Cardiac Catheterization and Coronary Intervention (2nd Edition, 2020) [PDF]

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OXFORD MEDICAL PUBLICATIONS



Cardiac Catheterization and Coronary Intervention



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Oxford Specialist Handbooks in Cardiology



Cardiac Catheterization and Coronary Intervention SECOND EDITION



Andrew Mitchell Consultant Cardiologist, Jersey General Hospital, Saint Helier, Jersey; and Honorary Consultant Cardiologist, John Radcliffe Hospital, Oxford, UK



Giovanni Luigi De Maria Consultant Cardiologist, John Radcliffe Hospital, Oxford, UK



Adrian Banning Professor of Cardiology and Consultant Cardiologist, John Radcliffe Hospital, Oxford, UK



1



1 Great Clarendon Street, Oxford, OX2 6DP, United Kingdom Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and in certain other countries © Oxford University Press 2020 The moral rights of the authors have been asserted First Edition published in 2008 Second Edition published in 2020 Impression: 1 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by licence or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above You must not circulate this work in any other form and you must impose this same condition on any acquirer Published in the United States of America by Oxford University Press 198 Madison Avenue, New York, NY 10016, United States of America British Library Cataloguing in Publication Data Data available Library of Congress Control Number: 2019957198 ISBN 978–​0–​19–​870564–​2 Printed and bound in China by C&C Offset Printing Co., Ltd. Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-​to-​date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-​pregnant adult who is not breast-​feeding Links to third party websites are provided by Oxford in good faith and for information only. Oxford disclaims any responsibility for the materials contained in any third party website referenced in this work.







Foreword ‘The only good is knowledge and the only evil is ignorance’ Socrates (469 BC–399 BC) ‘An investment in knowledge always pays the best interest’ Benjamin Franklin (1706–1790) Can the history and techniques of cardiac catheterization really be encompassed in a pocket-sized handbook? Clearly the answer is ‘yes’. This handbook succinctly summarizes the historical advances in d­ iagnostic and therapeutic coronary angiography from its origins in 1929 when Werner Forsmann performed right heart catheterization on himself, through the advent of percutaneous intervention with the first balloon angioplasty by Andreas Gruentzig in 1977, up to the current drug-eluting stent era. The main focus however is the practical applications and techniques of current practice in the catheterization laboratory, including radiation ­protection, vascular access, view selection for diagnostic angiography, and a detailed summary of current interventional techniques and devices. The chapter on complications, including a summary of when such issues are likely to occur and details of how to manage each predicament, ­deserves particular attention. This manual will prove to be a valuable guide to anyone wishing to learn the indications and practical techniques of cardiac catheterization, from ­cardiology trainees and other catheter laboratory personnel as well as serving as a useful quick reference guide for more experienced cardiologists. Professor Patrick W. Serruys, MD Thorax Centre University Hospital Rotterdam, The Netherlands



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Preface This latest edition of Cardiac Catheterization and Coronary Intervention expands on the practical success of the original edition but without losing the main purpose of the book. The text is written to offer a practical guide to coronary angiography and cardiac intervention, incorporating tricks and tips, hints and suggestions for the cardiology trainee learning cardiac catheterization, the nurse, or the technician assisting the case, or the senior cardiologist needing a reminder about certain conditions. Coronary angiography and cardiac catheterization remain a key component of modern cardiac care. Since the first edition of this book, the development of complementary cardiac imaging techniques such as cardiac computed tomography has resulting in more focused and selected patient care allowing targeted revascularization strategies using coronary intervention. The assessment of flow haemodynamics, changes in interventional techniques and stent delivery, as well as revised indications for revascularization mean that the world of interventional cardiology remains a rapidly evolving field. New sections in this edition are included on these topics as well as the role of the heart team, trends in vascular access, and on the use of pressure wire assessment and associated interventional imaging techniques. The challenges faced during primary angioplasty and its clinical and practical difficulties are explored. The book will act as an easily accessible reference for all members of the team in times of need. Using hints and tips from experts in the field, the familiar Oxford Handbook style, and with clear diagrams and illustrations, we expect this guide will remain the standard text for guiding cardiac catheterization and coronary angiography. ARJM GLDM AB November 2019



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Acknowledgements We are grateful for all of the help, support, advice, tips, and tricks from the many wonderful catheter laboratory teams and staff that we have had the honour and pleasure to work with, many of whom will have indirectly contributed to the quality and content of this book. ARJM: dedicated to Claire, Oliver, and Imogen for their continued love and support. GDM: dedicated to Michela and Milena. AB: dedicated to Anne, Amy, and Eve.



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xi



Contents Symbols and abbreviations  xiii Contributors  xvii References  xix 1 Introduction 2 The team 3 Vascular access 4 Cardiac catheterization 5 Specific conditions 6 Coronary angiography 7 Coronary artery bypass graft angiography 8 Percutaneous coronary intervention 9 Additional procedures 10 Complications 11 Post procedure Index  323



1 25 43 71 107 129 165 183 253 277 315







Symbols and abbreviations % cross-​reference M website ACC American College of Cardiology ACT activated clotting time AHA American Heart Association AL Amplatz left ALARA as low as reasonably achievable ALARP as low as reasonably practicable Ao aorta AP anteroposterior AR Amplatz right ASD atrial septal defect BMS bare-​metal  stent BRS bioresorbable scaffold CABG coronary artery bypass surgery CAD coronary artery disease CathLab catheterization laboratory CHIP complex high-​risk indicated patients CPR cardiopulmonary resuscitation CTO chronic total occlusion Cx circumflex DC direct current DES drug-​eluting  stent DOAC direct oral anticoagulant EAPCI European Association of Percutaneous Cardiovascular Interventions ECMO extracorporeal membrane oxygenation EDV end-​diastolic  volume ESV end-​systolic  volume FFR fractional flow reserve fps frames per second GPI glycoprotein IIb/​IIIa inhibitor GTN glyceryl trinitrate Gy gray IABP intra-​aortic balloon pump iFR instantaneous wave-​free ratio



xiii



xiv



S YMBOLS AND ABBREVIATIONS INR



international normalized ratio Ionising Radiation (Medical Exposure) Regulations IRA infarct-​related  artery IV intravenous JL Judkins left JR Judkins right kV kilovolt LA left atrium LAD left anterior descending LAO left anterior oblique LE lead equivalent LIMA left internal mammary artery LMS left main stem LV left ventricular LVEDP left ventricular end-​diastolic pressure mA milliampere MACE major adverse cardiac events MCS mechanical circulatory support MI myocardial infarction MINOCA myocardial infarction with non-​obstructive coronary arteries MR mitral regurgitation OTW over the wire PA pulmonary artery or posteroanterior PCI percutaneous coronary intervention PCWP pulmonary capillary wedge pressure PES paclitaxel-​eluting  stent PET positron emission tomography POBA plain old balloon angioplasty PPE personal protective equipment PTCA percutaneous transluminal coronary angioplasty PVC premature ventricular complex PVR pulmonary vascular resistance RA right atrium RAO right anterior oblique RIMA right internal mammary artery RV right ventricular SCAI Society for Cardiovascular Angiography and Interventions SPECT single-​photon emission computed tomography STEMI ST-​segment elevation myocardial infarction Sv sievert IR(ME)R



S YMBOLS AND ABBREVIATIONS  xv SVG SVR SVT TAVI TLR VF VSD VT WHO



saphenous vein graft systemic vascular resistance supraventricular tachycardia transcatheter aortic valve intervention target lesion revascularization ventricular fibrillation ventricular septal defect ventricular tachycardia World Health Organization







Contributors Dr Angie Ghattas Interventional Cardiologist, University Hospital of Coventry and Warwickshire, Coventry, UK Professor Paul Leeson Professor of Cardiovascular Medicine, University of Oxford, and Consultant Cardiologist, Oxford University Hospitals NHS Foundation Trust, Oxford, UK Professor Nick West Consultant Cardiologist and Clinical Lead for Coronary Intervention, Papworth Hospital, Royal Papworth NHS Foundation Trust, Cambridge, UK



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References Reference textbooks Grossman W (2013). Grossman and Baim’s Cardiac Catheterization, Angiography, and Intervention, 8th edition. Wolters Kluwer. Samady H, Fearon WF, Yeung AC, et al. (2018). Interventional Cardiology, 2nd edition. McGraw-​Hill Professional. Sorajja P, Lim MJ, Kern MJ (2019). Kern’s Cardiac Catheterization Handbook, 7th edition. Elsevier.



Websites Abbott Vascular: M https://​www.cardiovascular.abbott/​us/​en/​home. html American College of Cardiology: M http://​www.acc.org/​ American Heart Association: M http://​www.americanheart.org/​ Boston Scientific: M http://​www.bostonscientific.com/​ British Cardiovascular Intervention Society: M http://​www.bcis.org.uk/​ Cordis: M http://​www.cordis.com/​ European Society of Cardiology: M http://​www.escardio.org/​ Guidant: M http://​www.guidant.com/​ Medtronic: M http://​www.medtronic.com/​ St. Jude Medical: M http://​www.sjm.com/​ Transcatheter Cardiovascular Therapeutics: M http://​www.tctmd.com/​



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Chapter 



Introduction Background  2 Definitions  2 History of cardiac catheterization  3 Indications for cardiac catheterization  4 Indications for coronary angiography  6 Cardiac CT or invasive angiography?  8 Radiology equipment  10 Fluoroscopy and acquisition  12 Radiation safety  14 Dose excess  18 Patient preparation  20 Catheter laboratory preparation  22



1



2



Chapter    Introduction



Background In the last couple of decades, there has been a progressive increase in the provision of invasive cardiology techniques and access to coronary revascularization, particularly percutaneous coronary intervention (PCI). These techniques are largely learnt by apprenticeship with the training guided by the skills and beliefs of the trainer. For the training cardiologist (and also for the fully trained), it is important to have an independent reference guide for performing and interpreting cardiac catheterization and coronary angiography studies. This handbook has been written to provide key points, hints, and tips to the reader in an easily accessible style.



Definitions • Cardiac catheterization is the passage of a catheter into the left and/​ or right heart to provide diagnostic information about the heart and/​or blood vessels. • Coronary angiography is a procedure where contrast material is injected into the coronary arteries under X-​ray guidance in order to define the coronary anatomy and determine the degree of luminal obstruction. It remains the standard investigation for patients with known or suspected coronary artery disease (CAD).



