vein (LSPV). (B) The waist and RA disk being released sequentially. Failure of LA disk to disengage from the LSPV. (C) The loading cable being pushed against the RA disk to induce a secondary torque in order to facilitate disengagement of LA disc. (D) Release of LA disc from the LSPV resulting in deployment of the device

Balloon assisted technique (BAT)19 (Figs. 17 and 18): An Occlutech balloon (Boston Scientific, Watertown, MA, USA) is positioned in the right atrium and pushed against the interatrial septum over a superstiff wire positioned in the LSPV. The ASO delivery sheath is positioned in the right superior pulmonary vein. The balloon is then inflated followed by sequential release of the left atrial disk, waist and the right atrial disk. This is followed by gradual deflation of the balloon to allow deployment of the device across the ASD.

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Figures 15A and B: (A) Hausdorf sheath (Cook, Bloomington, IN) is a specially designed long sheath with two posterior curves at its end, allowing for a better alignment of the left atrial disk parallel to the septum. (B) Sidecutting sheath—is a modified Mullins sheath with the creation of a bevel at the inner curvature, also allowing a more parallel alignment of the left atrial disk to the interatrial septum

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The advantages of BAT are that it is a simple, safe, effective across all ages, has a short learning curve and most importantly is predictable in terms of technical success. Its limitations include requiring an additional venous access, additional hardware (cost), need for additional personnel to hold the balloon against the IAS and large venous access which can cause problems pertaining to hemostasis. Two modifications of BAT have been described; one in which an elongated instead of round balloon is used and the other wherein the balloon is positioned across the defect rather than in the right atrium.20,21

POSTPROCEDURAL CARE The patient is extubated on table if the procedure is done under general anesthesia. Patient is shifted to the recovery room or intensive care unit (ICU) where the vitals are monitored for another 6 hours. An ECG is done immediately after shifting the patient to the recovery room/ICU. Intravenous antibiotics are continued usually for another two doses. A repeat ECG and TTE are performed on the following day before planning for discharge. All the patients are discharged the next morning.

FOLLOW-UP Oral Aspirin is continued for 6 months after the procedure. Follow-up with clinical evaluation, 12 lead ECG and TTE are performed at 1 week, 1 month, 6 month, 1 year and yearly for

Figure 16: Wahab technique (dilator assisted technique): following deployment of the left atrial disk, a long dilator is advanced into the left atrium, holding the anterosuperior part of the left atrial disk to prevent it from prolapsing

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Figures 17A to C: (A) An Occlutech balloon (Boston Scientific, Watertown, MA, USA) is positioned in the right atrium and pushed against the interatrial septum over a superstiff wire positioned in the LSPV. The ASO delivery sheath is positioned in the right superior pulmonary vein. (B) The balloon is inflated followed by sequential release of the left atrial disk, waist and the right atrial disk. (C) The balloon is gradually deflated to allow deployment of the device across the ASD

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Figures 18A to C: (A) The balloon catheter being pulled back into the inferior vena cava before releasing the device. (B) The superstiff wire now pulled back into the inferior vena cava before releasing the device. (C) Device position confirmed in left anterior oblique view and released

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2 years and then once in 3–5 years or if there is chest pain, giddiness, shortness of breath or any other unusual symptom. Infective endocarditis prophylaxis is recommended for 6 months postprocedure.

COMPLICATIONS Some of the common complications encountered include: 1. Air embolism: This is evident by ST segment changes in inferior leads on the ECG (Figs. 19A and B). These are usually transient and can be avoided by consciously avoiding injecting air through peripheral lines and checking for adequate back flow of blood from catheters and sheaths placed in the left atrium/pulmonary vein. Meticulous preparation of the device at the time of loading and slenderizing also helps to prevent air embolism. Also, in patients breathing spontaneously during the procedure, the dilator and the wire should be removed from the delivery sheath by holding the sheath under water below the level of the heart. 2. Left atrium disk deformation (cobrahead formation): Here the left atrium disk maintains a high profile mimicking a cobrahead. This can happen if the left atrium disk is opened in the pulmonary vein or left atrium appendage or if the device itself is defective. Once it happens, try to recapture the device and withdraw it within the sheath. The same device can be reused to deploy if it forms normally in vitro. If deformation persists in vitro, which is rarely the case, the device needs to be changed. 3. Arrhythmia: Hill et al.22 noted supraventricular ectopy in 63% immediately after device closure including 23% with non-sustained supraventricular tachycardia. In elderly population, atrial fibrillation (AF) may get precipitated while entering the pulmonary veins or while moving the catheter in the RA. Gentle catheter manipulations within the atria and while entering the pulmonary veins help in preventing occurrence of AF. 4. Atrioventricular block: Suda et al.23 reported that 6.2% patients presented with new-onset or aggravation of

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Figures 19A and B: (A) Air embolism as noted by ST segment changes on ECG. (B) Air embolism is usually transient as noted by return of ST segment to baseline

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pre-existing AV block. Thirty percent occurred during the procedure and remaining were noted between 1 and 7 days after procedure. All resolved or improved spontaneously with no recurrence at mid-term follow-up. 5. Device embolization: This is a rare complication with an incidence of 0.55%.24 Embolization (Fig. 20A) usually occurs in those with large ASD and deficient rims. The device can embolize to either side of the atrial septum. A majority of the embolized devices do not cause acute hemodynamic collapse. Most of them can be snared and retrieved percutaneously (Fig. 20B). Principles of percutaneous device retrieval have been well described in the literature.25 6. Cardiac erosion/perforation (CP): This is the most dreaded complication with a reported incidence of 0.1%.26 Amin et al. reported that all erosions occurred at the dome of the atria near the aortic root. Their study concluded that the risk of erosion was higher with deficient aortic or superior rim and with use of oversized device. Patients with CP may present with pericardial effusion, chest pain, dyspnea, syncope, hemodynamic collapse, or even sudden death. CP can be confirmed on CT angiography where protrusion of the device into the pericardial space can be identified. However, this cannot be performed at the bedside and is expensive. In order to distinguish erosion from other etiologies of pericardial effusion, we utilized a strategy of injecting an LV contrast agent intravenously and trying to see whether it leaks into the pericardial cavity (Figs. 21A and B).27

LONG-TERM RESULTS

Long-term follow-up data after ASD device closure is now available.28,29 The incidence of residual shunt ranges from 0% to 3%. Right ventricular remodeling may persist in up to 10% of adults (>40 years of age). Nearly 97% have symptom free survival. Pre-existing AF may persist/recur in those more than 40 years of age in spite of device closure of the defect.

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Figures 20A and B: (A) An ASO embolized to the right ventricle. (B) ASO embolized into the aorta being retrieved by a snare retrograde from the arterial side

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Figures 21A and B: (A) A 2-dimensional echocardiographic (2D-Echo) image taken in the left parasternal short axis view showing opacification of the right ventricular cavity by the ultrasound contrast agent injected intravenously. There was no opacification visualized in the pericardial space. (B) 2D-Echo image showing subsequent appearance of the contrast agent in the left ventricle. Note that there is still no appearance of contrast within the pericardial space {RV: Right ventricle; LV: Left ventricle: PE: Pericardial effusion}.

REFERENCES 1. King TD, Mills NL. Non-operative closure of atrial septal defects. Surgery. 1974;75(3):383-8. 2. Feltes TF, Bacha E, Beekman RH 3rd, Cheatham JP, Feinstein JA, Gomes AS, et al. Indications for cardiac catheterization and intervention in pediatric cardiac disease: a scientific statement from the American Heart Association. Circulation. 2011;123:2607-52. 3. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease. J Am Coll Cardiol. 2008;52(23):e143–263. 4. Webb G, Gatzoulis MA. Atrial septal defects in the adults: recent progress and overview. Circulation. 2006;114(15):1645-53. 5. Jung JW. Echocardiographic evaluation of atrial septal defect device closure. J Cardiovasc Ultrasound. 2007;15(1):1-7. 6. Vaidyanathan B, Simpson JM, Kumar RK. Transesophageal echocardiography for device closure of atrial septal defects: case selection, planning, and procedural guidance. JACC Cardiovasc Imaging. 2009;2(10):1238-42. 7. Medford BA, Nathaniel TW, Cabalka AK, Cetta F, Reeder GS, Hagler DJ, et al. Intracardiac echocardiography during atrial septal defect and patent foramen ovale device closure in pediatric and adolescent patients. J Am SocEchocardiogr. 2014;27:984-90. 8. Roberson DA, Cui VW. Three-dimensional transesophageal echocardiography of atrial septal defect device closure. Curr Cardiol Rep. 2014;16(2):453. 9. Giannakoulas G, Dimopoulos K, Engel R, Goktekin O, Kucukdurmaz Z, Vatankulu MA, et al. Burden of coronary artery disease in adults with congenital heart disease and its relation to congenital and traditional heart risk factors. Am J Cardiol. 2009;103(10):1445-50. 10. Tzifa A, Gordon J, Tibby SM, Rosenthal E, Qureshi SA, et al. Transcatheter atrial septal defect closure guided by colour flow Doppler. Int J Cardiol. 2011;149(3):299-303. 11. Nyboe C, Hjortdal VE, Nielsen-Kudsk JE. First Experiences with the GORE Septal Occluder in Children and Adults with Atrial Septal Defects. Catheter Cardiovasc Interv. 2013;82:929-34. 12. Latson LA, Jones TK, Jacobson J, Zahn E, Rhodes JF. Analysis of factors related to successful transcatheter closure of secundum atrial septal defects using the HELEX septal occluder. Am Heart J. 2006;151:1129. e7-11. 13. Jones TK, Latson LA, Zahn E, Fleishman CE, Jacobson J, Vin-cent R, et al. Results of the U.S. multicenter pivotal study of the HELEX septal

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occluder for percutaneous closure of secundum atrial septal defects. J Am Coll Cardiol. 2007;49:2215–21. 14. Kazmouz S, Kenny D, Cao QL, Kavinsky CJ, Hijazi ZM. Transcatheter closure of secundum atrial septal defects. J Invasive Cardiol. 2013;25(5):257-64. 15. Pinto R, Jain, S, Dalvi B. Transcatheter closure of large atrial septal defects in children using the Left atrial disc engagement— disengagement technique (LADEDT)—technical considerations and short term results. Catheter Cardiovasc Interv. 2013;82:935-43. 16. Fu YC, Cao QL, Hijazi ZM. Device closure of large atrial septal defects: technical considerations. J Cardiovasc Med (Hagerstown). 2007;8:30-3. 17. Spies C, Boosefeld C, Schrader R. A modified Cook sheath for closure of a large secundum atrial septal defect. Cathet Cardiovasc Interven. 2007;70:286-9. 18. Wahab HA, Bairam AR, Cao QL, Hijazi ZM. Novel technique to prevent prolapse of the Amplatzer septal occluder through large atrial septal defect. Cathet Cardiovasc Interven. 2003;60:543-5. 19. Dalvi BV, Pinto RJ, Gupta A. New technique for device closure of large atrial septal defects. Cathet Cardiovasc Interven. 2005;64:102-7. 20. Kammache I, Mancini J, Ovaert C, et al. Feasibility of transcatheter closure in unselected patients with atrial septal defects, using Amplatzer devices and a modified sizing balloon technique. Cathet Cardiovasc Interven. 2011;78:665-74. 21. Wahab HA, Almossawy A, Al Bitar I, Hijazi ZM. Tips and tricks to prevent prolapse of the Amplatzer septal occluder through large atrial septal defects. Cathet Cardiovasc Interven. 2011;78:1041-4. 22. Hill SL, Berul CI, Patel HT, Rhodes J, Supran SE, Cao QL, et al. Early ECG abnormalities associated with transcatheter closure of atrial septal defects using the Amplatzer septal occluder. J Interven Cardiol Electrophysiol. 2000;4:469-74. 23. Suda K, Raboisson MJ, Piette E, Dahdah NS, Miró J. Reversible atrioventricular block associated with closure of atrial septal defects using the Amplatzer device. J Am Coll Cardiol. 2004;43:1677-82. 24. Levi DS, Moore JW. Embolization and retrieval of the Amplatzer septal occluder. Cathet Cardiovasc Interven. 2004;61:543-7. 25. Shirodkar S, Patil S, Pinto R, Dalvi B. Successful retrieval of migrated Amplatzer septal occluder. Ann Ped Cardiol. 2010;3:83-6. 26. Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv. 2004;63:496-502. 27. Jain S, Pinto R, Dalvi B. Use of contrast during echocardiography to diagnose cardiac perforation after device closure of atrial septal defect. Catheter Cardiovasc Interv. 2014. doi: 10.1002/ccd.25373. (Epub ahead of print). 28. Tomar M, Khatri S, Radhakrishnan S, Shrivastava S. Intermediate and long-term follow-up of percutaneous device closure of fossa ovalis atrial septal defect by the Amplatzer septal occluder in a cohort of 529 patients. Ann Ped Cardiol. 2011;4(1):22-7. 29. Knepp MD, Rocchini AP, Thomas R, Aiyagari RM. Long-term follow up of secundum atrial septal defect closure with the Amplatzer septal occluder. Congenit Heart Dis. 2010;5:32-7.