History of cardiac catheterization



History of cardiac catheterization The first human heart catheterization studies were performed using a modified urinary catheter that was inserted via the internal jugular vein into the right atrium. This work was initially performed on cadavers but, by performing the procedure on himself using fluoroscopic control and a mirror, Werner Forssmann was able to take a chest X-​ray and document the first right heart catheterization study in 1929. The work was taken up by André Cournand in 1941, who catheterized the right ventricle and performed more detailed right heart studies. In 1947, Zimmerman performed the first simultaneous left and right heart catheterization study. A few years later in 1953, Sven-​Ivar Seldinger developed his eponymous technique for percutaneous vascular access (% p.44). Forssmann, Cournand, and co-​ worker Dickinson Richards were awarded the Nobel Prize in Physiology or Medicine for their contributions in 1956. Mason Sones, working at the Cleveland Clinic, determined a new technique for selective coronary angiography in 1959. In 1977, Andreas Grüntzig performed the first coronary angioplasty in Zurich on a severe proximal left anterior descending coronary artery lesion in a 38-​year-​old man (% p.184). The first coronary artery stents were implanted in 1986. Since the early 1990s, there has been a rapid and successful development of percutaneous coronary intervention (PCI) procedures and devices.



Further reading Cournand A. Catheterization of the right auricle in man. Proc Soc Exp Biol Med 1941; 46: 462–​66. Forssmann W. The probing of the right heart. Clin Wkly J 1929; 8: 2085–​87. Gruntzig AR. Transluminal dilatation of coronary artery stenosis. Lancet 1978; 1: 263. Sones FM. Cine coronary arteriography. Mod Concepts Cardiovasc Dis 1962; 31: 735–​38.



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4



Chapter    Introduction



Indications for cardiac catheterization Cardiac catheterization is usually indicated to identify the degree and extent of CAD and to complement data obtained from non-​invasive imaging modalities. This includes the evaluation of left ventricular function, the assessment of valvular heart disease, pericardial disease, congenital heart disease, and cardiomyopathies. In general terms, the only absolute contraindication to cardiac catheterization is refusal of patient consent; however, there are a number of relative contraindications.



Relative contraindications • Acute kidney injury. • Pulmonary oedema. • Known radiographic contrast allergy. • Uncontrolled hypertension. • Active gastrointestinal haemorrhage. • Acute stroke. • Untreated coagulopathy. • Untreated (or unexplained) febrile illness.



Indications for cardiac catheterization



5



6



Chapter    Introduction



Indications for coronary angiography Coronary angiography is primarily used to determine the coronary anatomy and to identify any luminal stenoses. It provides some information on the nature of the stenosis, such as the extent of coronary ­atherosclerosis (% p.154), the presence of thrombus (% p.202), coronary spasm (% p.152), myocardial bridging (% p.163), and coronary dissection (% p.300). Coronary angiography remains the standard investigation for determining coronary anatomy but the technique is limited by its inability to see beyond the coronary lumen. Coronary angiography is therefore a procedure of ‘lumenography’ or ‘lumenology’.



Class 1 indications The current American College of Cardiology (ACC)/​American Heart Association (AHA) class 1 indications for coronary angiography include the following: • In patients with known or suspected coronary heart disease who have stable angina with: • Canadian Cardiac Society class 3 or 4 angina on medical treatment. • High-​risk criteria on non-​invasive testing. • Patients who have been resuscitated from sudden cardiac death or who have sustained ventricular tachycardia (VT) or non-​sustained polymorphic VT. • In patients with unstable coronary syndromes with: • High or intermediate risk for adverse outcome with unstable angina refractory to initial adequate medical therapy or recurrent symptoms after initial stabilization. • High risk for adverse outcome in patients with unstable angina. • High-​or intermediate-​risk unstable angina that stabilizes after initial treatment. • Initially low short-​term-​risk unstable angina that is subsequently high risk on non-​invasive testing. • In patients with acute ST myocardial infarction: • As a prelude to primary PCI within 12 hours of the onset of symptoms. • As a prelude to revascularization in patients with cardiogenic shock within 18 hours of onset of shock. • In patients with recurrent (stuttering) episodes of symptomatic ischaemia. • In patients recovering from myocardial infarction who have ischaemia at a low level of workload with electrocardiogram (ECG) changes (≥1 mm of ST depression).



Coronary angiography during valve assessment • Diagnosing coronary artery stenoses can be difficult using non-​invasive techniques in patients with significant valvular pathology. • It remains routine practice therefore to consider diagnostic coronary angiography in symptomatic patients who are undergoing assessment for valve surgery.



Indications for coronary angiography



• The small risks of the additional procedure are believed to be outweighed by the potential consequences of missing severe coronary disease. • The information obtained should also be considered an important part of overall surgical risk assessment. • For example, the addition of coronary artery bypass surgery (CABG) to aortic valve replacement in elderly patients significantly increases the operative risk. • In patients with mitral valve disease, undiagnosed coronary disease may be the mechanism responsible for mitral regurgitation. • Practice varies according to institution but a useful guide would be to perform coronary angiography in all patients over the age of 40 years with one or more cardiac risk factors (e.g. diabetes mellitus, hypertension, family history), in asymptomatic patients with suspected myocardial ischaemia, and in patients with left ventricular systolic dysfunction. • In patients with endocarditis, coronary angiography is only recommended before surgery in those with multiple cardiac risk factors or in those with evidence of coronary embolization.



Other indications There are other groups of patients who may benefit from cardiac catheterization and/​or coronary angiography. These include: • Patients with typical angina in spite of antianginal medication. • Those with atypical chest pain and recurrent hospitalization. • Patients who are unsuitable for non-​invasive testing. • Patients with heart failure of unknown aetiology. • Pilots and bus drivers with borderline investigations. • Patients presenting with chest pain soon after coronary revascularization. It is extremely unusual for asymptomatic patients with no evidence of cardiac ischaemia to undergo coronary angiography.



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Chapter    Introduction



Cardiac CT or invasive angiography? Two main factors have contributed to make invasive coronary angiography the technique of choice for assessment of coronary anatomy so far: • Good spatial resolution (allowing accurate imaging of small structures, such as coronary vessels). • Good time resolution (allowing accurate imaging of moving structures, again such as coronary vessels). Initially, no non-​invasive technique could match these standards. However, this has changed with cardiac computed tomography (CT) allowing image acquisition of up to 320 slices in one rotation, covering the complete volume of the heart in one short breath-​hold. These features account for significant improvement in both spatial and time resolution. At the time this book was written, both European and American guidelines recommended functional non-​invasive tests (cardiac magnetic resonance, stress echocardiography, single-​photon emission computed tomography (SPECT), or positron emission tomography (PET)) as a first-​line strategy to assess ischaemia in patients with suspected CAD and to guide decisions about revascularization. It should, however, be acknowledged that new evidence about coronary CT-​derived fractional flow reserve and perfusion CT is likely to evolve this. The evidence collected so far has confirmed a consistent high sensitivity and high negative predictive value of cardiac CT (which can go up to 100%). The specificity and consequently positive predictive value, however, are significantly lower (1000). • Large body mass index. • Previous coronary stenting (CT accuracy for instent restenosis decreases with stent size 1.4



40



Mild stenosis



1.5



70%).



Quantification of stenoses



Fig. 6.17 How angiography may underestimate disease severity. Two views of the same artery taken in different projections (shown schematically) generate different visual estimates of lesion severity. MLD, minimum luminal diameter; RD, reference diameter



Fig. 6.18  Reduction in vessel diameter stenosis compared with cross-​sectional area. The diagram illustrates the problem of inter-​observer variability with moderate lesions (those with diameter stenosis 40–​80%); lesions do not generally become flow-​limiting until they exceed 70% diameter/​90% area stenosis



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Quantitative coronary angiography • Computer software has been developed to aid assessment of severity of coronary stenoses (and measurement of structures during angiography); most modern catheter laboratories are equipped with such programs, many allowing online (live) analysis during the procedure. • Quantitative coronary angiography requires calibration, usually with the known diameter of the catheters being used in the study. • Sophisticated edge-​detection algorithms define the opacification of the lesion and compare minimum luminal diameter with the vessel reference diameter either side; the diameter stenosis, length of lesion, vessel calibre, and (by mathematical assumptions) area of stenosis may be calculated.



Alternative imaging modalities When angiographic imaging leaves uncertainty as to the severity of a given lesion, further information may be sought by interrogation of the lesion by adjunctive methods. The two methods in common use are: • Pressure wire—​measurement of fractional flow reserve to give further physiological information (% p.212). • Intravascular imaging—​direct imaging from within the vessel to give further anatomical information (% p.210). Both methods add to the interpretation of coronary angiograms, but often time and financial constraints may limit their use in routine practice.



Quantification of stenoses



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Chapter 6   Coronary angiography



Tips for interpretation Orientation and nomenclature • Inexperienced operators may find difficulty in reliably discriminating the LAD from the Cx. A simple rule to remember is that in all views of the LCA, the Cx is the vessel closest to the spine. • The angle of projection can also be worked out using the assumption that if the spine is on the left then the view is a RAO projection, and if the spine is on the right of the image then the image is a LAO projection. • When viewing angiographic images it is important to look at arteries in more than one imaging plan. For example, an oval lesion may appear severe in one view but normal in another. • Branches of the LAD running towards the Cx territory (the lateral wall) are termed diagonals; those running towards the right ventricle (and hence the interventricular septum) are termed septals. • Side branches of the Cx running towards the LAD territory (the lateral wall of the left ventricle) are termed obtuse marginals; the final marginal may be called the terminal marginal. There is often a Cx branch that continues towards the base of the heart in the atrioventricular (AV) groove; this is referred to as the AV Cx. • The RCA often has one or more right ventricular (RV) marginal branches that pass anteriorly towards the septum, but supply predominantly RV myocardium.



Normal vessel anatomy • The LAD usually tapers as it courses distally; the normal proximal LAD calibre is 3.5–​4.0 mm in men, and 3.0–​3.5 mm in women. • The Cx also tapers, but not until its mid-​portion and usually after the first obtuse marginal bifurcation. • The RCA is usually of uniform calibre until its bifurcation into the PDA and the posterior ventricular wall branch (at the ‘crux’).



Common pitfalls



Common pitfalls Inexperienced operators or outdated equipment may produce angiographic studies that are incomplete or misinterpreted/​misreported.



Inadequate/​incorrect projections • Simply performing a ‘standard’ set of views may not provide the necessary information. • Operators should ensure that major vessels are visualized without overlap and not in foreshortened projections. • Use should be made of cranial and caudal angulations; relying on straightforward LAO/​RAO projections provides inadequate imaging, particularly for the LCA.



Underuse of contrast media • Inadequate volume of contrast injected will fail to opacify the coronary satisfactorily; typical volumes required are 5–​10 mL for the LCA and 3–​5 mL for the RCA. Imaging of grafts may require larger volumes. • Inadequate speed/​pressure of injection will lead to the appearances of ‘streaming’ in the coronary (mixing of opacified and non-​opacified blood); this makes stenosis quantification difficult. • Ideally, contrast should be injected fast enough and in enough volume to fill the coronary for 3 beats, and to result in reflux of contrast past the catheter retrogradely into the aortic root.



Catheter-​tip spasm • Over-​engagement of diagnostic catheters may result in spasm (% p.152), especially in the RCA. • Typically, the monitored coronary pressure will decline a few seconds after engagement as spasm develops. The catheter should be withdrawn and nitrates administered if required. • Provocation testing for coronary artery spasm using an injection of intracoronary ergonovine is now rarely performed due to the risk of intractable spasm resulting in myocardial infarction.



Selective engagement/​injection • Super-​selective engagement of coronary vessels may occur as a result of variant anatomy (e.g. short LMS) or due to poor technique and over-​ engagement (see earlier); a test injection should alert the operator to this occurrence. • If the LMS is short or non-​existent, and a Judkins left catheter selectively engages the LAD, a catheter one size larger will normally engage the Cx. • Selective engagement in the RCA usually involves the proximal conus branch and may result in ventricular fibrillation (% p.288) if a large volume of contrast is injected into this small vessel.



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Unusual coronary anatomy • Variant/​anomalous coronary anatomy is found in 1–​2% of unselected patients undergoing coronary angiography. • The commonest forms of variant anatomy are separate ostia in the left sinus of Valsalva for LAD and Cx vessels, and an anterior origin of the RCA. These are sufficiently common to be considered normal variants rather than anomalies. • Anomalous anatomy (commonly an anomalous Cx vessel) may be overlooked if the operator fails to recognize that an area of the myocardium remains unsupplied from the vessels imaged (% p.161) (Fig. 6.19). • Anomalous anatomy includes unusual origin, course, and distribution of coronary arteries and the presence of fistulae. • The importance of coronary anomalies depends on the course of the vessels concerned and predisposition to coronary disease: sudden death has been reported in patients with anomalous LCA vessels that pass between the aorta and pulmonary artery, presumably due to dynamic compression and ischaemically mediated arrhythmias.



Anomalous origin of the circumflex • The commonest anatomical abnormality (0.2–​0.7%). • The Cx arises from the proximal portion of the RCA, or arises separately from the right sinus. It then pursues a retro-​aortic course onto the posterolateral aspect of the left ventricle. • It may be diagnosed by the ‘dot’ sign at ventriculography (the anomalous vessel end-​on), or by the absence of a vessel supplying the lateral wall. • If overlooked at angiography, it may lead to incomplete revascularization or ligation during valve replacement surgery. The vessel is often very small in the retro-​aortic segment and may be difficult to graft.



Anomalous coronary artery origins • Many varieties of this anomaly exist. • Common types include the RCA arising from the left sinus of Valsalva, the LMS arising from the right sinus, or the coronary ostia in the ascending aorta. • Rarer variants include LMS/​isolated LAD origin from the pulmonary artery.



Unusual coronary anatomy



Fig. 6.19 Anomalous left circumflex anatomy. Note ‘dot’ sign on left ventriculogram (top left panel), absence of circumflex in RAO caudal projection of LCA (top right panel), and outline of anomalous circumflex seen during RCA injection (bottom left panel). Selective intubation of anomalous vessel (bottom right panel) revealed critical proximal stenosis (indicated by arrow)



Tips for selective intubation of anomalous coronaries • There are no hard and fast rules as to which catheters are ideally suited to selectively intubating anomalous coronary arteries. • The choice of catheter will be determined by the anomalous vessel and its ostium and proximal course, which may be discerned by aortography. • Anomalous vessels arising in the right sinus may be engaged with a JR4 catheter, but an Amplatz (AL or AR) shape is often needed. • Anomalous vessels arising from the left sinus may be engaged with a JL catheter, sometimes of an unusual size, or an AL shape. • Multipurpose catheters may be useful, but operators should be aware of iatrogenic dissection due to their aggressive angle of engagement.



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Single coronary artery • Very rare (5 years) and may result in distal thrombotic embolization, fistula formation, compression of adjacent structures, and even graft rupture. Risk factors for SVG failure Patient factors • Diabetes mellitus. • Hypercholesterolaemia. • Chronic kidney disease. • Younger age. Procedural factors • Poor quality of the vein. • Increased vein diameter. • Multiple distal anastomoses or poor distal vessel. • Surgical handling during harvesting and anastomosis. • Grafting to non-​ischaemic target vessel.   



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Chapter 7   Coronary



artery bypass graft angiography



Treatment of SVG failure • SVG failure is known to be associated with significant morbidity; however, the majority of SVG failure events are clinically silent. • The likelihood of SVG resulting in symptoms is dependent on the extent of myocardial territory supplied by the graft, the extent and severity of native vessel coronary disease, and the function of other contributing grafts and/​or collaterals. • The risk of SVG failure can be decreased by lifestyle changes (e.g. smoking cessation) and addressing established cardiovascular risk factors (e.g. hypertension). Aspirin and statins have also been recommended for the prevention of SVG failure. • Treatment of SVG failure depends on the timing of the event, the severity of symptoms, and the relative risks/​benefits to an individual patient. • Repeat surgical revascularization can be considered for graft failure, but redo surgery is associated with increased mortality and may not be appropriate for many patients. Operative techniques involve the creation of new vein conduits either anastomosed more distally on the target artery or onto the existing vein graft if the distal anastomosis is still preserved. • PCI is another possible revascularization method for SVG failure, usually with the implantation of a drug-​eluting stent (% p.202). Consideration should be given to using a distal protection device during PCI to limit downstream embolization of thrombotic or plaque material during the procedure (% p.244).



Saphenous vein grafts



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Chapter 7   Coronary



artery bypass graft angiography



Competitive filling If a patent coronary artery is also supplied by a bypass graft, then wash out of contrast distal to the anastomosis may be seen. This is termed competitive filling. Occasionally, back filling of the graft may also be seen (Fig. 7.8).



Fig. 7.8  Selective injection (left) of the circumflex (Cx) coronary artery and (right) the saphenous vein graft (SVG) revealing back filling of the distal graft



Collateral filling



Collateral filling Each of the three main coronary territories has the ability to develop collateral vessels to the others. During angiography of one coronary artery you may identify collaterals supplying other territories. This suggests that the blood supply to that territory is reduced (e.g. a blocked native vessel or graft). Failure to identify collaterals in the presence of an occluded native vessel implies that the supplying graft may still be patent (Fig. 7.9).



Fig. 7.9  Left-​sided injection of the circumflex coronary artery and obtuse marginal (OM) vessel demonstrating collateral filling of the occluded left anterior descending artery (arrowed) and graft



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Chapter 7   Coronary



artery bypass graft angiography



Arterial grafts Left internal mammary artery The LIMA ostium arises anteroinferiorly from the left subclavian artery a few centimetres beyond the vertebral artery (% p. 179 ). When proceeding transfemorally either a JR4 or LIMA catheter is usually selected to engage the LIMA ostium. When proceeding via the left transradial approach, either a 3DRC (Williams) or a BC (Bartorelli-Cozzi) catheter are preferable ­options to engage the LIMA ostium (% p.82). Accessing the left subclavian artery • Advance the catheter over a guide wire (e.g. 0.035 inch J) to the aortic arch, just past the ostium of the left subclavian artery. • Using an AP or LAO projection, the guide wire can be withdrawn slightly to allow the tip of the catheter to become more flexible. • The catheter is then gently rotated anticlockwise with slow withdrawal to engage the left subclavian artery. • In elderly patients or in those with extensive aortic calcification, it is good practice to advance the guide wire just out of the catheter tip before rotation to minimize the risk of aortic trauma. • If there are difficulties cannulating the subclavian artery, then try a non-​selective injection of contrast to delineate anatomy and check for subclavian stenosis. Accessing the LIMA • Once the subclavian artery has been selected, carefully advance the guide wire into the vessel, halting immediately if any resistance is felt. • Ensure that the guide wire tracks smoothly down towards the left arm and does not enter the vertebral artery. • A hydrophilic wire (e.g. J-​tipped Terumo) can be helpful for accessing tortuous vessels. • The LIMA catheter has a longer tip than the JR4 and provides easier access to the LIMA. If necessary, use a long exchange wire (% p.76) and change catheters, taking care not to lose access to the vessel. • Advance the catheter over the wire until positioned after the vertebral artery. • Withdraw the guidewire, aspirate blood from the catheter, and then connect up to the pressure line. • Ensure a good-​quality pressure trace before manipulating the catheter further. • Consider recording the pressure waveform at this stage, as a dampened pressure may suggest subclavian stenosis. • The ostium is engaged by slowly withdrawing the catheter and rotating it anticlockwise (bringing the tip anteriorly) using small non-​selective injections of contrast to guide progress. • Cannulation is usually indicated by a slight jump or dip in the catheter tip. • Check the pressure tracing to ensure no damping and give a small test injection of contrast. Collecting images • During image acquisition, warn the patient that they can develop a warm or burning sensation over the left chest and arm due to contrast dissipation (Fig. 7.10).



Arterial grafts



Fig. 7.10  Selective coronary angiography of the left internal mammary artery (LIMA) to the left anterior descending (LAD) coronary artery in different patients and views. The catheter tip can be seen entering the LIMA just after the vertebral artery (VB)



Fig. 7.11  LIMA to LAD anastomosis



• For LIMA to LAD grafts, image acquisition is typically performed in the AP projection (to examine the LIMA ostium), an RAO cranial view (to examine the mid LAD), and in the LAO cranial and left lateral views (to examine the distal anastomosis; Fig. 7.11). • To examine the entire LIMA, the radiographer will have to move the table to follow the course of the artery. • To examine the anastomosis (e.g. left lateral view), the image can be pre-​positioned over the heart. Ensure that the catheter tip has not displaced before starting an acquisition.



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Difficulties in LIMA cannulation • The LIMA can be fragile and prone to dissection, particularly in the elderly. Selective injections of contrast should therefore be made slowly. • If the LIMA cannot be cannulated then a non-​selective acquisition can be made from the subclavian artery to confirm LIMA patency. • Inflating a blood pressure cuff on the left arm will help direct contrast down the LIMA. • In very difficult cases, switching to a smaller catheter (5 F) may help or access can be obtained using a left radial approach (% p.50).



Right internal mammary artery The RIMA is used as an in situ graft to the native coronary arteries occasionally or dissected free from the subclavian artery and used as a free graft from the aorta. It is cannulated in a similar manner to the LIMA (% p.178) though access to the vessel can be quite challenging (Fig. 7.12). • Advance the JR4 or LIMA catheter to the aortic arch just past the origin of the innominate artery. • Gently withdraw the catheter while slowly rotating anticlockwise. • Be careful not to access the right common carotid artery. • To selectively cannulate the RIMA, the catheter should be rotated clockwise (to bring the tip anteriorly). • Selective injections should be made slowly to avoid potential for ostial dissection.



Fig. 7.12 Right internal mammary artery (RIMA) graft to the right coronary artery. The location of clips give a clue to the vessel path and insertion



Arterial grafts



Radial artery Antispasm drugs have improved graft survival but patency rates are still not as high as hoped. Radial arteries are usually used as free grafts attached to the aorta in similar locations to vein grafts. Occasionally, they are used as jump or sequential grafts from the LIMA or RIMA. Radial artery grafts are generally smaller and with smoother calibres than SVGs. Access and imaging of free radial grafts is performed in a similar manner to vein grafts (% p.170).