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17 Renal Stenting: Rationale and Techniques Sanjay Tyagi, Subhendu Mohanty, Dhruv Tyagi

INTRODUCTION Renovascular hypertension represents a secondary and potentially remediable form of hypertension. Elevated blood pressure is only one of a broad array of pathophysiologic consequences that are associated with decreased renal perfusion.

ETIOLOGY Common causes of RAS are: 1. Atherosclerosis is responsible for 70–90% of all renovascular stenotic lesions. It is often associated with lesions in aorta, coronary, cerebral and peripheral arteries. 2. Fibromuscular dysplasia is a non-atherosclerotic, noninflammatory disease that most commonly affects renal arteries in young. Medial fibroplasia is the histological finding in nearly 80– 5% of all cases of FMD. This type occurs in females and commonly involves both the renal arteries. It has characteristic “string of beads” appearance. Bilateral disease occurs in 60% of patients (Fig. 1). Takayasu’s arteritis is the commonest cause of RAS in children and young adults in India and Southeast Asia. RAS is seen in 34–85% of patients with Takayasu’s arteritis, orifice and proximal segment are involved and stenosis is often bilateral (Table 1). Other rare causes of RAS include William’s syndrome, neurofibromatosis, postradiation therapy, retroperitoneal fibrosis, etc.

CLINICAL CLUES TO THE DIAGNOSIS OF RAS Various clinical clues pointing toward RAS include: yy Onset of hypertension before the age of 30 years or severe hypertension after the age of 55 years yy Accelerated, resistant or malignant hypertension

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yy Development of new azotemia or worsening renal function after administration of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blockers (ARB) agent yy Unexplained atrophic kidney or size discrepancy between kidneys greater than 1.5 cm yy Sudden unexplained pulmonary edema yy Unexplained renal dysfunction, including starting renal replacement therapy yy Multivessel coronary artery disease yy Unexplained CHF yy Refractory angina with hypertension.

CLINICAL IMPACT OF RAS 1. Hypertension: This occurs due to hypoperfusion of the kidney stimulating renin-angiotensin system, causing classic RVH. In atherosclerotic RAS, this may cause acceleration of pre-existing essential hypertension. 2. Cardiac destabilization syndrome: Renal artery stenosis may exacerbate coronary ischemia and CHF by peripheral arterial vasoconstriction and/or volume overload. CHF may occur gradually due to hypertension causing diastolic dysfunction and later systolic dysfunction and often CHF. 3. Renal dysfunction: Progressive vascular occlusion leads to tissue hypoxia, vascular rarefaction, inflammatory injury and tissue fibrosis. Continued renal hypoperfusion leads to ischemic renal dysfunction. This was traditionally thought to be due to severe RAS of both the kidneys or RAS of solitary-functioning kidney. Several studies have challenged the conventional wisdom and suggested that revascularization of unilateral RAS can improve or stabilize renal function and decrease proteinuria.

WHEN THERE IS RAS Important considerations are: 1. What degree of stenosis → RVH/ischemic nephropathy? 2. Is it the cause of hypertension? 3. Is it the cause of renal insufficiency? 4. Will treatment improve either? Selecting patients for renal artery stenting who actually will benefit from revascularization shall also decrease the unnecessary complications inherent with any interventional procedure.

ENDOVASCULAR MANAGEMENT OF RAS Indications for Intervention for Atherosclerotic RAS 1. Failure to adequately control blood pressure with a good three-drug antihypertensive regimen

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Figure 1: Renal artery stenosis due to medial fibromuscular disease before and after balloon angioplasty showing good improvement

Table 1: Three major forms of renal artery disease Cause

Age (in years)

Location of lesion and appearance

Natural history

Atherosclerosis >50

Proximal 2 cm; branch Progression in 50% disease rare often to total occlusion

Aortoarteritis

Proximal main renal artery

16 yr) follow-up. Patient is normotensive

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Table 4: Randomized controlled trials for revascularization versus medical therapy in atherosclerotic RAS Study Scottish and Newcastle Renal Artery Stenosis Collaborative Group (1998) Dutch Renal Artery Stenosis Intervention Study Cooperative Group (2000) STAR (2009)

Population 135 participants >40 years, hypertension, RAS > 50%

Intervention PTRA and medical therapy vs medical therapy alone

Findings Significant fall in BP after PTRA in bilateral RAS only

No difference in 106 participants, PTRAA and medical therapy BP or renal funchypertension, RAS > 50% vs medical tion outcomes between groups therapy alone

Stent placement had no impact on renal function. Significant complications with procedures ASTRAL (2009) 806 participants, PTRAA with or No difference in BP, renal funcwithout stenthypertension ing and medical tion or mortality RAS > 60% between groups uncertainty as therapy vs medical therapy to benefit of alone revascularization CORAL (2013) 947 participants, PTRAA with No difference in hypertension stenting and incidence of CV and CKD, medical therapy and renal events or RAS > 80% (or vs medical all-cause mortality. 60–80% with therapy alone 2 mm Hg improvepressure gradiment in systolic BP ent) in stent group 140 participants, CrCl < 80 mL/min, RAS > 50%

PTRAA with stenting and medical therapy vs medical therapy alone

CONCLUSION Renovascular hypertension is the most common cause of secondary hypertension. In our country aortoarteritis is the most common cause of RVH in patients less than 40 years of age and atherosclerosis accounting for the majority in patients older than 40 years of age. Whereas balloon angioplasty is still the method of choice for the treatment of FMD and aortoarteritis; stent implantation is indicated in ostial atherosclerotic RAS. However, randomized controlled trials have not proven a beneficial outcome of atherosclerotic RAS revascularization compared to medical management. Currently, PTRA for severe atherosclerotic RAS is indicated only in patients with the highest risk presentations such as flash pulmonary edema, rapidly declining renal function and severe resistant hypertension. Results of PTRA are very gratifying in younger patients with RAS due to FMD and aortoarteritis. These patients show marked improvement in hypertension after angioplasty.

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SUMMARY Renal artery stenosis (RAS) is considered to be one of the more frequent causes of secondary arterial hypertension. It can also present as renal failure (ischemic nephropathy), or congestive heart failure (CHF). The common causes of RAS are atherosclerosis, aortoarteritis (Takayasu’s disease) and fibromuscular dysplasia (FMD). Atheromatous RAS is associated with increased incidence of cardiovascular events and increased cardiovascular mortality. There is a dilemma regarding role of revascularization in RAS as atherosclerosis, hypertension and renal insufficiency coexist commonly. Recent evidence from large clinical trials has led clinicians away from recommending interventional revascularization toward aggressive medical management. There is no current rationale for “drive-by” interventions. Hence, careful patient selection for intervention is required, with focus on intervening only in patients with the highest risk presentations such as flash pulmonary edema, rapidly declining renal function and severe resistant hypertension. Severe (>80%) bilateral RAS or stenosis due to a solitary functioning kidney may also be considered for revascularization. Careful attention to technique is essential for good result and to minimize the complications. Revascularization of a stenosed renal artery may be associated with better control of hypertension, unstable angina and CHF. Best response to angioplasty is seen in FMD, followed by aortoarteritis and atherosclerosis. Severity of RAS and, most importantly, underlying renal disease affect outcome after successful correction of RAS. Recent studies have shown that renal fractional flow reserve assessment and elevated baseline brain natriuretic peptide (BNP) levels closely correlate with hypertension improvement after angioplasty. Renovascular disease is also present in about 10–40% of patients with endstage renal disease. Pediatric renovascular hypertension (RVH) in our country is caused by aortoarteritis (≥90%), followed by FMD. At this age angioplasty is especially useful in providing long-term freedom from antihypertensive medications, besides preserving renal function.

SUGGESTED READINGS 1. Böhlke M, Barcellos FC. From the 1990s to CORAL (Cardiovascular Outcomes in Renal Atherosclerotic Lesions) Trial Results and Beyond: Does Stenting Have a Role in Ischemic Nephropathy? Am J Kidney Dis. 2015. pii: S0272-6386(14)01538-8. 2. George JC, White CJ. Renal artery stenting: lessons from ASTRAL (Angioplasty and Stenting for Renal Artery Lesions). JACC Cardiovasc Interv. 2010;3(7):786-7. 3. Chen W, Kayler LK, Zand MS, Muttana R, Chernyak V, DeBoccardo GO. Transplant renal artery stenosis: clinical manifestations, diagnosis and therapy. Clin Kidney J. 2015;8(1):71-8. 4. Jenks S, Yeoh SE, Conway BR. Balloon angioplasty, with and without stenting, versus medical therapy for hypertensive patients with renal artery stenosis. Cochrane Database Syst Rev. 2014;12:CD002944.

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5.

Chrysant SG. Treatment of hypertension in patients with atherosclerotic renal artery stenosis, updated. Postgrad Med. 2014;126(7):59-67. 6. Riaz IB, Husnain M, Riaz H, Asawaeer M, Bilal J, Pandit A, et al. Metaanalysis of revascularization versus medical therapy for atherosclerotic renal artery stenosis. Am J Cardiol. 2014;114(7):1116-23. 7. Weber BR, Dieter RS. Renal artery stenosis: epidemiology and treatment. Int J Nephrol Renovasc Dis. 2014;7:169-81. 8. Jennings CG, Houston JG, Severn A, Bell S, Mackenzie IS, Macdonald TM. Renal artery stenosis-when to screen, what to stent? Curr Atheroscler Rep. 2014;16(6):416. 9. Marshall RH, Schiffman MH, Winokur RS, Talenfeld AD, Siegel DN. Interventional radiologic techniques for screening, diagnosis and treatment of patients with renal artery stenosis. Curr Urol Rep. 2014;15(6):414. 10. Meyers KE, Cahill AM, Sethna C. Interventions for pediatric renovascular hypertension. Curr Hypertens Rep. 2014;16(4):422. 11. Zeller T, Macharzina R, Rastan A, Beschorner U, Noory E. Renal artery stenosis: Up-date on diagnosis and treatment. Vasa. 2014;43(1):27-38. 12. Gulati AS, Patnaik AN, Barik R, Kumari R, Srinivas S. Renal angioplasty for atherosclerotic renal artery stenosis: Cardiologist’s perspective. J Postgrad Med. 2013;59(4):289-99. 13. Sattur S, Prasad H, Bedi U, Kaluski E, Stapleton DD. Renal artery stenosis—an update. Postgrad Med. 2013;125(5):43-50. 14. Chrysant SG. The current status of angioplasty of atherosclerotic renal artery stenosis for the treatment of hypertension. J Clin Hypertens (Greenwich). 2013;15(9):694-8. 15. Textor SC, Lerman LO. Renal artery stenosis: medical versus interventional therapy. Curr Cardiol Rep. 2013;15(10):409. 16. Meier P. Atherosclerotic renal artery stenosis: update on management strategies. Curr Opin Cardiol. 2011;26(6):463-71. 17. Colyer WR, Eltahawy E, Cooper CJ. Renal artery stenosis: optimizing diagnosis and treatment. Prog Cardiovasc Dis. 2011;54(1):29-35. 18. Lao D, Parasher PS, Cho KC, Yeghiazarians Y. Atherosclerotic renal artery stenosis—diagnosis and treatment. Mayo Clin Proc. 2011;86(7):649-57. 19. White CJ. Catheter-based therapy for atherosclerotic renal artery stenosis. Circulation. 2006;113(11):1464-73. 20. Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid DM, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med. 2014;370(1):13-22. 21. Tyagi S, Singh B, Kaul UA, Sethi KK, Arora R, Khalilullah M. Balloon angioplasty for renovascular hypertension in Takayasu’s arteritis. Am Heart J. 1993;125(5Pt1):1386-93. 22. Tyagi S, Kaul UA, Satsangi DK, Arora R. Percutaneous transluminal angioplasty for renovascular hypertension in children: initial and long-term results. Pediatrics. 1997;99(1):44-9.