Gastroepiploic artery • This artery is not used routinely for coronary artery bypass but can be useful when internal mammary and vein grafts are unavailable. • It is typically used for distal RCA grafting. • Access to the artery is usually performed using a cobra catheter inserted into the common hepatic artery via the coeliac artery. • A guide wire (such as a hydrophilic Terumo wire) is advanced into the gastroduodenal artery and then to the right gastroepiploic artery. • The cobra catheter can then be exchanged for a MPA1 or JR4 to allow selective angiography (Fig. 7.13).



Coeliac artery



Fig. 7.13  Gastroepiploic artery graft cannulation using a cobra catheter from the coeliac artery



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Percutaneous coronary intervention History  184 Indications for PCI  186 Imaging the lesion  188 Lesion classification  190 Guiding catheters  192 Angioplasty guide wires  194 Angioplasty balloons  196 Intracoronary stents  198 Restenosis  200 Drug-​eluting stents  202 Bioresorbable scaffolds  204 Stent thrombosis  206 The PCI procedure  208 Intravascular ultrasound  210 Pressure wire  212 Optical coherence tomography  216 IVUS or OCT?  217 Antiplatelet therapy  218 Anticoagulation therapy  224 Specific techniques in complex PCI  225 PCI in acute myocardial infarction  226 Primary PCI  228 Facilitated PCI versus a pharmaco-​invasive strategy  230 Cardiac arrest in STEMI  230 Primary PCI in cardiogenic shock  231 Primary PCI in multivessel disease: culprit-​only versus non-​culprit  PCI  232 Multivessel PCI  234 Bifurcation lesions  236 Bifurcation PCI techniques  238 Left main stem PCI  240 Chronic total occlusion PCI  242 Vein graft PCI  244 The ‘no-​reflow’ phenomenon  246 Rotational atherectomy  248 Aspiration catheters  252



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History The first percutaneous transluminal coronary angioplasty (PTCA) in a conscious human was performed in Zurich, Switzerland, on 16 September 1977 by Andreas Gruentzig, a Swiss cardiologist (Fig. 8.1). This landmark event in interventional cardiology had been preceded by years of pioneering work by Gruentzig in developing a balloon suitable for intracoronary inflation and then putting it to trial, first in animals, then in postmortem specimens, and finally in living humans. The first human angioplasties were performed in peripheral arteries and then (with a miniaturized balloon) in coronary arteries during coronary bypass surgery. But Gruentzig’s work owes a debt of gratitude to work by Charles Dotter and Melvin Judkins in the mid 1960s, who reported on the successful use of sequentially larger coaxial sheaths to dilate arteries in the legs of patients with severe peripheral rest ischaemia. However, it was with Gruentzig’s realization that radial, rather than longitudinal, force on the vessel wall provided a better mechanical means of dilating stenoses that balloon angioplasty, and indeed modern interventional cardiology, was born.



The first PTCA The patient, a 37-​year-​old insurance salesman, had been suffering from exertional angina and was found to have a severe proximal LAD lesion at angiography. The balloon catheter was advanced across the lesion without event and then inflated twice to relieve the trans-​lesion pressure gradient. To the surprise of all present, the procedure was completed successfully with a good angiographic result, without the patient experiencing chest pain, ST segment shift, or arrhythmia (Fig. 8.2).



Subsequent developments In the four decades since the first PTCA, technological advances have made the world of interventional cardiology almost unrecognizable:  PTCA has evolved into PCI (percutaneous coronary intervention), encompassing balloon dilatation, deployment of intracoronary stents, and a host of adjunctive therapeutic and imaging techniques, many of which will be discussed further in this chapter. The development of intracoronary stents (pioneered by Julio Palmaz and Richard Schatz) to prevent abrupt vessel closure and, in particular, to scaffold balloon-​induced coronary dissection, has revolutionized practice and enhanced procedural safety. Universal uptake of such devices (to near 100% in present-​day PCI) has paralleled the reduction in requirement for urgent CABG surgery and the risk of procedural mortality to less than 1%.



History



Fig. 8.1  Andreas Gruentzig. The pioneer of modern-​day interventional cardiology at work in the catheter lab at Emory University, Atlanta, GA, USA



Fig. 8.2  The first PTCA in a human. Cineangiograms taken before PTCA (left) and at 10-​year routine follow-​up angiography (right). Several years later, the patient received a stent to the proximal LAD. Reproduced from Douglas, Jr, J.S., King, III, S.B. Techniques of Percutaneous Transluminal Angioplasty and Atherectomy of the Coronary Arteries. Hurst’s The Heart. 8th ed. P.1346, with permission from McGraw-​Hill



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Indications for PCI PCI is generally indicated for the relief of symptoms of angina; at the present time, no study has clearly identified any prognostic benefit from PCI (in contrast to CABG for multivessel or LMS disease). Gruentzig’s original selection criteria for angioplasty demanded that the patient have: • Stable angina. • Documented ischaemia on functional testing. • Single-​vessel disease (preferably proximal, non-​occluded, and non-​ calcified lesion). • No features precluding CABG (if required as bailout), for example, malignancy, severe LV dysfunction, pulmonary disease, etc. While such criteria may seem conservative by today’s standards, there is little doubt that such patients are not only eminently suitable for PCI, but will obtain good results with a low risk of complication. Advances in interventional technology have resulted in lesion and patient subsets of increasing complexity being tackled, including: • ‘Unstable’ patients: • Primary PCI for acute MI. • PCI in ACS. • PCI in cardiogenic shock. • Multivessel disease. • Bifurcation lesions. • LMS disease. • Vein graft disease. • Patients deemed unsuitable/​unfit for CABG.



Recommendations for PCI All patients undergoing PCI should have: • Symptoms consistent with myocardial ischaemia (chest pain, dyspnoea). • Evidence of myocardial ischaemia (acute ECG changes or positive functional imaging). • Technically suitable coronary anatomy. • Appropriate consent for the procedure taken.



Indications for PCI



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Imaging the lesion For any PCI procedure to be successful, the target lesion must be imaged adequately before the procedure to examine its anatomy and, after the procedure, to assess the final result. Angiographic analysis of the lesion is expected, but increasing use is being made of adjunctive techniques to provide further anatomical or functional information (e.g. intravascular ultrasound (IVUS) % p.210, pressure wire % p.212), especially where stenosis severity is in doubt.



Diagnostic angiography versus PCI Diagnostic coronary angiography: • Outlines the extent and severity of coronary artery disease. • Is used to inform the decision as to whether the patient should pursue medical therapy, or be considered for revascularization by percutaneous or surgical methods. In contrast, when undertaking PCI, angiographic information obtained must be more focused, concentrating on a more discrete portion of the coronary anatomy (the target lesion), and should define: • The length of the lesion. • The reference diameter of the ‘normal’ vessel either side of the lesion. • Features indicative of procedural complexity, including proximity to side branches, vessel tortuosity, and the presence of calcification or luminal thrombus. Radiographic views The target lesion should be imaged: • In at least two angiographic projections, preferably at right angles (orthogonal views). • Avoiding overlap with other coronary vessels. • Providing the least amount of foreshortening (if the vessel is not imaged at 90° to the X-​ray source, the lesion may appear shorter and more severe). Sometimes, due to the location of the target lesion, separate views may be required to adequately image the proximal and distal limits of the lesion. • The operator should also be aware of the radiation dose to both the patient and him/​herself (% p.14); for prolonged PCI procedures, the radiographic view utilized should be varied in order to reduce the likelihood of causing a radiation burn to the patient’s skin. Many new imaging systems include a skin dosimeter to indicate when acceptable exposure has been exceeded. • Appropriate views for PCI will vary on an individual patient basis, and by operator preference. Table 8.1 indicates some recommended views as a starting point. See % p.139 for more diagnostic imaging planes.



Imaging the lesion



Table 8.1  Recommended views for PCI Target vessel



Recommended views



Proximal LAD



RAO 30° caudal 20° RAO 30° cranial 30° LAO 45° caudal 25° PA caudal 30°



Mid/​distal LAD



LAO 50° cranial 30° LAO 10° caudal 35–​40° PA cranial 30°



Circumflex



RAO 30° caudal 20° PA caudal 30° LAO 45° caudal 25° LAO 60°



Proximal/​mid RCA



LAO 40–​50° RAO 30°



Mid/​distal RCA (including crux)



PA cranial 30° LAO 45° cranial 30°



Further reading Di Mario C, Sutaria N. Coronary angiography in the angioplasty era: projections with a meaning. Heart 2005; 91: 968–​76.



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Lesion classification • Various systems of lesion classification have been developed to describe the complexity of a lesion, and to predict PCI success and the likelihood of procedural complications. • The system in widest use is the ACC/​AHA classification, initially published in 1988, then revised in 1990.



The ACC/​AHA classification • This system evaluates up to 11 features of each lesion, classifying lesions into three groups (A, B, C). See Table 8.2 for a summary of features. • The 1990 revision subdivided type B lesions into two subgroups, depending on the number of ‘B’ features present: B1 (one ‘B’ feature) or B2 (two or more ‘B’ features). • It should be noted that this system was devised and validated in the PTCA or POBA (‘plain old balloon angioplasty’) era, and despite its widespread contemporary use, newer classification systems predict success and outcome more accurately since stent deployment has become routine. • Current data suggest procedural success in 99% of type A, 92% of type B, and 90% of type C lesions (in stark contrast to initial estimates in the POBA era of >85%, 60–​85%, and 90°)



Non-​angulated segment Moderately angulated segment (45–​90°)



Occlusion >3 months old



Smooth contour



Irregular contour



Bifurcation with unprotected side branch



Light or no calcification



Moderate or heavy calcification



Degenerate saphenous vein graft



No side branches adjacent



Occlusion 7 F >6 F) offer increased support for PCI. • Forward planning of the strategy for the PCI procedure and anticipation of the potential need for a larger-​calibre catheter, for techniques such as rotational atherectomy (% p.248) or complex two-​stent procedures (% p.237), may enable the operator to avoid the cumbersome switching of guiding catheters mid-​PCI. Table 8.4  Guide catheters and level of catheter support Increasing catheter support l Target vessel



+



++



+++



LAD



JL3.5/​4



AL2



XB/​EBU3.5



Cx



JL4/​5



AL2



Voda/​XB/​EBU3.5/​4



RCA



JR4a



AR1/​2



Hockey Stick/​AL1/​2



a



JR4 may offer more support if ‘deep-​throated’ into the target vessel without inducing trauma.



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Angioplasty guide wires Following positioning of the guiding catheter, a guide wire must be positioned distally in the coronary bed to allow tracking of balloon/​stent catheters and other intracoronary devices to the intended target lesion.



Guide wire construction Most angioplasty guide wires are manufactured at a calibre of 0.014 inches, and are multilayer constructions: • Core element (usually stainless steel, steel alloy, or nitinol): tapers at variable points towards wire tip to impart differential stiffness along the wire’s length. • Terminal coil segment (often 30 mm length; usually radio-​opaque material, e.g. platinum/​iridium alloys): gives flexibility and allows wire tip to be shaped per operator requirements. • Coating: most wires have a silicone or Teflon® outer coating to aid easy advancement. Some are coated with a hydrophilic polymer coating that becomes a gel when wet to reduce surface friction and increase wire ‘slipperiness’.



Guide wire characteristics Construction of the wire influences the following characteristics: • Push: ability to transmit manual movements to advance wire in the coronary. • Torque: ability to transmit rotational movements of wire. • Support: allows advancement of balloon catheters without buckling/​ kinking of wire. • Elasticity: wire resistance to bending and ability to maintain shape/​form. • Visibility: not all wires are radio-​opaque and may be difficult to visualize during fluoroscopy. Wires with elongated core segments (‘core-​to-​tip’ design) will tend to be stiffer, with enhanced push, torque, and support, whereas wires with longer core tapers that do not reach the tip of the wire (the terminal segment is termed a ‘shaping ribbon’) will be floppier, with relatively less push and support but increased flexibility and are less likely to cause trauma to the vessel.



Guide wire selection Every manufacturer produces a range of wires that may be utilized in different settings, and every operator will develop their own favoured wires for particular situations. • Workhorse wire: most operators will opt for a default choice that has a balance between stiffness/​support and a flexible tip with shaping ribbon, for use in the majority of lesions. • Stiff wires: offer extra support for tortuous/​calcified coronary anatomy. • Floppy wires: may be useful when vessel trauma is a concern (e.g. re-​ crossing a dissected lesion). • Coated wires: hydrophilic coatings reduce friction and may be helpful in crossing occluded target vessels (% p.242).



Angioplasty guide wires



Preparation and placement of the guide wire The guide wire tip should be manually shaped according to the angulation of the target vessel and the lesion to be crossed: • Once shaped, the wire is passed through the guiding catheter into the coronary artery; it is good practice to enter the vessel with continuous fluoroscopy to ensure side branches are not engaged and that the wire is not buckling against obstructions. • The wire should be advanced with continuous tip movement (repeated short rotations of the wire shaft) to ensure that the tip does not lodge in the lesion or vessel wall and cause an iatrogenic dissection. • Some operators find the use of a torqueing device (a small plastic handle) to aid wire rotation is helpful. • Some wires have a pre-​shaped tip, also known as a ‘preformed J’ and may not require further shaping prior to use (Fig. 8.4). Optimum guide wire positioning The guide wire should be placed as distally as possible in the target vessel; most wires have differential stiffness, and this allows extra support at the lesion when attempting to cross with balloon/​stent catheters. Distal positioning also reduces the chance of the wire becoming displaced backwards across the lesion and necessitating re-​crossing during the procedure. Care should be taken to avoid vessel perforation when positioning wires with hydrophilic coatings very distally in the coronary vasculature.



Fig. 8.4  (a) Angioplasty wire construction. (b) Preparation of the guide wire. The guide wire is shaped manually, with or without the aid of the introducer needle (centre and right panels)



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Angioplasty balloons Like other pieces of equipment used in PCI, the balloon catheters in use today bear little resemblance to the bulky and limited devices used in the era of Gruentzig.



Balloon catheter construction The balloon catheter is essentially a device designed to deliver the key component of the device (the balloon itself ) to the target lesion, using the angioplasty wire as a guide. The balloon catheter comprises: • Low-​profile hypotube with connection for inflation device. • Monorail segment. • Balloon itself with radio-​opaque markers to aid visualization. • Chamfered (tapered) nosecone to prevent local trauma (Fig. 8.5).



Monorail versus ‘over-​the-​wire’ balloons Almost all balloon catheters now in routine use utilize monorail ‘rapid exchange’ technology. • The short monorail segment is the only part of the balloon catheter through which the guide wires passes, enabling the operator to easily exchange balloon and stent catheters without recourse to cumbersome use of very long guide wires. • ‘Over-​the-​wire’ (OTW) balloon catheters, where the angioplasty guide wire passes along the entire length of the catheter were historically the norm; changing balloon or stent catheters necessitates long ‘exchange length’ guide wires. Use of such balloons is now usually restricted to PCI in CTOs (% p.242).



Balloon compliance Balloons are generally manufactured from a polyethylene polymer; balloon characteristics depend on the material of manufacture, and generally are described as: • Compliant: balloon expands as greater pressure is applied; the standard type of balloon used for pre-​dilation of lesions. Degree of expansion may be unpredictable at high pressures. • Non-​compliant: balloon expands very little as greater pressure is applied; used for post-​dilating stents after deployment. • Semi-​compliant: described as having ‘controlled compliance’, with more predictable expansion at high pressure than compliant balloons.



Fig. 8.5  Monorail balloon catheter



Angioplasty balloons



Balloon expansion Pressure is applied to expand the balloon by the inflation device via the hypotube. The external diameter of the balloon will expand as the pressure is increased, governed by balloon compliance. Two specific levels of pressure should be noted: • Nominal pressure: the pressure (bar) at which the balloon will have expanded to the manufacturer-​specified size; that is, for a 2.5 mm diameter balloon expanded to nominal pressure, its external diameter should be 2.5 mm. • Rated or ‘burst’ pressure: the pressure beyond which the balloon is not designed to be inflated and may risk rupture, with consequent dissection of the vessel.



Balloon sizing Angioplasty balloons are manufactured in varying sizes and lengths; the specific size chosen should be determined by lesion characteristics. It is important to maximally dilate the target lesion prior to stent deployment; attempting to ‘crack’ a resistant lesion after stenting can be very difficult. • Balloon diameter: should be chosen to be no larger than the calibre of the vessel at the target lesion. Over-​sizing of balloons may lead to dissection or rupture, and under-​sizing to incomplete lesion preparation. • Balloon length: should be appropriate for the lesion. Balloons that are too short may ‘melon-​seed’ (move to and fro across the lesion) as they are inflated, and those that are too long may damage normal sections of vessel wall adjacent to the lesion.



Cutting balloon angioplasty The cutting balloon has one or more atherotomes (cutting blades) attached longitudinally to its outer surface; inflation of the balloon allows these to incise fibrotic or calcified lesions and allow subsequent balloon inflations to be successful. Atherotomes are sharper than surgical scalpels and may perforate gloves and/​or skin, as well as damaging coronary vessels if the device is not allowed to fully deflate before withdrawal (Fig. 8.6).



Fig. 8.6  Cutting balloon. Cutting blades/​atherotomes are seen mounted on the angioplasty balloon (left panel); as the cutting balloon is inflated, the atherotomes incise fibrous/​calcified tissue. Images courtesy of Boston Scientific



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Intracoronary stents History Intracoronary stents were initially developed as ‘bail-​out’ devices to avoid CABG when abrupt closure followed angioplasty-​induced dissection of the target vessel. Initial devices, despite needing to be hand-​crimped onto balloon catheters and being bulky by today’s standards, were remarkably effective, and were subsequently shown to reduce restenosis compared with POBA.



Stent construction and characteristics • Stent design has evolved rapidly since the first Palmaz–​Schatz devices were developed, although the initial design template (‘closed-​cell’) continues to be used in some of the current generation of stents (Fig. 8.7 and Fig. 8.8). • Stent design is complex, with ever-​evolving technology aimed at improving physical properties, including handling, delivery, immediate recoil, flexibility, radial strength, visibility, etc. No one design is optimal in all regards, and final properties depend on both material and design. Stent materials • Stents are generally manufactured from 316 L stainless steel, with increasing use of cobalt/​chromium, cobalt/​nickel alloys and other metals. • Work is currently being undertaken evaluating prototype metallic and polymer-​based bioabsorbable stent designs. Stent design Stents fall into three broad categories of structural design: • Tubular slotted: stents laser-​cut from stainless steel tubes and crimped onto the balloon catheter. Typically, such stents are of ‘closed-​cell’ design, resulting in a high degree of metal coverage at the target lesion (metal:artery ratio) and high radial strength but less flexibility (Fig. 8.8). • Modular: stents based on repeating identically designed units, again laser-​ cut, linked together by welded struts, giving an ‘open-​cell’ design. Such stents offer less metal coverage, particularly around the articulated welds but are more flexible and offer better side-​branch access (Fig. 8.9). • Coil: stents based on a continuous wire coil stretching the entire length of the design; this design has been largely superseded due to limited vessel scaffolding and radial strength despite high flexibility.



Stent delivery • Stents are pre-​mounted on monorail balloon catheters (% p.196) for easy delivery and are sized by final expanded diameter and length. • Self-​expanding stents have fallen out of favour for coronary work despite their continuing role in peripheral arterial intervention, principally due to unacceptably high restenosis rates (% p.200).



Stent usage • Increased elective stent usage during PCI (now near-​universal) has paralleled the reduction in procedural death, MI, and emergent CABG. • Stents have been clearly demonstrated to reduce restenosis (% p.200) in a variety of lesion subsets when compared with POBA alone.



Intracoronary stents



Fig. 8.7  The Palmaz–​Schatz stent. Based on repeating modules (two or three Palmaz stents linked by short struts), this stent was the first in widespread use. These stents were provided in a deployed state and needed to be hand-​crimped onto angioplasty balloons before use. Stent dislodgement from balloon catheters was not uncommon



Fig. 8.8  Closed-​cell stent design. Although modern closed-​cell stents have relatively large cells, the cells themselves are boundaried by stent struts as part of the design. Picture of Boston LiberteTM stent courtesy of Boston Scientific



Fig. 8.9  Open-​cell/​modular stent design. Multiple repeating modules are linked at certain points of the design, giving flexibility but less metal:artery coverage. Image of Medtronic DriverTM stent courtesy of Medtronic



Strut thickness • Stent strut thickness is a major determinant of risk of restenosis (% p.200) in bare-​metal stents (BMSs), with randomized comparisons clearly showing an advantage for stents with lower strut thickness (and hence metal:artery ratio). • In the era of drug-​eluting stents (DESs), such concerns are much reduced; the stent design providing the worst restenosis rates in such studies is now the platform for the successful Cypher® sirolimus DES (% p.203).



Further reading Pache J, Kastrati A, Mehilli J, et al. Intracoronary stenting and angiographic results: strut thickness effect on restenosis outcome (ISAR-​STEREO-​2) trial. J Am Coll Cardiol 2003; 41: 1283–​88. Serruys PW, de Jaegere P, Kiemenieij F, et al. A comparison of balloon-​expandable stent implantation with balloon angioplasty in patients with coronary artery disease. Benestent study group. N Engl J Med 1994; 331: 489–​95.



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Restenosis The Achilles heel of modern-​day PCI.



Definition • Renarrowing occurring at the site of a successful intervention.