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18 Retrieval of Foreign Bodies During Cardiac Catheterization Vijay Trehan, Sanjeev Kathuria

INTRODUCTION The removal of foreign bodies from the heart and vasculature has shifted from the domain of the radiologist and even the thoracic and vascular surgeon to interventional cardiologist and, in turn, from the radiographic suite or operating room to cardiac catheterization laboratory. Interventional procedures to retrieve devices are useful additions to the skill set of endovascular specialists. These objects have been previously classified as long and skinny and round and slippery (Fig. 1).1 Every endovascular specialist will, at some time or another, be confronted with the problem of a device that has malfunctioned, fractured, or migrated and requires removal.

Figure 1: Percutaneous devices currently used by interventional cardiologists and radiologists

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Coronary artery stent migration and subsequent retrieval are the most commonly reported device misplacements because these are the devices most commonly used, but the incidence is still less than 0.5%.2 Some of the devices, physicians may encounter, are listed in the Classifications of Intravascular Foreign Bodies sidebar. The reasons for migration of devices are numerous, but the most common is a misjudgment of the relative size of the device and the intended site of placement. Coronary stents are the exception because these are mostly dislodged by calcified plaque before or during placement. Different methods of retrieval are needed for each type of object. This article discusses methods for non-surgical foreign body retrieval, interventional procedures for removing malfunctioned, fractured or migrated devices.

Long and Skinny yy Segment of central venous catheter yy Fragment of inferior vena cava (IVC) filter yy Fractured guidewire yy Balloon and/or tip of angioplasty catheter yy Migrating stents.

Round and Slippery Bullets and shotgun pellets Embolization coils Ureteric and bile duct calculi Atrial septal occluders Pressure balls and beads.

BACKGROUND The incidence of device loss during percutaneous interventions has significantly declined in recent years (improvement in equipment design and technology, universal use of premounted stents). However, device loss still occurs and it could represent a hard experience because the operator may not be familiar with retrieval techniques and equipment and these latter are not so frequently used. Most devices that are lost during percutaneous coronary intervention (PCI) are stents and rarely wire tip fragments, balloons and balloon-fragments.

RETRIEVAL DEVICES There are many kinds of commercially available snares and graspers for retrieval. However, it is easy to make a loop snare with a standard 5F angiographic catheter and a 180 cm, 0.018 inch underwire (Figs. 2A to C). This is our most commonly used snare. Mallmann et al.3 reported 100% success using this type of device, but its usefulness was well known before this recent

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Figure 2A: A selection of loop snares. From the top, a simple loop snare (i) comprising a 5F, 0.038 inch endhole Cobra 2 catheter and a 0.018 inch, 180 cm long guidewire. This has the advantage of being able to enlarge to fit differently sized vessels. The loop can be moved independently of the catheter tip by pushing or pulling on one of the ends of the guidewire. This loop must be preloaded before the catheter is inserted into the vessel. The second loop snare (ii) is from an endoscopy set. This is designed to be positioned by the endoscope tip, and the snare is of limited size and has no intrinsic steerability. The third snare (iii) is from a Cook Medical (Bloomington, IN) IVC filter retrieval set. This is designed to fit the IVC and engage a hook on the superior aspect of the IVC filter. It is difficult to use in curved vessels. The lowermost snare (iv) has the same loop as the top snare, except the apex of the guidewire loop has been kinked with forceps. This makes it possible to afterload the snare once the catheter is adjacent to the foreign body. The kink allows more aggressive deflection of the snare to either side by alternately pushing or pulling one of the wire guide ends

publication. The advantages of this type of snare are that it has a variable size loop and that it is inexpensive. If the end of the loop is kinked with forceps, this snare can be deflected to either side more predictably. The other advantage is that the angiographic catheter has a shaped tip (most commonly a Hick or Cobra 2 shape) and, usually, better translational torque than a commercial snare. Commercial devices include 0.038 inch single-arm forceps, snares and graspers for IVC filter removal, stone retrieval baskets and loop snares designed for embolization coil retrieval (Fig. 3). There are several cleverly designed forceps and graspers for laparoscopic use, but they are generally too short, rigid and large in terms of caliber for endovascular use. Although the concept of grasping forceps is attractive, in most cases, it is easier to grasp the wall of the cavity or vessel rather than the foreign body itself. In small tubes such as the bile duct or ureter, commercial stone baskets or a simple balloon

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Figure 2B: Loop snares of different size

Figure 2C: First device used for the retrieval of endovascular foreign

bodies

catheter are effective. In the case of the bile duct, a stone just needs to be ejected into the duodenum. Ureteric stones can be delivered through a nephrostomy or per urethra. Most of the foreign bodies in the airways and upper alimentary tract are removed endoscopically without the assistance of endovascular specialists. Urethral foreign bodies usually damage the posterior urethra. This subject was reviewed by Forde et al.4 Retrieval devices are available in small sizes which fit with any catheter or sheath used for diagnostic procedure. The use of guide catheters or large sheaths depends on the size

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Figure 3: Tools available for foreign body retrieval have rapidly evolved in the past decade

of the device to retrieve. Nitilol Goose-neck snares have no sharp edges, but very smooth and flexible, so extremely safe for intravascular use. Forceps and baskets have rigid tips and can potentially grasp the vessel wall next to the foreign body and require more caution and experience. Snares can be effectively used when the foreign body or the device has free and/or located on a guidewire. Frequently, endovascular lost device should be manipulated by wires or catheters (pigtail or different shape) into another position until it moves to a more favorable position for snaring (from a perpendicular position to a parallel position to the vessel). These maneuvers can also complicate the procedure of retrieval because of uncontrolled embolization (following the blood flow direction).

Prerequisites to Attempting the Retrieval yy Foreign body retrieval from the vascular space involves introduction system of the retrieval, or grabbing, mechanism contained in a “carrier grabbing mechanism at the distal end of the carrier catheter is catheter”, activated by a control mechanism that extends out of, or is part of the proximal end of the catheter. Proximal mechanism moves the distal retrieval mechanism in and out of the carrier catheter and opens and closes the retrieval mechanism. yy Long sheaths with radio-opaque bands at their distal tips are very helpful for precise positioning. They should be available in at least 85 cm lengths and in a variety of diameters, up to and including at least 16F, as part of the standard retrieval equipment. These large sheaths are available from a variety of manufacturers. yy The back-bleed valves with a flush port are fixed as part of the larger diameter long sheaths, while some of the smaller diameter long sheaths have detachable back bleed/flush

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valves. A detachable back-bleed valve has the advantage of allowing even the most irregularly shaped foreign body to be withdrawn completely out of the proximal end of the sheath without having to remove the sheath from the vascular system, Tuohy back-bleed valves.

METHODS In almost every case it is possible to remove the foreign body without resorting to open operation, in some cases, a large and rigid object can be captured and brought to a superficial site where simple surgical removal under local anesthesia is possible. Occasionally intracardiac devices such as stents can become entangled during migration5 or retrieval and in these cases a surgical approach from the right atrium is preferable. The best time to remove a device is as soon as possible after it becomes unwanted. This axiom applies to IVC filters as well as other devices. Intravascular objects become covered with endothelium rather quickly and if the foreign body becomes incorporated with the vessel wall, it may not be possible to engage or remove it without causing significant endothelial damage.6 In the case of large-caliber devices, such as atrial septum occluders, there is a risk of aortic or large branch vessel thrombosis, and usually, open or laparoscopic surgery is required.7 It is not uncommon to see pieces of IVC endothelium attached to long dwelling IVC filters that have close sections in contact with IVC endothelium (Figs. 4A to C). Sections of silicone catheters from venous access devices may become closely applied to the wall of the pulmonary artery and cardiac chambers. This makes it difficult or impossible to engage the tubing with a conventional snare. In this situation provided the tubing is flexible, a catheter can be passed beneath the tubing near a less fixed portion and a snare used to complete the capture (Figs. 5A and B). The steps in removal are deciding what to capture the foreign body with, positioning the retrieval system, engaging the foreign body, and bringing the retrieval device and foreign body to the retrieval systems point of entry. It is very important to consider how the foreign body is engaged, as it may not be possible to extract a long and skinny object that may not bend easily unless it is captured near one end (Figs. 6A and B). Consideration should be given to the delivery method of the foreign body; it may be easier to pull a stent or catheter through the tissues to the puncture site than to insert a very large sheath. For extravascular foreign bodies, a combination of fluoroscopy and computed tomography may be useful.8 If bare delivery is planned, the access site should be planned so that forceps can be used to ensure that the foreign body is not lost at the access site (Fig. 7). The most frequently lost device is stent, slipping of the delivery balloon in the coronary circulation. The stent may

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Figures 4A to C: When an IVC filter with cross-links becomes deeply embedded in the wall of the IVC; removal of the filter requires moderate force and will result in shreds of endothelium at the site of removal. (A) A CT endovascular reconstruction confirmed deep embedding of the central filter struts of an OptEase IVC filter (Cordis Corporation, Bridgewater, NJ). (B) An axial CT image showed that the endothelium covers a closed section of the filter limbs. (C) The venogram after removal shows a ragged collection of endothelial tags that had previously covered the filter limbs

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Figures 5A and B: In this patient, a long section of Hickman catheter (Bard Peripheral Vascular, Inc., Tempe, AZ) tubing was retained when the catheter fractured during removal. As one end was embedded in a small branch pulmonary artery and the other in the right ventricle, a catheter was passed behind the Hickman tubing, replaced with a guidewire, and snared from the opposite side of the tubing. The images show the loop snare around the wire guide before removal (A); once the capture was complete, the assembly was withdrawn (B). Traction should only be applied to the snare to avoid pulling the wire guide through the loop. This technique is only possible if the foreign body is flexible and will bend. It avoids unnecessary manipulation in the right ventricle

A

B

Figures 6A and B: Intracardiac migration of a self-expanding nitinol stent. A coronal CT reconstructions show the stent lying across the tricuspid valve (A). Cardioversion was administered by an eager cardiologist because of ventricular tachycardia caused by attempts to capture the stent in the right atrium, and the stent migrated to the pulmonary artery as a result. This made capture of the stent much easier, but if the procedure had failed, subsequent surgery would have been more complicated. Using a simple loop snare, the stent was captured near one end (B) and moved gently to the IVC. The tricuspid valve should be treated with great care to avoid damage to the valve and subsequent tricuspid incompetence

stripped free of the delivery balloon while it is being advanced into a diseased artery. After unsuccessful attempts to advance the stent through the target lesion (particularly in calcified and tortuous lesions), the stent may become stuck within the lesion when withdrawn back, the stent may come free of the balloon. After unsuccessful advancement of the stent, withdrawing the system back into guiding catheter, the proximal edge of the stent may catch the guide catheter tip and the stent may be

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Figure 7: Migration of an ALN Optional IVC filter (ALN, Bormes les Mimosas, France) to the left brachiocephalic vein during planned retrieval. Control of this filter was lost when the grasper failed to function correctly. As a result of actions to keep the filter from entering the right ventricle, it became positioned in the left brachiocephalic vein with buckled legs. Although a large-bore catheter was inserted from the left jugular vein, retrieval through this side proved impossible. Using a pair of simple loop snares and two buddy wires, the filter was retrieved inverted to the right jugular vein where it was extracted with forceps percutaneously