Pathophysiology • Three separate processes may contribute: • Elastic recoil after balloon dilatation—​immediate. • Inflammation and neointimal proliferation—​weeks/​months. • Negative remodelling—​months/​years. • Elastic recoil and negative remodelling have largely been eliminated by use of intracoronary stents. However, the inflammatory cascade leading to neointima formation remains an issue, as cellular proliferation may occur between stent struts, renarrowing the vessel at PCI sites. Inflammation and neointima formation • Vessel injury by balloon inflation and stent deployment leads to platelet activation, local thrombus formation and recruitment of neutrophils, monocytes, and lymphocytes by cytokines and growth factors. • Inflammatory mediators generated by activated leucocytes and platelets stimulate smooth muscle cell proliferation, producing intimal hyperplasia and restenosis. • Timing and extent of these processes varies depending on patient factors including mode of presentation (acute/​elective) and extent of injury inflicted during PCI.



Epidemiology of restenosis • Restenosis was far commoner in the era of balloon angioplasty, occurring in around 30–​60% of patients at 6 months after PCI; successive generations of technological improvements in BMSs has reduced restenosis risk from around 25% to 10–​15%. • Restenosis occurs more commonly in longer lesions, smaller calibre vessels, complex lesions, diabetes mellitus, and renal failure. • Angiographic restenosis (i.e. that detected during angiography) is much commoner than clinical restenosis (i.e. that causing symptoms associated with recurrent myocardial ischaemia). Clinical restenosis commonly occurs in only approximately 10% of patients. • Angiographic restenosis as an endpoint in clinical trials is therefore a controversial surrogate, especially as the finding of restenosis without symptoms at planned follow-​up angiography has been shown to result in inflated repeat revascularization rates.



Prevention of restenosis • Strict attention to PCI technique, including correct stent sizing, optimal expansion at deployment, and complete lesion coverage is important. • Use of IVUS (% p.210) to guide stent deployment has been demonstrated to reduce the risk of restenosis. • Pharmacological therapies have yet to be proven in the prevention of restenosis.



Restenosis



Treatment of restenosis • Use of balloon angioplasty, with or without use of the cutting balloon (% p.197), may be useful in compacting the restenotic intima. • Use of intracoronary brachytherapy has largely been superseded by repeat stenting with DESs (% p.202). • IVUS in the treatment of in-​stent restenosis is important in assessing expansion of the original stent and close apposition of any further stents that are deployed (Fig. 8.10). • Severe diffuse or recurrent restenosis may be an indication for CABG.



Fig. 8.10  In-​stent restenosis. Angiographic images taken before and after contrast injection to illustrate stent position in proximal LAD and presence of severe in-​stent restenosis, occurring 5 months after stent implantation



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Drug-​eluting stents History With virtual elimination of immediate elastic recoil and late negative remodelling by routine use of intracoronary stents, intimal proliferation’s role in restenosis became the focus of much research work. Similarities between the rapid proliferation of smooth muscle cells in the nascent neointima and the proliferation of malignant neoplastic cells in tumours sparked interest in anticancer and immunomodulatory agents.



Stent delivery of drug • Stents are ideal vectors to carry drug agents, targeting geographically the site of intimal proliferation and potentially limiting systemic toxicity. • Drug delivery is usually achieved by combining the drug with a biocompatible polymer which can then be used to coat the stent. Such polymers will also allow a gradual elution of the drug (dependent on polymer characteristics) to ensure that the agent is released during peak neointimal proliferation.



Antiproliferative agents • Many agents have been researched, but only a few of those with potential promise have evolved into clinically effective choices for DESs. • Currently available DESs deliver either cytotoxic (paclitaxel) or cytostatic (sirolimus and analogues) agents to either kill proliferating cells or arrest cell cycle-​driven replication. Paclitaxel • Derived from the bark of the Pacific yew tree (Taxus brevifolia), paclitaxel stabilizes microtubules and exerts a potent cytotoxic effect. • Extensive studies have assessed the safety and clinical utility of paclitaxel-​eluting stents (PESs) in a variety of patient groups. It is clear that PESs reduce major adverse cardiac events (MACE), particularly due to reduced restenosis rates and therefore less need for target lesion revascularization (TLR). Sirolimus • The immunomodulatory agent sirolimus was first discovered during a visit to Easter Island (the original drug name, rapamycin, derives from the island’s name, Rapa Nui). Sirolimus has been widely used in prevention rejection following kidney and other organ transplantation, and additionally has been shown to possess antimitotic properties. • Again, clinical trial evidence has amassed for the sirolimus-​eluting stent (SES), similarly demonstrating safety and clinical efficacy in terms of reduced MACE and TLR (Fig. 8.11). Sirolimus analogues • Agents structurally similar to sirolimus have also been investigated, with zotarolimus and everolimus the latest agents to be used successfully on DES platforms; evidence continues to accrue for these DES.



Drug-eluting stents



Fig. 8.11  The Cypher® sirolimus-​eluting stent. Based on a closed-​cell bare-​metal stent design which had performed poorly in randomized comparisons, the Cypher® stent was the first available drug-​eluting stent that clearly improved restenosis and clinical outcomes



Indications for DESs • Lesions/​patients with a high risk of restenosis (% p.200). • Treatment of restenotic lesions. • National Institute for Health and Care Excellence (NICE) guidance in England recommends the use of DESs where vessel calibre is less than 3 mm and/​or lesion length is greater than 15 mm.



Considerations with DESs • High cost. • Relatively short-​term efficacy and safety data at present. • Unknown effects of DES combinations. • Possible hazard of stent thrombosis (% p.206). Differences between DESs • Controversy persists as to which DES is superior, and indeed with regard to how clinicians should assess such superiority. • The bulk of evidence (both randomized and registry) relates to PESs and SESs; both DES types reduce TLR (to 0.89 defer revascularization.



Pressure wire



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Optical coherence tomography IVUS and optical coherence tomography (OCT) are the two main techniques of intravascular imaging adopted in the CathLab. OCT differs from IVUS in: • The way the image is generated. • Spatial and temporal resolution. • Tissue penetration. OCT is an intravascular imaging technique using infrared light to provide a highly detailed depiction of intraluminal and transmural coronary anatomy. Optical imaging in a non-​transparent tissue is difficult due to the high scattering of light produced by human tissues. This obstacle in OCT is represented by red blood cells. For this reason, OCT requires displacement of blood from the vessel segment under investigation. This was achieved with an occlusive balloon in first-​generation OCT. Currently, thanks to faster acquisition time in the newer-​generation OCT system, blood displacement is achieved with injection of (translucent) contrast.



Differences between IVUS and OCT See Table 8.6. Table 8.6  Differences between IVUS and OCT



Catheter size (F)



IVUS



OCT



3.2–​3.5



2.4–​2.7



Max. frame rate (frames/​sec) 30–​60



200



Pullback speed (mm/​sec)



0.5–​1.0



18–​36 (up to 40)



Pullback length (mm)



150



54–​75 (up to 150)



Type of pullback



Mechanical or manual



Mechanical



Need for blood clearance



No



Yes



Tissue penetration (mm)



4–​8



2–​3.5



Axial resolution (μm)



80–​100



10–​20



Lateral resolution (μm)



200–​250



20–​40



IVUS or OCT?



IVUS or OCT? Because of these technical specifications, when compared to IVUS, OCT can offer faster image acquisition and higher image resolution with greater definition of: • Calcium. • Thrombus. • Intima hyperplasia/​thickening. • Atherosclerotic plaque (fibrosis/​lipidic core). • Dissection flaps. • Stent parameters. Due to lower tissue penetration of infrared light (compared to ultrasound) and because of no need to inject contrast to obtain vessel imaging, IVUS remains a better intravascular imaging option for: • Large vessels. • LMS. • Aorto-​ostial lesions. • Ectatic/​aneurysmal segments. • Patients with impaired kidney function.



Indications for OCT Pre-​intervention Vessel sizing • Lumen area and diameter at proximal and distal references. • Minimal lumen area and diameter. • Areas and diameters measurements can be based on lumen contour detection or media-​to-​media definition. Identification of culprit vessel/​lesion in ACS • Plaque rupture. • Plaque erosion. Identification of high-​risk plaque • Fibrous cap smaller than 65 μm. • Lipidic core with posterior attenuation. • Lipidic arch greater than 90°. • Macrophages infiltration. Post intervention Identification of acute of suboptimal stent result • Struts malapposition. • Stent underexpansion. • Geographical miss. • Stent edge dissection. • Tissue prolapse. Identification of mechanisms of stent failure (restenosis/​thrombosis) • Stent malapposition. • Stent underexpansion. • Neoatherosclerosis.



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Antiplatelet therapy Antiplatelet therapy Antiplatelet therapy in patients with coronary artery disease (CAD) has two main justifications: CAD not treated with PCI • Prevention of first or recurrent coronary ischaemic events. CAD treated with PCI • Prevention of first or recurrent coronary ischaemic events. • Prevention of stent thrombosis.



PCI: a thrombogenic process • Balloon inflation disrupts the intima, revealing the prothrombotic lipid core of plaques, exposing tissue factor, von Willebrand factor, and so on which activate platelets (Fig. 8.17). • Angioplasty equipment in the arterial circulation during the procedure may encourage adherent thrombus. • Stents deployed in the coronary circulation may occlude due to thrombosis if anticoagulation is inadequate. • A variety of agents, targeting different parts of the coagulation/​ thrombosis cascades may be used in different combinations.



Aspirin • Aspirin has been used universally since the first balloon angioplasty procedures, and has been shown to reduce the incidence of procedural MI. • Mode of action: inhibition of platelet cyclooxygenase 1 (COX-​1), blocking thromboxane 2 (TxA2) synthesis and thus preventing platelet aggregation. • Dosage: 300 mg loading dose and then 75 mg once daily orally indefinitely.



Clopidogrel • Clopidogrel improves outcomes in ACS with and without PCI; combination with aspirin in dual antiplatelet therapy has simplified and improved safety in post-​PCI care. • Mode of action: a thienopyridine, it acts by blocking the platelet P2Y12 receptor for adenosine diphosphate (ADP). • Dosage: 75 mg once daily orally. Patients should be preloaded with 300 mg as a single dose at least 72 hours before the PCI procedure, or with 600 mg if less time is available. • Its main limitation is still due to inter-​individual variability in response, mainly related to genetic polymorphisms of genes codifying for cytochrome P450 responsible for hepatic conversion of the prodrug form into active drug. • Duration of clopidogrel therapy is the subject of debate, especially with regard to the issue of stent thrombosis (% p.206). Clopidogrel should be continued for at least 4 weeks after deployment of BMSs, and at least 6 months after DESs. Many centres now recommend 12 months or longer, particularly following complex PCI.