Figure 8: If stent is lost distally with a wire still across can probably best be left in situ and gradually expanded from low profile to normal ballooning

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Figure 9: If stent is lost proximally, with a wire still across the retrieval of the stent can be attempted by crossing the stent with a small balloon, inflating the balloon distally to the stent and retrieving guiding catheter, balloon wire and the stent all together. Retrieval of lost stent with the “Two Wire Technique”

A

C

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Figures 10A to D: (A) Dislodged stent on the wire; (B) A second wire is advanced through the stent struts or beside the stent; (C) Twisteing the two wire together, the twisted end can trap the stent; (D) Withdraw the two wires with the stent to guiding catheter then the whole system (catheter, wires and stent)

stripped from the balloon. The risks for stent loss during PCI include patients-related factors; equipment-related factors and operator-related factors.9 Stents are designed to remain at sites within the vascular system. It might be difficult to remove them because of their size and rigidity. The first consideration with lost stents is to evaluate if it is possible to deploy the stent at the loss position or to move

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Figure 11: If stent is lost proximally without a wire across goose-neck snaring can be attempted to retrieve the stent, leaving a safety wire beside

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Figures 12A to C: Migration of a Palmaz iliac stent (Cordis Corporation). This stent was intended for the left common iliac vein but migrated to the IVC as it was ballooned. To ensure the guidewire remained through the stent, the wire guide was advanced and entered the right ventricular outflow tract. A small-diameter angioplasty catheter was passed along the guidewire and through the stent; the balloon was then inflated to stop further migration (A). The initial plan was to reconfigure the proximal end of the stent to allow reinsertion in the left common iliac vein. A loop snare was passed over the inflated balloon to avoid the loop of the snare from becoming caught on the bare stent ends (B). When it became obvious that the stent could not be positioned in the common iliac vein, a decision was made to “park” the stent permanently in the right brachiocephalic vein and use a 25-mm angioplasty balloon to lock the stent in place (C). Follow-up at 1 year shows the stent is securely in place without any sequelae.

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it to a stable and safer alternate site. The weigh risks associated with the retrieval maneuver, such as permanent vascular wall trauma, vessel peroration or rupture, against the benefit to the patient from the percutaneous procedure. The rescue technique used for the retrieval of incorrectly positioned stents depends in great degree on the type of stent involved (self- or balloonexpandable, size, radio-opacity, flexibility, compressibility, rigidity, the radial expansion force) (Figs 8 to 11). As an alternative to removal of a misplaced stent can be re positioned where it will be innocuous. The final resting place should be where branch vessels are not compromised and the stent can be securely fixed without the risk of further migration (Figs 12A to C).

CONCLUSION Every interventionist will, at some time or the other, be confronted with the problem of device loss, fractured or migration. Endovascular retrieval of foreign bodies and misplaced devices is a simple technique, and there is a large array of instruments available for this purpose. For most situations, a simple loop snare is as effective and at a far lower cost than commercial snares. In most cases, open or even laparoscopic surgery can be avoided. It is important to remember that although no job is too small, some jobs are too hard. In the latter case, the interventionist can always either leave it alone or resort to open surgery.

REFERENCES 1. Bako B. Foreign body retrieval. Presented at the Interventional Radiology Society of Australasia; 2005; Queesntown, New Zealand. 2. Adair JD, Harvey KP, Mahmoood A. Inferior vena cava filter migration to right ventricle with destruction of tricuspid valve: a case report. J Trauma. 2008;64:509-11. 3. Mallman CV, Wolf KJ, Wacker FK. Retrieval of vascular foreign bodies using a self-made snare. Acta Radiol. 2008;49:1124-8. 4. Forde JC, Casey RG, Grainger R. An unusual penpal: case report and literature review of posterior urethral injuries secondary to foreign body insertion. Can J Urol. 2009;16:4757-9. 5. Hussain F, Moussa T. Migration of an embolized deployed stent from the left main with subsequent crushing: a new use for the IVUS catheter? J Invasive Cardiol. 2010;22:E19-22. 6. Jahrome AKH, Stella PR, Leijdekkers VJ, Guyomi SH, Moll FL. Abdominal aortic embolization of a Figulla atrial septum occlude device, at the level of the celiac axis after an atrial septal defect closure: hybrid attempt. Vascular. 2010;18:59-61. 7. Collacchio G, Scianneli V, Palena G, Coggia M. Total laparoscopic intra-aortic foreign body retrieval. Eur J Vasc Surg. 2008;35:737-8. 8. Amoretti N, Hauger O, Marcy PY, Hovorka I, Lesbats-Jacquot V, Fonquerne ME, et al. Foreign body extraction from soft tissue by using CT and fluoroscopic guidance: a new technique. Eur Radiol. 2010;20:190-2. 9. Brilakis ES, Best PJ, Elesber AA, et al. Incidence, retrieval methods and outcomes of stent loss during percutaneous coronary intervention: a large single-centre experience. Catheter Cardiovasc Interv. 2005;66:333-40.

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19 Nuclear Cardiology: Basics and Beyond Prasanta Kumar Pradhan, Shashwat Verma, Amitabh Arya

INTRODUCTION Cardiovascular events remain one of the major causes of morbidity and mortality globally. These cardiovascular events can be predicted early by various radioisotopic procedures, which have been evolved since more than four decades from simple radionuclide ventriculography, i.e. equilibrium radionuclide angiography (ERNA) or multi-gated acquisition (MUGA) to present day single photon emission computed tomography (SPECT)/computed tomographic coronary angiography (CTCA) and positron emission tomography (PET)/ CTCA myocardial perfusion and metabolism of myocytes along with luminal narrowing of coronary arteries and their fusion. It seems the fusion imaging with SPECT, PET and CTCA might play a greater role being a better screening protocol for intermediate probability of coronary artery disease (CAD) for diagnosis and prognosis of stable CAD. Similarly, stressors have evolved from physical to pharmacological that too with vasodilators from oral dipyridamole, then IV dipyridamole and presently IV adenosine. Various protocols of stress procedure have evolved with time, which significantly reduce duration of the study and decrease radiation burden. Nuclear cardiology comprises a number of studies, viz. yy Myocardial perfusion imaging (MPI) yy Metabolic imaging yy Ventricular imaging yy Receptor imaging yy Apoptosis imaging. Amongst them, MPI is the most widely used nuclear medicine procedure pertaining to cardiology and it constitutes almost half of all nuclear medicine procedures annually. It is performed with the help of a gamma camera using SPECT technology. It is a simple noninvasive imaging modality

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rou-tinely used in the diagnosis and for assessing the prognosis of CAD. MPI is gated to ECG so as to assess the function of the left ventricular (LV) myocardium. MPI gives a 3D image of the perfusion distribution of the LV myocardium. The clinical success of gated MPI SPECT relies on an understanding of the physics and technical aspects of SPECT imaging, as well as the technical limitations and quality assurance requirements of the system.

HISTORY OF MYOCARDIAL PERFUSION IMAGING Planar MPI used to produce a 2D image of a 3D organ, which used to be obscured by the underlying structures resulting in under reporting and loss of image resolution. Single photon emission computed tomography on the other hand gives us a 3D representation of the perfusion of the myocardium. It allows separation of target regions from overlying structures and therefore has improved diagnostic accuracy over planar imaging. The sensitivity of CAD detection has been shown to be far superior with SPECT (93%) than with planar imaging (77%) because of following reasons (Figs. 1 and 2).1 yy Improved resolution yy Ability to differentiate overlying and underlying tissues yy Improved sensitivity and specificity of diagnosis yy Ability to reconstruct images in same orientation irrespective of cardiac position yy Ability to reconstruct images in a format comparable with other cardiological images.

Figure 1: Planar views

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Figure 2: Planar left anterior oblique image of Tl-201 MPI showing visually and semiquantitatively significant fill in that is redistribution of Tl201 implying severe ischemia in anterior wall and moderate fill in that is redistribution in inferior wall that is moderate ischemia in an asymptomatic peripheral vascular disease patient having underlying CAD

Gated MPI SPECT The cardiac cycle is divided into various frames with the help of the software and the data/counts corresponding to different phases or intervals of the cardiac cycle are acquired from R wave to R wave. Gated MPI SPECT scans have increased temporal resolution. In a gated acquisition, counts from each phase of the cardiac cycle are associated with a temporal frame within the computer. Reconstruction of each interval of a gated MPI SPECT into a tomographic image set allows for visual or quantitative estimation of functional parameters, such as myocardial motion and thickening. Areas of scar have absent or diminished motion and thickening. Areas with decreased activity due to attenuation will show normal motion and thickening. Gated MPI SPECT wall motion is often visualized using bulls eye plots and allows the reporting physician to distinguish between fixed defects from artifacts. Gated SPECT is also used to calculate the end-diastolic volume (EDV) and end-systolic volume (ESV), and as a result, calculate the left ventricular ejection fraction (LVEF).2 Gated MPI SPECT is not possible in case of changes in heart rate may be due to patient anxiety or arrhythmia or due to technical problems (Fig. 3).

THE PREREQUISITES FOR MPI— MACHINE AND MATERIAL The Gamma Camera It is the imaging system for most of the nuclear medicine procedures and named because of imaging of emitted radiation (emission imaging) from the organ of interest or whole body.

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Figure 3: ECG Gated SPECT

There is a large, relatively thin (9–25 mm) sodium iodide scintillation crystal that is doped with a small amount (~0.7%) of thallium to form NaI (Tl). It has density of 3.67 g/cm3 and a moderate response time of 230 nanoseconds. The crystal is optically coupled to an array of photomultiplier tubes (PMT), which detect light and are used to measure the position and energy of the incident photon. The light photons are then viewed by all of the PMTs depending on their proximity to the point of interaction between the gamma ray and scintillation crystal. By measuring the amount of light detected by each PMT, the event can be localized to a relatively high degree of accuracy (Fig. 4).

Collimators The gamma rays, which are emitted from the patient travel in various directions and cannot be focused. Hence, a collimator is used to selectively absorb or transmit gamma rays into the detector. The collimator is made of a lead plate with several holes in it with thick septa between the holes. Only those gamma rays travelling in a particular direction to the holes are transmitted with rest of the rays being absorbed by the lead septa. The direction, diameter and length of the holes influence the sensitivity and resolution of the image.

Data Acquisition It is done with the help of multiple detectors mounted with the collimators. The detectors rotate around the patient to acquire the counts from the injected radioactivity, which is transformed into the image by the camera circuitry. Generally, a 180° data acquisition [from 45° right anterior oblique (RAO) to 45° left anterior oblique (LPO)] is preferred to 360° data acquisition in both single and multiple-headed gamma

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Figure 4: The gamma camera with its components (Adapted from Kathryn Adamson. Principles of myocardial SPECT imaging. Integrating Cardiology for Nuclear Medicine Physicians. New York:Springer-Verlag Berlin Heidelberg; 2009. pp. 191-211.)

camera systems. The avoidance of posterior projections lessens noise contamination due to significant attenuation and decreased image resolution owing to the greater distance between the heart and the detector.3 A 180° acquisition is preferred for nonattenuation-corrected images because of better spatial resolution, higher contrast and less attenuation. To reduce artifacts due to attenuation, a scintillation camera with attenuation correction hardware and software may be used. Either a step-and-shoot acquisition with 32 or 64 stops separated by 3–6° or continuous acquisition may be used. The duration of acquisition at each stop varies with the protocol and radiopharmaceutical that is used (Fig. 5).4-6

Image Orientation With the help of the reconstruction software available, the images obtained by the gamma camera are processed and displayed in various projections. They are namely short axis (image perpendicular to the long axis of the heart), vertical long axis (VLA) and horizontal long axis (HLA) slices, which are oriented at 90° angles to each other (Fig. 6).

Interpretation The software displays the images in the slices as described above. The stress and rest images are aligned row-wise for direct comparison amongst each other (Fig. 7) (Table 1).

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Table 1: Interpretation of myocardial perfusion images in stress and rest Perfusion

Stress image

Rest image

Interpretation

Reduced

Normal

Ischemia

Reduced

Reduced

Hypoperfused

Absent

Absent

Infarction

Normal

Normal

Normal

Figure 5: 180° circular and elliptical orbits

Source: Kathryn Adamson. Principles of myocardial SPECT imaging. Integrating Cardiology for Nuclear Medicine Physicians. New York: Springer-Verlag Berlin Heidelberg; 2009. pp. 191-211.

Figure 6: Image orientation

High-risk Markers on Myocardial Perfusion Imaging yy Extent of infarcted myocardium. yy Transient ischemic dilatation (Fig. 7) yy Increased lung uptake with Thallium-201 only yy Low ejection fraction (EF). Both uncorrected and corrected data should be reviewed to minimize the likelihood of misinterpretation. Because misregistration of the attenuation correction map from

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Figure 7: Summary display of a normal MPI along with polar plot and quantitative functional parameters

Figure 8: Ischemia quantification

CT and the emission data is a potential source of artifacts, a fused image demonstrating the relation of these two datasets should be reviewed before evaluation of the attenuation correction emission data.6 All these visual and semiquantitative para-meters for ischemia (Figs. 8 and 9) and functional parameters like LVEF, ESV, EDV, systolic thickening can be seen in (Fig. 10) following images of a symptomatic CAD patient and summary page in Figure 11 which is combined.

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Figure 9: Ischemia anterior, lateral and inferior wall

Figure 10: Polar map with functional parameters in same patient demonstrating fall in ejection fraction in stress and abnormal thickening

Factors Af fecting MPI Images Hepatobiliary Clearance and Gut Uptake 99mTc sestamibi is excreted through the hepatobiliary system into the duodenum and bowel.7 Exercise stress studies result in lower liver activity when compared with rest images whereas pharmacological stress tests result in higher liver and gut uptake with slower clearance than exercise stress imaging that’s why adenowalk is the best form of stress protocol if patient can do little exercise.

Photon Attenuation It means that those photons emitted from the organ, which have not reached the detector due to the overlying tissue or due to low energy are considered as attenuated. It will result in

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Figure 11: Summary displaying moderate fill in i.e. ischemia in anterior, lateral and inferior wall with semiquantitative polar plot

a loss of resolution and reduced contrast in the projection data and consequently the reconstructed data. Males have decreased activity in inferior wall because of diaphragmatic attenuation where as females have relatively decreased activity in the anterior wall, apex, or lateral portion of the heart, secondary to breast attenuation. To perform MPI a patient is intravenously given a radiopharmaceutical i.e. a pharmaceutical labeled with a small amount of radioactivity or tracer, which emits gamma rays. The ideal tracer would have the following desirable properties: yy Distribute in the myocardium in linear proportion to blood flow yy Efficient myocardial extraction from the blood on the first pass through the heart yy Stable retention within the myocardium during the scan yy Rapid elimination allowing repeat studies under different conditions yy Be readily available yy Good imaging characteristics, e. g. emit gamma rays with energy of 100–200 keV.1

Advantages of 99mTc sestamibi over 201Tl chloride: yy Higher quality images due to the higher energy photons and photon flux yy Shorter half-life than 201Tl

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yy Larger amounts of radiopharmaceutical to be administered with lower radiation dose to the patient yy Imaging can be delayed for a short while after injection and scans can also be repeated without loss of sensitivity.

IMAGING PROTOCOLS IN MYOCARDIAL PERFUSION IMAGING Introduction Imaging protocols for stress MPI include: yy Performing the stress procedure yy Choice of radiopharmaceuticals yy Data acquisition process yy Data analysis for reporting yy Logistics of patient attendance, such as inability to attend on two separate days yy Logistics of the department or nuclear cardiology laboratory.

Stress Procedure There are various stress protocols well described in published literature and one need to choose appropriately i.e. physical exercise or pharmacological. Mostly vasodilator stress is preferred nowadays with adenosine intravenous infusion because of its proven equivalence to exercise and its safety factor by 10 times in comparison to exercise or dobutamine (Tables 2 and 3).

Limitations of Physical Stress yy Who cannot perform exercise yy Medications which blunt the heart rate response (such as beta-blockers and calcium channel blockers) yy Peripheral vascular disease yy Musculoskeletal abnormalities.

Indication for Dobutamine (Inotropic Stress)— Contraindication for Adenosine (Vasodilator Stress) yy Severe bronchospasm yy Pulmonary disease i.e. bronchial asthma with rhonchi and crepitations yy Systemic hypotension (systolic BP < 90 mm Hg )

Table 2: Types of stress Physical

Pharmacological

Treadmill test (TMT)

Vasodilators—Adenosine Dipyridamole Regadenoson

Bicycle ergometer

Inotropic—Dobutamine Arbutamine

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Table 3: Contraindication and limitations of physical stress Contraindication

Limitation

Unstable angina with recent (< 48 hours) angina

Pulmonary complaints

CHF

Peripheral vascular disease

Acute myocardial infarction

Musculoskeletal abnormalities

Systolic BP > 220 and diastolic BP > 120 mm Hg

Lack of motivation.

Pulmonary hypertension

Not comprehending the exercise protocol.

Untreated life-threatening arrhythmias, Advanced atrioventricular block (without a pacemaker) Acute myocarditis, acute pericarditis, severe mitral or aortic stenosis HOCM {BP: blood pressure; CHF: Congestive heart failure; HOCM: Hypertrophic obstructive cardiomyopathy}.

yy Severe mitral valve disease yy Hypersensitivity to dipyridamole or adenosine yy Patients requiring methylxanthine containing medications and steroid to control their bronchospasm yy Patients with advanced (second- or third-degree) atrioventricular block.

Indication for Adenosine (Vasodilator Stress)— Contraindication for Dobutamine (Inotropic Stress) In patients with ventricular tachyarrhythmias (Fig. 12). yy Aortic stenosis (mild and moderate degree) yy Unstable angina yy Aortic aneurysm yy Hypertrophic obstructive cardiomyopathy (HOCM) yy Recent pulmonary embolism yy Deep vein thrombosis (DVT) yy Active endocarditis, myocarditis and pericarditis yy Systolic blood pressure > 220 mm Hg and diastolic > 120 mm Hg yy On beta blockers. Dobutamine is usually a secondary pharmacological stressor and is used in patients who cannot undergo exercise stress and have contraindications to using vasodilator stress. It increases regional myocardial blood flow and results in direct β1 (beta) and β2-receptor stimulation, with a dose-related increase in heart rate, blood pressure and myocardial contractility (Table 4).8 Dobutamine infusion begins with 5 ug/kg/min for 3 minutes,

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Figure 12: Adenosine stress protocol

Table 4: Pharmacologic stressors and their properties Adenosine

Dipyridamole

Dobutamine

Half-life

< 10 sec

30–60 minutes

2 minutes

Mean time to peak coronary flow velocity

55 sec

6.5 minutes

10 minutes

Onset of action

Few seconds

2 minutes

1–2 minutes

Side effects requiring medical intervention

0.6%

16%

5%

then increased to 2-8 times at 3 minutes interval till maximum of 40 ug/kg/min is achieved or when patient has achieved 85% maximal predicted heart rate and continue infusion of another one minute. If target heart rate is not achieved,the Atropine injection in dose of 0.5–1 mg given.

Indication for Terminating a Stress Procedure yy Patient requests to stop yy Technical/mechanical difficulties yy Suspected myocardial infarction yy Serious dysrhythmias yy Drop in systolic BP > 40 mm Hg yy Severe angina yy ST elevation > 1 mm without history of myocardial infarction yy Poor perfusion yy Tired or shortness of breath (SOB) yy Claudication yy Supraventricular tachycardia (SVT) yy Systolic blood pressure> 240 mm of Hg,diastolic blood pressure > 120 mm of Hg yy Exercise induced bundle branch block (BBB).

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Protocol for Stress—Rest Imaging One-day imaging protocol: In this technique a smaller dose of 7–10 mCi (250–370 MBq) of radiotracer is injected followed by three times dose of 21–30 mCi (740–1110 MBq) 2–3 hours later on the same day. Two-day imaging protocol: This is the protocol of choice in patients who are overweight and in whom a relatively lower dose of radiopharmaceutical will result in suboptimal images. In this, radiotracer doses of 10–15 mCi for rest and 10–15 mCi for stress are used (Box 1). Same day stress and rest 99mTc acquisition protocol: This protocol is useful for patients who have low likelihood of heart disease. There is a definite advantage of this protocol that if a preliminary analysis of the “stress” images reveals normal perfusion to all myocardial walls; then there is no need for further imaging for rest. Same day rest and stress 99mTc acquisition protocol: In this protocol, the rest study is done first followed by stress. The relative advantage of this approach is that anxious patients may be prepared whereby they are gradually introduced to the stress component of the study, and they are therefore better prepared and less likely to move during data acquisition (Table 5).

What is the Basis of Myocardial Perfusion Imaging? yy Cardiac metabolism is aerobic. yy The oxygen extraction by the myocardium is maximum at rest. yy Increased myocardial oxygen uptake is achieved by increased blood flow. yy Insufficient blood flow will produce ischemia. yy Flow is pulsatile and most flow to the myocardium occurs in diastole and at high heart rates, diastole shortens more.

Box 1: One day and two day protocols One day protocol  Ill and elderly patients  Inpatients  Patients with high likelihood of CAD  Coming from too far  Patients who need urgent report  Renal patients on dialysis Two day protocol  Busy department/scheduling issues  Obese patients  Low likelihood of CAD (Adapted from Kathryn Adamson. Principles of myocardial SPECT imaging. Integrating Cardiology for Nuclear Medicine Physicians. New York: Springer-Verlag Berlin Heidelberg; 2009. pp. 191-211.)

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Table 5: Advantages and disadvantages of one day and two days stress-rest procedures Same day stress—rest protocol Advantage Convenient Quicker diagnostic information Good choice for patients with low likelihood for CAD If stress study is normal then no need for rest Limitation Reversibility may be underestimated due to presence of remaining activity from the stress study Stress—rest sequence may result in an increased number of ischemic segments incorrectly identified as fixed defects Two day stress rest protocol Advantages Good quality image Less noise and more contrast Same amount of radioactivity administered for both stress and rest If stress is normal then no need for rest study Ability to image obese patients Better patient scheduling Less radiation burden to patient and staff Good for patients with low likelihood for CAD Limitation Patient has to come on different days Slight delay in diagnosis

Ef fect of Coronary Stenosis on Flow A stenosis is not considered significant until it is 70% but coronary flow reserve drops at 40–60% stenosis. Resting flow is maintained up to 90% stenosis. Oxygen consumption is higher in subendocardium. It is the first area to be affected in ischemia. Significant CAD is defined angiographically as CAD with greater than or equal to 70% diameter stenosis of at least one major epicardial artery segment or greater than or equal to 50% diameter stenosis of the left main coronary artery.

Indications of Myocardial Perfusion Imaging yy Diagnosis of CAD yy Evaluation of known coronary disease, location and extent of ischemia yy Evaluate the effectiveness of medical therapy yy Risk stratification postmyocardial infarction yy Preoperative evaluation in high risk cases for major noncardiac surgery in patients with known CAD9,30 yy Assessment after coronary artery bypass grafting yy Determine the cause of change in symptom pattern in patients with known CAD.

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Myocardial Perfusion Imaging and Risk Assessment in Various Sub Groups yy Acute coronary syndrome (ACS) yy Acute myocardial infarction yy Preoperative evaluation in high risk cases30 yy Diabetes mellitus yy Postrevascularization.