Antiplatelet therapy



Fig. 8.17  Simplified illustration of coagulation cascade/​platelet interactions. Note central roles of factor Xa and thrombin in stabilizing thrombus by aiding fibrin generation. ADP, adenosine diphosphate; COX, cyclooxygenase; TXA2, thromboxane A2



Prasugrel • Prasugrel is a third-​generation thienopyridine with a more effective metabolism, allowing more potent and rapid action and significantly lower risk of low or non-​responsiveness compared to clopidogrel. • The TRITON TIMI 38 study has confirmed the superiority (in terms of reduction of ischaemic events) of prasugrel compared to clopidogrel, in combination with aspirin, in patients with ACS treated with PCI. This benefit was, however, offset by an increased risk in major and fatal bleedings. • It is not recommended in the elderly (>75 years old), in patients with low body weight ( bleeding risk



Bleeding risk > ischaemic risk Mid bleeding risk



High bleeding risk



1st month



A+C+O



A+C+O



C+O



6th month



A+C+O or



A+O or C+O



12th month



A+O or C+O



After 12th month



O



O



O



A, aspirin; C, clopidogrel; O, oral anticoagulation.



Table 8.11  Interruption of therapy for surgery Restart on day_​_​_​ after surgery



Prasugrel



7



1–​4



Clopidogrel



5



Ticagrelor



3



Aspirin



Do not stop (case-​by-​case decision)



SURGERY



Stop _​_​_​ days before surgery



1–​4 1–​4 —​



Interruption of antiplatelet therapy in patients going for surgery See Table 8.11.



Further reading Lopes RD, Heizer G, Aronson R, et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med 2019; 380: 1509–​24. Valgimigli M, Bueno H, Byrne RA, et  al. 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS. Eur Heart J 2018; 39: 213–​54.



Antiplatelet therapy



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Anticoagulation therapy Heparin • Heparin has been used as standard peri-​PCI anticoagulation since the early days of balloon angioplasty; the trend has been to use lower doses to reduce bleeding complications while maintaining adequate anticoagulation. • Mode of action: inactivates thrombin and procoagulant proteases (including factor Xa) via antithrombin III activation. • Dosage: varies at operator discretion; usually 70–​100 IU/​kg patient weight administered intra-​arterially. • The activated clotting time (ACT; measured by bedside assay) is used by some operators to assess anticoagulation during procedures; it should be maintained at greater than 250–​300 seconds. • Recent data suggest that low-​molecular-​weight heparins and the factor Xa antagonist fondaparinux may reduce bleeding complications when used in PCI.



Glycoprotein IIb/​IIIa antagonists • Inhibition of the platelet glycoprotein IIb/​IIIa receptor prevents platelet aggregation and may de-​aggregate clumped platelets. • Glycoprotein IIb/​IIIa inhibitors (GPIs) have become established in the medical management of non-​STEMI and in PCI for both patients presenting with ACS and those with complex disease, particularly when thrombus is present, and in insulin-​treated diabetics. • GPIs are used in combination with heparin. • Abciximab: a monoclonal antibody fragment, producing non-​competitive irreversible platelet blockade. Administered by weight-​adjusted IV (or intracoronary) bolus followed by 12-​hour infusion. • Tirofiban, eptifibatide: small molecule GPIs providing competitive and reversible blockade of platelet aggregation during infusion, with short (50%). • CvLPRIT study: angiography based (stenosis >70%). • DANAMI PRIMULTI study: FFR based (FFR ≤0.80). • COMPARE ACUTE study: FFR based (FFR ≤0.80). The second question is when to complete revascularization: • PRAMI trial: at the time of primary PCI (‘all in one go’). • COMPARE ACUTE and CvLPRIT trials: either at the time of primary PCI or later during the same admission. • DANAMI-​PRIMULTI trial: staged during the same admission. Due to the lack of comparison of the two strategies (immediate vs staged), current guidelines recommend complete revascularization to be achieved before discharge.



Further reading Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-​segment elevation. Eur Heart J 2018; 39: 119–​77. Neumann FJ, Sousa-​ Uva M, Ahlsson A, et  al. 2018 ESC/​ EACTS Guidelines on myocardial revascularization. Eur Heart J 2019; 40: 87–​165.



PRIMARY PCI IN MULTIVESSEL DISEASE



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Multivessel PCI Background • Despite Gruentzig’s original affirmation that PCI should only be considered in single-​vessel disease, improvements in imaging, equipment, operator technique, and above all patient safety, have led to multiple lesions in multiple vessels being tackled in a single procedure or in staged procedures.



Complete revascularization • ‘Complete revascularization’ of all compromised territories is associated with improved survival; therefore, CABG has traditionally been viewed as the gold standard for revascularization in multivessel disease. • Real-​world registries (as opposed to randomized trials) indicate that PCI-​driven anatomical revascularization may only be complete in 30–​ 70% of patients. • Use of the pressure wire to measure FFR (% p.212) and guide functional revascularization by PCI shows promise, but randomized data are required.



PCI versus CABG • Initial studies of balloon angioplasty versus CABG (BARI, EAST) demonstrated similar outcomes in terms of death and MI, but increased event rates driven by repeat interventions in the angioplasty group. • Stent-​era studies show some reduction in need for further PCI (SoS, ARTS), and when compared with historical controls, DESs compare favourably with CABG (ARTS-​II). • Ongoing randomized studies (SYNTAX, FREEDOM) will address the question of the utility of multivessel (including LMS) stenting with DESs versus CABG.



Technical aspects of multivessel PCI • Where traditional indications for CABG are present, the patient should be appropriately advised and consented. • Operators may choose not to tackle all lesions at one sitting, especially if one or more are CTOs, bifurcations, and so on; subsequent PCI are referred to as staged procedures. • Operator preference may dictate the order of lesions tackled: many operators prefer to tackle the most challenging lesion first, reserving the option of CABG if unsuccessful, rather than leave the patient only partially revascularized. Complications • As for any PCI procedure. • Increased risk of hypotension/​haemodynamic compromise if target vessel occlusion occurs in the setting of multivessel stenoses. • Increased number of stents/​stent length deployed may increase the risk of restenosis and stent thrombosis.



Multivessel PCI



PCI in patients with diabetes Diabetic patients offer a particular challenge for revascularization; they are more likely to have diffuse multivessel disease in small-​calibre vessels, in the setting of impaired LV function, cerebrovascular disease, and renal impairment. Historical trials have favoured CABG as the mode of revascularization of choice, as it appears to offer diabetics a mortality benefit. The following measures should be considered when optimizing the patient for the procedure: • Maintenance of glycaemic control (glycated haemoglobin ≤7.0%) prior to the procedure. • Pretreatment with statins to lower cholesterol and reduce periprocedural myonecrosis. • Prehydration, administration of N-​acetylcysteine, and minimizing contrast load (% p.312) where renal function is impaired. • Consideration should be given to administration of GPIs (% p.224), especially in insulin-​treated diabetics. • DESs (% p.202) should be considered in view of the high risk of restenosis in diabetics.



Further reading ARTS II Investigators. Sirolimus-​eluting stent implantation for patients with multivessel disease: rationale for the arterial revascularization therapies study part II. Heart 2004; 90: 995–​98. Chaitman BR, Rosen AD, Williams DO, et  al. Myocardial infarction and cardiac mortality in the Bypass Angioplasty Revascularization Investigation (BARI) randomized trial. Circulation 1997; 96: 2162–​70. King SB III, Kosinski AS, Guyton RA, et  al. Eight year mortality in the Emory Angioplasty versus Surgery Trial (EAST). J Am Coll Cardiol 2000; 35: 1116–​20. Serruys PW, Unger F, Sousa JE, et al. Comparison of coronary artery bypass surgery and stenting for the treatment of multivessel disease. N Engl J Med 2001; 344: 1117–​24. SoS Investigators. Coronary artery bypass surgery versus percutaneous coronary intervention with stent implantation in patients with multivessel coronary artery disease (the Stent or Surgery trial): a randomized controlled trial. Lancet 2002; 360: 965–​70.



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Bifurcation lesions Background • Up to 15% of all PCI target lesions are bifurcation lesions, that is, involving an adjacent side branch. • PCI for such lesions is challenging due to the increased risk of periprocedural complications (usually due to compromise/​occlusion of the side branch) and the variety of different strategies that may be employed in such cases.



Classification of bifurcation lesions • Bifurcation lesions may be classified according to the location of lesion(s) in the main/​parent vessel and the side branch (Fig. 8.19).



Protection of the side branch The need to electively consider a strategy that protects the side-​branch limb of a bifurcation (by either balloon prior to dilation or simply wiring the vessel) depends upon the side-​branch calibre, its area of distribution, and the degree of ostial involvement: • Vessels with a calibre less than 2.0 mm are rarely considered for treatment. • Side-​branch occlusion is rare when pretreatment ostial stenosis is less than 50%.



Approaches to bifurcation lesions • Several approaches (% p.238) have been developed for the treatment of bifurcation lesions, but there is little evidence to suggest any one approach has superiority over the relatively simple technique of ‘provisional T-​stenting’ (% p.238)—​stenting of the main vessel with balloon dilatation of the side branch, and subsequent stenting only if the vessel remains compromised.



Fig. 8.19  Medina classification of bifurcation lesions. x,y,z (0 = none, 1 = present) where x is a lesion in the proximal main vessel, y is a lesion in the distal main vessel, and z is a lesion in the side branch



Bifurcation lesions



‘Kissing’ inflations • A final simultaneous ‘kissing’ inflation, with two balloons deployed simultaneously in the main and side-​branch vessels is advisable, regardless of bifurcation stent technique, to ensure optimal stent expansion and shaping of the bifurcation carina. This technique has been demonstrated to improve outcomes (Fig. 8.20). • Most currently available 6 F guiding catheters have lumens large enough to accommodate two balloon catheters for kissing inflations.



‘Kissing’ inflation Fig. 8.20  Bifurcation lesion PCI. Type 1 LAD/​D1 bifurcation lesion treated by ‘provisional T’ technique; following main and then side-​branch dilation, single stent deployed in LAD. After wire exchange, kissing inflation performed to optimize result. Pre and post-​treatment angiograms in LAO 50° 30° projection shown



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Bifurcation PCI techniques There are a large number of techniques that have been described for PCI of bifurcation lesions. Fig. 8.21 shows ten different approaches.



Provisional Crossover Stenting technique • This technique involves pre-dilation and stenting of the main vessel with either no intervention or balloon dilatation (typically kissing balloon inflation) of the side-branch ostium (Fig. 8.21, part 5). When required (typically because of severe stenosis or impaired flow on the side branch due to significant plaque or carina shift) provisional crossover stenting technique can be converted into two stents techniques. Most common bail-out two-stents techniques after provisional stenting are T-stenting, T-stenting with a small protrusion (TAP) or culotte.



T-stenting and T with a small protrusion (TAP technique) • Both approaches can be used as “by-intention two-stents technique” or as “bail-out technique” after failed provisional-crossover. • T-stenting is to be preferred when the angle between the main and the side branch approaches 90°. TAP should be preferred when the angle between main and side branch is 33). • PCI on last patent vessel. High co-​morbidity burden • Heart failure. • Severe valvular disease. • Chronic obstructive pulmonary disease. • Kidney failure. • Diabetes. • Elderly. • Peripheral vascular disease. • Prior cardiac surgery. • Acute presentation. • Electric instability. Haemodynamic compromise • Ejection fraction less than 35%. • Systolic blood pressure less than 100 mmHg. • Cardiac Index less than 2.2 L/​min/​m2.