Acute Coronary Syndrome and Myocardial Perfusion Imaging A normal stress MPI in stable angina carries less than 1% annual risk of cardiac death. The extent and severity of ischaemia predicts outcome in chronic stable CAD and stratifies patients with indeterminate stress ECG. A negative study has a low risk of subsequent cardiac events when injected at rest up to 6 hours post pain. Those with an intermediate to high pre-test probability of CAD are considered the best candidates for MPI whereas it is deemed inappropriate for patients with low pre-test probability. In patients with stable symptoms, a normal stress Tc-99m sestamibi SPECT MPI was associated with a very low risk of death or nonfatal myocardial infarction (0.6% annually) in contrast to a 12-fold higher event rate (7.4% annually) in patients with abnormal images (fixed or reversible defects). A normal stress MPI study carries similar satisfactory outcomes in stable angina patients with significant angiographic disease. In the absence of markers of ischemia or obvious abnormalities on initial ECG (possible ACS), rest Tc-99m sestamibi perfusion imaging is appropriate and can reduce unnecessary hospitalizations among patients without acute ischemia. The negative predictive value (NPV) of SPECT MPI to exclude myocardial infarction in patients with acute chest pain ranges from 99% to 100% and the NPV for excluding future cardiac events during medium-term follow-up is approximately 97%.10 A small fixed perfusion defect indicates an excellent prognosis, and probably low benefit from revascularization. On the other hand, patients with markers of increased risk (number and severity of myocardial perfusion defects, transient LV dilation and increased tracer lung uptake in Thallium-201 only) could be referred for coronary angiography and revascularization.

Acute Myocardial Infarction and Myocardial Perfusion Imaging Nuclear imaging was first used in the detection of myocardial infarction more than 30 years ago. MPI provides a direct assessment of coronary blood flow and thus, appears to be an optimal tool for identifying patients with ACS, who initially

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appear at low risk based on ECG or clinical characteristics. In acute ischemic syndromes, myocardial hypoperfusion occurs before the onset of LV dysfunction, ECG changes, clinical symptoms and myocardial necrosis. Rest MPI becomes abnormal simultaneously with myocardial hypoperfusion.

Diagnostic Value of Acute Rest Myocardial Perfusion Imaging Acute rest myocardial perfusion imaging (ARMPI) has only moderate sensitivity for diagnosis of acute myocardial infarction as regional hypoperfusion also occurs in scar, unstable angina and even in chronic multivessel disease. Because the negative predictive value of ARMPI is very high (99%), patients with negative rest perfusion imaging have a very low probability of an ACS and can be safely discharged from the emergency department. Infarct size, which in itself is an important predictor of outcome, can easily be quantified by ARMPI in acute myocardial infarction. Similarly the size of myocardial perfusion abnormalities also correlates with longterm prognosis.11

Diabetes Mellitus and Myocardial Perfusion Imaging Not only do diabetics have a greater complexity and extent of vascular disease in general but they also have the additional disadvantages of having multisystem dysfunction involving endothelium, platelets and renal and neurological systems. The pathophysiology driving the disease process can be divided into four areas: endothelial dysfunction, platelet and clotting abnormalities, lipid abnormalities, and the consequences of hyperglycemia, including protein and collagen modifications. All four interact with each other to produce systemic organ damage. The consequence of this pathophysiological process on the coronary arterial vasculature is a tendency toward smaller caliber coronary vessels and a more severe diffuse type of coronary disease. Diabetes mellitus, type 2 in particular, has a universally established excessive predilection for CAD irrespective of race, ethnicity, gender or geography. People with diabetes and chronic kidney disease (CKD) are at high risk to both loss kidney function and experience major adverse cardiovascular events. In diabetic patients, myocardial ischemia due to coronary atherosclerosis is typically asymptomatic. More than 25% of type 2 diabetics have severe myocardial ischemia, myocardial infarction, or both, without experiencing chest pain or discomfort.12 This lack of warning symptoms (i.e. angina) during infarction and ischemia may reflect abnormalities in the perception of pain related to autonomic neuropathy. Consequently, multivessel atherosclerotic disease often develops before ischemic symptoms occur.13

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Myocardial Perfusion SPECT in Symptomatic CAD Patients with Diabetes Kang et al. have shown that the sensitivity, specificity and normalcy rates of ECG-gated SPECT stress myocardial perfusion SPECT (MPS) in diabetic patients symptomatic for CAD were not different from those observed in nondiabetic patients.14 They also prognosticated 1,271 diabetic patients with MPS and found an annual cardiac event rate (myocardial infarct or death) of 1–2% in the presence of normal MPS scans, 3–4% in those with mildly abnormal scans, up to more than or equal to 7% for moderately to severely abnormal scans. Giri et al. in a large multicenter retrospective study of 4,755 patients (including 929 diabetic patients with known or suspected CAD) followed for an average of 2.5 years, demonstrated that abnormal stress MPS was an independent predictor for myocardial infarct and cardiac death and that patients with diabetes had higher event rates than patients without diabetes, the highest being for diabetic patients with ischemia (17.1% infarction rate) and for multivessel fixed defect (13.6% cardiac death rate).15

Myocardial Perfusion SPECT in Asymptomatic CAD Patients with Diabetes In patients with diabetes mellitus, there could be several explanations for the lack of presence of chest pain, which include increased threshold of pain sensitivity, psychological denial, or the presence of autonomic neuropathy leading to sensory denervation. The latter seems to be more likely in diabetic patients, because autonomic neuropathy is a common feature of diabetes and in a study conducted by Faerman I et al. showed abnormalities of the autonomic nerve fibers demonstrated histologically in diabetic patients who died after painless myocardial infarction.16 Autonomic neuropathy in diabetics tends to be associated with a severe CAD and abnormality in pain perception is linked to sympathetic denervation as shown by diffuse abnormalities in m-iodobenzylguanidine imaging in silent ischemia.17 The multicenter study on Detection of Ischemia in Asymptomatic Diabetics (DIAD) is a prospective study aimed at defining the prognostic significance of abnormal stress MPS in asymptomatic diabetic patients. Results reveal a 22% prevalence of silent myocardial ischemia, including 5% with severe perfusion abnormalities.18

Role of Positron Emission Tomography Imaging in Coronary Artery Disease The use of positron emitting radionuclides, especially 18F labeled fluorodeoxy glucose (18F-FDG), have increased recently due to its role in oncology. This has paved the way to look for other uses for these agents.

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The use of PET as a noninvasive tool for imaging the heart to look for perfusion defects and viability has already been established.19,20 This has helped us to know the extent of myocardial blood flow, the metabolic changes occurring in the myocardium and changes in the cardiac autonomic innervations in various pathological conditions.

Why PET Rather than SPECT? Myocardial perfusion imaging to look for stress induced ischemia and viable myocardium using gamma rays emitting radionuclides and SPECT technique has been in use for more than three decades. The most commonly used radionuclide being 99mTc labeled with sestamibi or tetrofosmin. Positron emitting radionuclides undergo beta (+) decay resulting in the emission of a positron (mass similar to that of an electron but oppositely charged) which then rapidly combines with a nearby electron undergoing annihilation. This results in the emission of two 511-keV photons, which travel in opposite directions. The basic principle of PET lies in the coincidence detection of these photons in a ring scanner. The spatial resolution of reconstructed clinical PET images is currently in the range of 4–7 mm, and it is superior to conventional nuclear imaging techniques like SPECT.21 With the usage of the combined PET/CT imaging system, this can be further improved to be in the range of 1–2 mm.22 PET also has high temporal resolution, which allows for creation of dynamic imaging sequences. PET is also quantitative in nature, which is made possible because of the readily available correction algorithms for photon attenuation, scatter and random events. This quantitative character of PET can be used in predicting the absolute myocardial blood flow or glucose use. Most PET-CT scanners are now equipped with multislice CT, allowing for measurement of coronary calcium and/or CT coronary angiography in addition to PET imaging procedures. With the usage of contrast enhanced CT angiography, electrocardiogram-gated image acquisition for complementary functional analysis and the addition of respiratory gating for creation of motion-frozen images to reduce breathing artifacts, PET/CT imaging of the cardiovascular system is considered superior to other noninvasive imaging studies of the heart. Also comparative studies with 82Rb PET and 99mTc sestamibi show that PET has greater diagnostic accuracy when compared with SPECT (89% vs 79%) seen in Figure13A and B.4

Myocardial Perfusion Imaging Using Positron Emission Tomography Positron Emission Tomography Perfusion Tracers The most commonly used PET tracers used for myocardial perfusion imaging are listed in Table 6.

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Figures 13A and B: Advantage of PET over SPECT MPI. (A) It shows a fixed defect in the inferior wall on SPECT which is absent on PET, suggesting the presence of a SPECT attenuation artifact. This demonstrates the improved specificity of PET. (B) It shows stress-induced perfusion defects in the anterior and inferolateral walls (arrows), which are more clearly shown in PET rather than SPECT, thus demonstrating the improved sensitivity with PET.

Table 6: Positron emitter radionuclides and their characteristics for PET MPI Tracer

Half-life

Positron range (mm)

Mechanism of uptake

FDA ap- First pass proved extraction (%)

82

Rb

76 seconds

2.6

Na/K ATPase

Yes

65

13

NH3

10 minutes

0.7

Diffusion/ Metabolic trappinga

Yes

80

2 minutes

—

Diffusion( No freely diffusible/not trapped)

100

110 minutes

0.2

Mitochondrial binding

No

NA

110 minutes

0.2

Mitochondrial binding

No

NA

H215O

18

F-FBnTP*

18 Fflupiridaz*

a=Metabolic trapping by energy-dependent process. *=Under clinical trials 18F-FBnTP= F-18-fluorobenzyl triphenyl phosphonium; 18F-flupiridaz=18FBMS747158; FDA=Food and Drug Administration; H2O=Water; NA= Not Applicable NH3= Ammonia; Rb=Rubidium.

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13 NH3 and Rb-82 are utilized regularly in USA though more popular is Rb-82 because it is a generator produced radionuclide, analogous to Tl-201 and ultrashort half-life of 75 seconds. Thus, can be done repeated for rest and stress. H215O is superior to 82Rb and 13NH3, however it is utilized in few laboratories and utilized for research purpose because of high first pass extraction, and because it is metabolically inert and it is freely diffusible across cell membrane. Since the routinely used PET tracers have very short halflife, research for tracers with longer half-life is still undergoing. 18 F tagged with FDG is largely being used in PET for oncological imaging and follow-up. Since 18F has a half-life of 110 minutes, trials are undergoing to tag molecules with this agent and use for cardiac imaging. Two of these tracers are 18F-flupiridaz and 18 F-fluorobenzyl triphenyl phosphonium, which have entered human clinical trials.26-28 Details about these new tracers are discussed in below Table 6.

Protocol for Myocardial Perfusion The total duration of this PET MPI protocol is approximately 35–40 minutes and it is as follows as depicted in Flow Chart 1 (Table 7).25

For Absolute Flow Quantification Coronary flow reserve (CFR) is the ratio of peak myocardial blood flow (MBF) during near maximal pharmacologically induced vasodilatation to resting MBF. CFR is an index of the functional significance of a coronary stenosis. This can be quantified by PET/CT through compartmental modeling of multiframe dynamic acquisitions. Several studies have suggested the prognostic value of quantitative PET measurements of MBF and CFR for progression toward clinically overt CAD14,24 and in idiopathic and hypertrophic cardiomyopathies leading to emphasis on microcirculation and endothelial function.

Myocardial Viability Using Positron Emission Tomography Cardiac viability study is done with 18F-FDG PET tracer. This tracer has a half-life of 110 minutes, positron range of 0.2 mm and is FDA approved. FDG enters the viable cells via glucose transporters and then enters the anaerobic glycolysis cycle. It is metabolized by hexokinase into FDG-6-phosphate, which cannot be further metabolized and thus is trapped in the cell. The basic principle is that even though there are perfusion abnormalities, if the cells are viable they may pick up FDG. This might help in identifying hibernating or stunned myocardium, which are seen as tracer deficient area in perfusion studies but picks up FDG during viability study thus producing a perfusion—viability mismatch (Fig. 14). Immediate intervention, if done, may lead to improvement of these

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Flow Chart 1: Image acquisition protocol for PET perfusion study#

{CTCA—Computed tomographic coronary angiography}. #—This is for stress protocol. For rest imaging the second step is replaced by nitrate/nonnitrate augmented PET tracer injection. *—Radiotracer is injected at this step.

Table 7: Various interpretations of perfusion and metabolic cardiac imaging Perfusion study findings

Viability study findings Final impression

Normal

Normal

Normal

Abnormal

Normal

Mismatch (hibernating myocardium)

Abnormal

Abnormal

Match (nonviable)

Normal

Abnormal

Reverse mismatch (altered myocardial glucose metabolism)

regions. Hence, FDG viability study is considered the gold standard for myocardial metabolic assessment. However, the concordance between nitrate augmented MIBI SPECT and FDG PET is approximately 85–90% in published series.23 Molecular basis: The myocardium utilizes fatty acid as its substrate in the normal state for its energy, but in case of

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Figure 14: A mismatch with reduced rest perfusion (measured by 82 Rb) and preserved metabolism (measured by 18F-FDG) is shown in the inferolateral wall, indicating ischemically compromised but viable hibernating myocardium. (Bottom) A matched perfusion/metabolism defect is shown in the inferior wall, indicating nonviable scar

ischemia (low flow), the myocardium shifts to glucose as energy substrate, which is a protective mechanism since oxidative glycolysis needs lesser oxygen. Hence, glucose uptake is high during ischemia. When radiolabeled glucose is administered during ischemia, it localizes in the myocardium similar to the nonradioactive glucose and emits positrons and metabolic PET scan is obtained. It directly represents metabolic changes in the myocytes in the low flow state. Nuclear cardiology has addressed various diagnostic and prognostic aspects of CAD in various clinical scenarios since several decades. The wealth of information in published literature is enormous which has already empowered the cardiologists and physician for various clinical situations for better decision making in management with coronary intervention or medical management. With the help of newer gamma cameras, radiopharmaceuticals, technologies, software and targeted imaging, nuclear cardiology is at its zenith. The future for nuclear cardiology may lie in its ability to image physiological processes at a molecular level and explore many mechanisms involved in CAD.29 Future trends include Annexin-V apoptosis imaging, imaging for myocardial fatty acid metabolism with iodinated fatty acid analogue, 15-(p-[123I] iodophenyl)-3-(R,S) methyl pentadecanoic acid (BMIPP). In addition, FMISO is a tracer under development for the localization of myocardial hypoxia—useful in assessment of ischemia. CT data may be used to help produce accurate measures of quantitative

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tracer uptake and retention. The ability to coregister SPECT and CTCA data also makes SPECT/CT cameras an ideal tool for hybrid i.e. structural and functional imaging of heart. The development of cardiac CT, especially with hybrid systems including SPECT-CT and PET-CT modalities, may have the potential for adding value to the practice of nuclear cardiology, especially in attenuation correction and delineating hemodynamic significance of even branched coronary arteries like first diagonal branch (D1) or first obtuse marginal (OM1), etc. from fusion imaging of MPI and CTCA.

CONCLUSION Routinely performed radionuclide ventriculography, SPECT and PET are quantitative, noninvasive cardiac imaging techniques that is being increasingly used in risk stratifying and prognosticating each patient prior to clinical decision making in CAD. Despite high single test cost it shows overall cost-effectiveness as it can be used as an “one stop shop” for diagnosing myocardial perfusion abnormalities and viability study. With the inclusion of CT in PET and novel tracers being produced, the role of PET in cardiac imaging will still improve in the near future and it is expected to play greater role besides its present utility in attractive translational research tool in combination with molecular probes i.e. Cell therapy or Gene therapy.

REFERENCES 1. Kathryn Adamson. Principles of myocardial SPECT imaging. Integrating Cardiology for Nuclear Medicine Physicians. New York: Springer-Verlag Berlin Heidelberg; 2009. pp. 191-211. 2. Lee DS, Cheon GJ, Ahn JY, Chung JK, Lee MC. Reproducibility of assessment of myocardial function using gated 99Tcm- MIBI SPECT and quantitative software. Nucl Med Commun. 2000;21:1127-34. 3. American Society of Nuclear Cardiology. Imaging guidelines for nuclear cardiology procedures, part1. Myocardial perfusion stress protocols. J Nucl Cardiol.1996;3(3):G11-5. 4. Hesse B, Tagil K, Cuocolo A, Anagnostopoulos C, Bardiés M, Bax J, et al. EANM/ESC procedural guidelines for MPI in nuclear cardiology. Eur J Nucl Med Mol Imaging. 2005.32(7):855-97. 5. Husain SS. MPI protocols: is there an ideal protocol? J Nucl Med Technol. 2007;35(1):3-9. 6. Strauss HW, Miller DD, Wittry MD, Cerqueira MD, Garcia EV, Iskandrian AS, et al. Procedure Guideline for MPI. J Nucl Med Technol. 2008;36(3):155-61. 7. Peace RA, Lloyd JL. The effect of imaging time, radiopharmaceutical, full fat milk and water on interfering extra-cardiac activity in myocardial perfusion single photon emission computed tomography. Nucl Med Commun. 2005;26:17-24. 8. Iskandrian AS, Verani 1. MS, Heo J. Pharmacologic stress testing: mechanism of action, hemodynamic responses, and results in detection of coronary artery disease. J Nucl Cardiol. 1994;1:94-111. 9. Travain MI, Wexler JP. Pharmacological stress testing. Semin Nucl Med. 1999;29:298-318.

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10. Iskander S, Iskandrian AE. Risk assessment using single photon emission computed tomographic technetium-99m sestamibi imaging. J Am Coll Cardiol. 1998;32:57-62. 11. Ghanem FA, Movahed A. MPI for Risk Stratification in Suspected or Known Coronary Artery Disease: Current Status and Limitations. New York: Springer-Verlag Berlin Heidelberg; 2009. pp. 231-6. 12. Miller TD, Christian TF, Hopfenspirger MR, Hodge DO, Gersh BJ, Gibbons RJ. Infarct size after acute myocardial infarction measured by quantitative tomographic 99mTc sestamibi imaging predicts subsequent mortality. Circulation. 1995;92(3):334-41. 13. Di Carli MF, Hachamovitch R. Should we screen for occult coronary artery disease among asymptomatic patients with diabetes? J Am Coll Cardiol. 2005;45:50-3. 14. National Kidney Foundation. The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI™). [online] Available from www.kdoqi.org. [Accessed March, 2015]. 15. Kang X, Berman DS, Lewin H, Miranda R, Erel J, Friedman JD, et al. Comparative ability of myocardial perfusion single-photon emission computed tomography to detect coronary artery disease in patients with and without diabetes mellitus. Am Heart J. 1999;137(5):949-57. 16. Giri S, Shaw LJ, Murthy DR, Travin MI, Miller DD, Hachamovitch R, et al. Impact of diabetes on the risk stratification using stress single-photon emission computed tomography MPI in patients with symptoms suggestive of coronary artery disease. Circulation. 2002;105(1):32-40. 17. Faerman I, Faccio E, Milei J, Numez R, Jedzinsky M, Fox D, et al. Autonomic neuropathy and painless myocardial infarction in diabetic patients. Histological evidence of their relationship. Diabetes. 1977;26:1147-9. 18. Langer A, Freeman MR, Josse RG, Armstrong PW. Metaiodobenzylguanidine imaging in diabetes mellitus: assessment of cardiac sympathetic denervation and its relation to autonomic dysfunction and silent myocardial ischemia. J Am Coll Cardiol. 1995;25:610-8. 19. Wackers FJ, Young LH, Inzucchi SE, Chyun DA, Davey JA, Barrett EJ, et al. Detection of silent myocardial ischemia in asymptomatic diabetic subjects: the DIAD study. Diabetes Care. 2004;27(8):1954-61. 20. Schelbert HR, Phelps ME, Hoffman E, Huang SC, Kuhl DE. Regional myocardial blood flow, metabolism and function assessed noninvasively with positron emission tomography. Am J Cardiol. 1980;46:1269-77. 21. Weiss ES, Siegel BA, Sobel BE, Welch MJ, Ter-Pogossian MM. Evaluation of myocardial metabolism and perfusion with positronemitting radionuclides. Prog Cardiovasc Dis. 1977;20:191-206. 22. Pichler BJ, Wehrl HF, Judenhofer MS. Latest advances in molecular imaging instrumentation. J Nucl Med. 2008;49 Suppl 2:5S–23S. 23. Bateman TM, Heller GV, McGhie AI, Friedman JD, Case JA, Bryngelson JR, et al. Diagnostic accuracy of rest/stress ECG-gated Rb-82 myocardial perfusion PET: comparison with ECG-gated Tc-99m sestamibi SPECT. J Nucl Cardiol. 2006;13:24-33. 24. Nienaber CA, Ratib O, Gambhir SS, Krivokapich J, Huang SC, Phelps ME, et al. A quantitative index of regional blood flow in canine myocardium derived noninvasively with N-13 ammonia and dynamic positron emission tomography. J Am Coll Cardiol. 1991;17:260-9. 25. Goldstein RA, Mullani NA, Marani SK, Fisher DJ, Gould KL, O’Brien HA Jr. Myocardial perfusion with rubidium-82. II. Effects of metabolic and pharmacologic interventions. J Nucl Med. 1983;24:907-15. 26. Lortie M, Beanlands RS, Yoshinaga K, Klein R, Dasilva JN, deKemp RA. Quantification of myocardial blood flow with 82Rb dynamic PET imaging. Eur J Nucl Med Mol Imaging. 2007;34:1765-74. 27. Yu M, Guaraldi MT, Mistry M, Kagan M, McDonald JL, Drew K, et al.

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NIC Handbook of Interventional Cardiology BMS-747158-02: a novel PET myocardial perfusion imaging agent. J Nucl Cardiol. 2007;14:789-98. 28. Maddahi J, Schiepers C, Czernin J, Sparks R, Phelps M, Huang SC, et al. First human study of BMS747158, a novel F-18 labeled tracer for myocardial perfusion PET: dosimetry, biodistribution, safety, and imaging characteristics after a single injection at rest. J Nucl Med. 2011;52:1490-8. 29. Schindler TH, Nitzsche EU, Schelbert HR, Olschewski M, Sayre J, Mix M, et al. Positron emission tomography-measured abnormal responses of myocardial blood flow to sympathetic stimulation are associated with the risk of developing cardiovascular events. J Am Coll Cardiol. 2005;45:1505-12. 30. Hendel RC, Berman DS, Di Carli MF, Heidenreich PA, Henkin RE, Pellikka PA, Pohost GM, Williams KA. Hendel RC, Berman DS, Di Carli MF, Heidenreich PA, Henkin RE, Pellikka PA, Pohost GM, Williams KA. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging: a report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, the American Society of Nuclear Cardiology, the American College of Radiology, the American Heart Association, the American Society of Echocardiography, the Society of Cardiovascular Computed Tomography, the Society for Cardiovascular Magnetic Resonance, and the Society of Nuclear Medicine. Circulation. 2009;119:e561–e587.

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Index Page numbers followed by ‘f ’ and ‘t’ indicate figures and tables respectively. A Abbott BVS 100 vascular 13 wires 13 Ablation procedure tips 147 Access artery spasm 25 Activated partial thromboplastin time 29 Active backup support 16 endocarditis 280 Acute coronary syndrome 284 Acute myocardial infarction 115, 284 Acute stent thrombosis 201 Adenosine stress protocol 281f Air embolism 238f Allen’s 27 Allopurinol 121 Ambulation 24 Amplatz 17 Amplatzer delivery system 230f Amplatz guides 18 Anatomies during radial approach 24 Angiographic contrast 78 Angioplasty beyond 2 wire 35f Antiplatelet therapy 3 Antiproliferative agents 3 Aortic aneurysm 280 root angiogram 192f, 193f stenosis 280 variants and anomalies 34 Apoptosis imaging 270 Arterial anomalies 26 spasm grades 26 Asahi family of wires 13 ASO embolized to the right ventricle 239f Asymptomatic diabetics 286 Atherosclerotic ostial renal artery stenosis 250f right renal artery stenting 252f Atraumatic catheter 18 Atrial fibrillation 219 Atrial natriuretic peptides 121 Atrial septal defect 221 Atrioventricular block 153, 280

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B Balance middle weight 33 Balloon angioplasty 2 catheter 237f commissurotomy 217 crush stenting technique 169f mitral valvuloplasty 202, 205-206, 211, 214-215, 217 Barbeau’s test 27 Bare metal needle 29 stents 135 Beware of brachiocephalic 34 Bifurcation coronary lesions 159 lesions 149, 160f, 161 stenting strategy 161, 173 Bioabsorbable scaffold 96 polylactide-based polymer 99 stents 66 vascular scaffold 67, 92, 93 Borderline stenosis 251 Boston wires 13 Brachiocephalic 37 Bronchial asthma 279 Burr detachment 154 entrapment 154 movement 146 positioning 145 selection 143 speed 145 C CABG surgery 104 Calcified lesions 148 Calcium channel blockers 117 Cardiac erosion 239 magnetic resonance imaging 114, 115 Cardiomyocyte death 110 edema 109 swelling 113 Carotid angioplasty 182 artery occlusive disease 182 spasm 198 stenosis 182 dissection 200 endarterectomy 182 perforation 201 stent cell geometry 189f stenting step-by-step procedure 190

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stent selection 188 Case selection 221 Catheter preparation 80 Central layered circle 81 Changing the delivery sheath 234 Chronic total occlusions 15, 70, 148 Cilostazol 121 Cineangiograms 1 Cine-film demonstrating balloon mitral valvuloplasty 214f Claudication 281 Clinical impact of RAS 243 Coaxial technique 247 Collimators 273 Complications of renal angioplasty 251 Compression of the other artery 30 Contrast encephalopathy 200 Cordis corporation 268 wires 13 Core-to-tip design 8 Coronary angiography and adjunctive techniques 113 angiography documenting 45f artery bypass graft 95 disease 15, 93 lesions 176f looks 62 stent migration 259 catheterization 1 flow reserve 289 guidewire classification 9 commonly used 10 components of 7 core element 7 crossing 7 distal tip 7 flexibility 6 manipulation 12 performance 9 prolapse tendency 6 selection of 10 steeribility 6 support 7 tactile feedback 7 torque control 6 trackability 6 interventions 1 stents 3 Cougar XT 10 Cullotte stenting 179 stenting technique 168f Cyclosporine 121

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D Data acquisition 273 Dedicated bifurcation stents 170 Deep vein thrombosis 280 Delivery sheath and device 229, 232 Device embolization 225, 239 Diabetes mellitus and myocardial perfusion imaging 285 Diabetes patients 103 Diagnosis of RAS 242 Diagnostic catheters 17 Dilator assisted technique 234, 236 Disability-adjusted life years 94 Distal embolization 199 protection devices 185 protection during carotid angioplasty 185f tip 80f UPLM intervention 178 Dobutamine 279 Dynaglide foot pedal 139f E Eccentric atherosclerotic renal artery stenosis 250f Echocardiographic evaluation 204 Echogenicity analysis 96 Effect of coronary stenosis on flow 283 revascularization on hypertension 253 Eisenmengerised ASD 222 Electrocardiography 115 Endothelial blisters 109 Endovascular foreign bodies 261f management of RAS 243 Entrapped rotablation burr 155 EPD management 195 Exenatide 121 External carotid artery occlusion 201 F Factors affecting mpi images photon attenuation 277 Fibromuscular dysplasia 242, 253 Final angiographic evaluation 198 Finet’s law 162f First transcatheter device closure 221 Floppy guidewires 11 Foreign bodies during cardiac catheterization 258 Forte extra support 11 Fractal bifurcation geometry 162f Fractional flow reserve technique procedural details 42 step by step 42 value physiological interpretations 49

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suboptimal hyperemia 49 technical issues 49 G Gamma camera 272 Gated MPI spect scans 272 Gore helex device 228f Guide catheter back-up and control 38 selection 15, 143 Guidewire selection 144 Guidezilla 16 Guiding catheter related complications 252t technique for renal angioplasty 246f catheters used for renal angioplasty 248f H Hausdorf sheath 235f Hooking of coronary 38 Horizontal long axis 274 Hydrophobic coatings 9 Hypercholesterolemia 113 Hyperemia 52 Hyperemic pullback runs 56 Hyperperfusion syndrome 200 Hypertrophic obstructive cardiomyopathy 280 I Igaki-Tamai device 96 scaf fold 96 Image interpretation calcified plaque 83 evaluation of stents 85 fibrous plaque 83 lipid plaque 83 neoatherosclerosis 85 neointimal hyperplasia 85 normal vessel 82 red thrombus 84 stent apposition 85 thin cap fibro-atheroma 85 tissue prolapse 85 white thrombus 85 Incidence and clinical implications 109 Inotropic stress 279, 280 Inoue balloon catheter 211, 213f Instant wave-free ratio clinical practicality 52t compared to FFR 52 how to measure 52 implementation 55 physiological basis 50 tandem lesions and virtual stenting 55 In-stent restenosis 149

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Interventional cardiologists and radiologists 258f catheterization 1 Intra-arterial diltiazem 26 Intracardiac migration 265 Intracoronary Doppler measurements 114 Intracranial hemorrhage 199 Intraluminal endothelial protrusion 109 Intramyocardial hemorrhage 113 Intraprocedural imaging 225 Intravascular ultrasound basic setup of 61 examination technique 62 history of 60 plaque characterization 62 principle of 61 Intravenous midazolam 26 Iodophenyl 291 J Judkins guide catheters 18 Juxtaostially 17 K Kissing balloon inflations (KBIS) 162 L Lactic-co-glycolic acid 98 LAO projection 209 Left anterior oblique 37f Left circumflex coronary 70 Left internal mammary artery 17, 28 Left main coronary artery calcified lesions 70 complex bifurcation lesions 74 distal lesions 69 in-stent restenosis 70 proximal lad 74 stenosis 68 Lesion-specific indications 148 LMCA stenting 175 Long arterial sheaths 16 Lumen diameter 12 Luminal plugging 109 M MADS stenting technique 161f Magnesium bioabsorbable stent 97 Major adverse cardiac event 93 Maximal hyperemia 55 Measurement of mitral valve annular diameter 207f Medical therapy in atherosclerotic ras 255t Medtronic wires 13 Metabolic imaging 270 Metal allergies 104 Metallic stents 96 Microparticle debris 135f

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Microvascular constriction 113 obstruction 114 Minimal lumen area 64 Mitral balloon valvuloplasty 214 stenosis severity 205, 206t Molecular basis 290 Mother-child catheter techniques 16 Myocardial blood flow 111, 287 blush grade 107 contrast echocardiography 114 perfusion imaging limitations of physical stress 279 stress procedure 279 revascularization 134, 181 territory 109 Myocarditis and pericarditis 280 N Neoatherosclerosis 95 Neuroprotection systems 184 Nicorandil 117 Nitinol 8 Nonattenuation-corrected images 274 Non-distal uplm intervention 177 Nonspecific aortoarteritis 253 Nuclear cardiology basics and beyond 270 O Occlutech balloon 237f figulla flex ii 228, 229 Ohm’s law 50 Optical coherence tomographic imaging hardware 78 image interpretation 82 principles and basics 78 steps in image acquisition 80 Original coronary angiography 71 Origin of renal artery 247t Ostioproximal CTOS 16 P Palmaz iliac stent 268f Passive backup support 16 Pathogenetic components distal atherothrombotic embolization 111 ischemic injury 111 reperfusion injury 111 susceptibility of coronary microcirculation to injury 111 Patient populations for absorb 102 Percutaneous balloon mitral valvuloplasty 205 coronary intervention 15, 108, 175

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mitral balloon valvuloplasty 215, 216t transluminal coronary angioplasty 70, 157, 246 Peri-interventional protocol 190 Persuader 13 Piezoelectric crystal capable 61 Pinocytotic vesicles 109 Plain old balloon angioplasty 134 Planar views 271f Poor perfusion 281 Porcine model 137 Positron emission tomography perfusion tracers 287 Positron emitter radionuclides 288t Post-coronary artery bypass graft 28 Post dilatation 197, 200 Post-percutaneous coronary intervention 94 Postprocedural care 236 Postrevascularization 284 POT technique 163, 167 Preclinical data 102 Predilatation 196 Pre-procedure ultrasound of arm arteries 25 Pressure wire drift 44 Primary percutaneous coronary intervention 107 Proinflammatory cytokines 113 Protocol for myocardial perfusion 289 Protrusion technique 166f Provisional stenting technique 164f Proximal occlusion devices 186 protection device 187f protection devices 186, 187 right coronary artery 46f Pullback gradient 45f Pulmonary disease 279 hypertension 222 Puncture of access artery 28 Q Quick reference burr guide 144t R Randomized clinical trial 101 Rationale renal stenting 242 Receptor imaging 270 Renal artery disease 244t stenosis 244f stenting rationale 242 techniques 242 Renovascular hypertension 242, 255 Rest imaging one-day imaging protocol 282 same day rest and stress 99mTc acquisition protocol 282 two-day imaging protocol 282

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Retrieval devices 259 Retroesophageal right subclavian 34 Reva device 99 Revolutions per minute 141 Rheumatic heart disease 202, 203, 219 heart valve disease 202 mitral stenosis 203 Right brachiocephalic 35f internal carotid artery 184f renal artery and infrarenal aorta balloon angioplasty 254f Risk of stroke in asymptomatic patients 183f Rotablator burr cut inelastic tissue 136f console 138f system failure 154 Rotalink catheter connection 142f Rotational atherectomy 137, 150, 156, 157, 158, 177, 178, 251 RotaWire extra support guidewire 140 floppy guidewire 139f Routine deployment technique 230 Ruptured plaque 65 S Safety wire beside 268f Seldinger’s technique 29 Selecting device size 226 Selection of appropriate balloon size 206 Self-expanding nitinol stent 265f Semiquantitative polar plot 278 Serious dysrhythmias 281 Severe angina 281 Severe bronchospasm 279 Shaping the wire tip 12 Sheathless guides 23 Sheath sizing protocol 25f Short tip guide catheters 17 Single photon emission computed tomography 271 Single venous access 226 Sirolimus drug coating 100 Site of radial artery puncture 29f Slow flow 152 Small arteries 30 Squeezing effect 186 Stainless steel 7 ST-elevation myocardial infarction 49 Stent avulsion 201 deployment 196 mal-apposition 67 Step-by-step atrial septal defect closure 221 Stronger polymer 100 ST-segment elevation myocardial infarction 107

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Subclavian tortuosities 38 Subendocardium 109 Supraventricular tachycardia 281 Systemic embolism 205 Systolic blood pressure 280 T Tailored-approach 183 Takayasu’s arteritis 242, 257 Techniques of device delivery 230 TEE loops 233f Thrombectomy 36f Thrombolysis in myocardial infarction 107, 112 Thrombotic mileu 219 Thrombus burden 107 Thunder 11, 13 Tired or shortness of breath 281 Transbrachial routes 21 Transradial access 24 angiography 38 PCI 23 procedure failure 24 Transseptal puncture 208, 210f technique 207 Traversing the subclavian 32 T-stenting technique 165f Two-stent techniques 170t Typical rheumatic mitral stenosis 203f U Unstable angina 280 UPLM intervention 177, 178, 180 V Various guide catheter curves 19 Vascular access 198, 226 Vasodilators adenosine 117 antithrombotic therapy 118 calcium channel blockers 117 nicorandil 117 sodium nitroprusside 118 thrombolysis 119 Ventricular imaging 270 tachyarrhythmias 280 Verapamil 26 Very late stent thrombosis 95 Vulnerable plaque 183 W Wahab technique 234, 236f Wave intensity analysis 51f Whisper 11 Wiggle 11

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Wilkins score 204t WireClipTM torquer 141f Wire position during equalization of pressure 43f X X-ray chest in a child with atrial septal defect 223 position 209

therapy 182

Y Yellow line, measured FFR 48f Z Zeroing in on crossovers 32 Zinger light 11 marker 11 support 11

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