Choice of MCS In cardiogenic shock, selection of the MCS device should be made according to the severity and acuteness of shock. See Fig. 9.8. severe



Heart failure



ECMO



Impella Durable VADs



IABP



Heart transplant



moderate acute



chronic



Fig. 9.8  Choice of MCS depending on severity and chronicity of heart failure. ECMO, extracorporeal membrane oxygenation; IABP, intra-​aortic balloon pump; VAD, ventricular assist device



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As a general rule, cardiogenic shock is severe in the presence of the following: Clinical features • Blood pressure less than 90 mmHg. • Heart rate greater than 120 bpm. • Lactate greater than 4 mmol/​L. • Cool extremities. • Patient mentally obtunded. • Two or more inotropic/​vasoactive drugs required. Haemodynamic features • Cardiac Index less than 1.5 L/​min/​m2. • PCWP greater than 30 mmHg. • LVEDP greater than 30 mmHg. • Cardiac power less than 0.6 Watts. The selection should be based on the following • Amount of haemodynamic support needed. • Amount of cardioprotection needed (veno-​arterial extracorporeal membrane oxygenation (VA ECMO) offers the best haemodynamic support, but very poor cardioprotection). • Ease of use. • Risk of complications. • Contraindications.



Mechanical cardiopulmonary resuscitation



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Intra-​aortic balloon pump All cardiac CathLabs performing PCI should have immediate availability of an intra-​aortic balloon pump (IABP). Indications and contraindications for an IABP are shown in Box 9.1.



Mechanism • A long (34 or 40 cm) balloon is placed in the proximal descending aorta. Rapid expansion of the balloon in diastole displaces blood and promotes flow distally to the mesenteric, renal, and lower limb vessels. • Augmented flow also occurs proximal to the balloon, to the head and neck vessels and coronary arteries. • Flow in coronary vessels mainly occurs in diastole and use of an IABP is associated with a substantial improvement in coronary perfusion. • Abrupt balloon deflation at the start of systole decreases the afterload resistance to LV contraction, improving performance and decreasing cardiac work. • The balloon is inflated and deflated with helium via a pressurized line, fed from a reservoir cylinder. • Inflation and deflation cycles are timed from the surface ECG and adjusted so that the balloon inflates immediately after aortic valve closure and deflates at the end of diastole (Fig. 9.9).



Sizing • IABP balloons are generally sized according to the patient’s height. • The manufacturer, Datascope, recommends that the sizes of its balloons are: • 25 mL for height of less than 152 cm. • 34 mL for height of 152–​163 cm. • 40 mL for height of 164–​183 cm. • 50 mL for height of greater than 183 cm.



Practical considerations • Most patients with an IABP receive systemic anticoagulation with IV heparin; platelet count should be monitored with prolonged heparin infusion. • Distal pulses should be marked and checked regularly. • IABP therapy is less effective in patients with a tachycardia, especially if the rhythm is irregular. These patients may need careful review with inflation/​deflation cycles being triggered by changes in aortic pressure rather than the surface ECG. • In the event of IABP failure (balloon rupture, exhausted helium supply, ECG trigger failure), pumping must be resumed in 10–​15 minutes or the balloon catheter removed. A static IABP is a potential source of clot formation and distal arterial embolization. • Some patients require weaning from IABP support. The usual method is to reduce the balloon inflation frequency to every second, and later to every third cardiac cycle. • Though it is possible to draw arterial blood samples from the pressure monitoring line of an IABP, this should be avoided as the calibre of the line is narrow and prone to blockage if contaminated with blood.



Intra-aortic balloon pump



Box 9.1  Intra-​aortic balloon pump: indications and contraindications Indications • Cardiogenic shock. • Intractable myocardial ischaemia. • Severe pulmonary oedema. • Severe mitral regurgitation with cardiac failure. • Ventricular septal defect with severe cardiac failure (especially post MI). • Support during CABG and coronary angioplasty (% p.231). Contraindications • Significant aortic regurgitation. • Significant aortic stenosis. • Hypertrophic obstructive cardiomyopathy with significant gradient. • Known aortic dissection. • Significant peripheral vascular disease (relative contraindication). Cautions • May sometimes worsen renal blood flow. • Peripheral vascular compromise can occur, usually affecting the leg on the side of insertion, though ischaemia of the contralateral limb can also occur. A cold, pale, and painful limb with reduced pulses demands immediate specialist attention.



Fig. 9.9 Augmented diastolic flow



Fig. 9.10  Intra-​aortic balloon catheter. Designed for sheathed or sheathless insertion



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• IABP catheters can be inserted directly or via a sheath into the femoral artery. At the time of removal, the used balloon will not usually retract through the sheath. The IABP catheter should be slowly withdrawn until the balloon reaches the sheath. At this point, resistance will be encountered. The sheath and balloon catheter are then pulled out together as a single unit (Fig. 9.10). • Pressure haemostasis will be required as for any arterial line (% p.55). • IABP devices tend to be 7.5 F or larger and prolonged compression will be required. Insertion tips for the Datascope system • Obtain arterial access using the Seldinger technique (% p.44) and then use the dilator over the wire. • Remember to use the introducer wire from the balloon pump kit. It is smaller in diameter than a standard exchange wire and will not fit down the balloon lumen. • Attach the one-​way valve to the balloon and, using a large syringe, apply a vacuum to the balloon. • Advance the balloon over the guide wire until the tip lies just distal to the left subclavian artery. Use X-​ray screening if available to confirm position. • Advance the sheath seal into the hub of the sheath (if used) and secure it to the patient’s leg. • Remove the guide wire and aspirate 3 mL of blood. • Flush the inner lumen to ensure there is no trapped blood in the circuit and attach the pressure circuit. • Remove the one-​way valve yellow lumen insert from the balloon. • Connect the balloon to the catheter extender and then connect this to the pump (Fig. 9.11).



Transport Transfer of an unstable patient with an IABP may be required for revascularization or cardiac surgery. If a patient is being transferred with an IABP then ensure: • The ambulance or aircraft is suitably equipped with adequate loading and equipment securing capabilities. • The transporting personnel are suitably trained to work an IABP. • The power supply is sufficient (bring a spare battery). • The receiving centre has a pump available to switch to. • Plans are made to return the IABP machine. • Telephone communication is available for advice.



Timing Inflation and deflation of the balloon are usually timed to the ECG. Machines allow pressure traces to be frozen to allow examination and optimization of the timing (Fig. 9.12). Balloon inflation should begin immediately after the aortic valve closes (the dicrotic notch) and deflation at just before systole (the R wave). See Figs. 9.13–​9.17.



Intra-aortic balloon pump



Fig. 9.11  Coronary angiography of the left coronary artery during intra-​aortic balloon pumping. The balloon inflates during diastole (see ECG). Catheters for coronary angiography or PCI can be exchanged past the balloon



Fig. 9.12  IABP screen. Detailed information provided on the screen of an IABP machine. The IABP is being triggered (top right) by pressure. Heart rate is 79 bpm. Augmented pressure is 140 mmHg. Aortic pressure waveform and balloon waveform are shown. The machine is running low on battery. There is a good supply of helium in the tank



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Fig. 9.13 Normal inflation/​deflation cycle. Balloon inflation occurs just after aortic valve closure, resulting in augmented diastolic pressure, reduced aortic end-​diastolic pressure, and reduced systolic pressure. A = unassisted aortic end-​diastolic pressure; B = unassisted systolic pressure; C = diastolic augmentation; D = assisted aortic end-​ diastolic pressure; E = assisted systolic pressure



Fig. 9.14  Early inflation of IABP. The balloon inflates before aortic valve closure so the diastolic augmentation (C) encroaches upon the systolic wave (B). This can result in early aortic valve closure, aortic regurgitation, elevation of the LVEDP, and increased myocardial oxygen requirement



Fig. 9.15  Late inflation of IABP. The balloon inflates after aortic valve closure so the diastolic augmentation (C) is suboptimal



Intra-aortic balloon pump



Fig. 9.16  Early deflation of IABP. The balloon deflates early with a sharp, suboptimal drop in augmented pressure (C to D). There may be retrograde blood flow and myocardial oxygen demand may increase



Fig. 9.17  Late deflation of IABP. The balloon deflates while the aortic valve is starting to open. The diastolic augmentation period (C) is prolonged with similar assisted (D) and unassisted (A) aortic pressures. There is a prolonged period of assisted systole (E). There is little (if any) afterload reduction and myocardial work may increase as the left ventricle is contracting against the balloon



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Impella® The LV Impella® system consists of an intravascular microaxial blood pump inserted into the left ventricle through the aortic valve. A pigtail is present at the distal end of the device to allow atraumatic resting within the LV cavity. The pump is placed underneath the aortic plane and it aspirates blood from the left ventricle shifting it into the ascending aorta.



The LV Impella® allows LV support by • Increasing cardiac output. • Reducing myocardial O2 consumption. • Reducing PCWP. Compared to an IABP it does not require a native LV systolic pulsation to be present. In other words, the more dysfunctional the left ventricle is, the more functional the LV Impella® becomes. Compared to an IABP, the LV Impella® requires larger vascular access (thus a higher risk of access-​related complications), requires prolonged anticoagulation, is more expensive, and presents a longer learning curve. The device is inserted via the femoral or axillary artery and it is available in three different sizes. More recently, a new iteration of the device, the Impella® RP, has been introduced specifically to address the failing right ventricle. It is inserted via the femoral vein into the main pulmonary artery. See Fig. 9.18. It currently is indicated in the following contexts • RV infarction with refractory failure. • RV failure post LV assist device. • RV failure post cardiac surgery. • Biventricular failure. • Acute RV failure from massive pulmonary embolism.



Contraindications for Impella® use • LV thrombus. • Mechanic aortic valve. • Severe aortic stenosis. • Moderate/​severe aortic regurgitation. • Significant peripheral vascular disease. • Contraindications to anticoagulation.



Possible Impella®-​related complications • Device migration. • Device thrombosis. • Limb ischaemia. • Vascular trauma. • Haemolysis. • Stroke. • Infection.



IMPELLA ®



LV IMPELLA®



Cardiac output: 2.5 L/min Access site size: 12 F Cardiac output: 3.5 L/min Access site size: 14 F Cardiac output: 5.0 L/min Access site size: 21 F



IMPELLA® RP



Fig. 9.18  The LV Impella® and Impella® RP systems



Cardiac output: 4 L/min Access site size: 23 F



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Extracorporeal membrane oxygenation Due to its relatively simpler mode of insertion, ECMO is probably the most adopted modality of extracorporeal life support (ECLS) in the CathLab. According to the position of the cannulas, it is possible to distinguish between: • Veno-​arterial (VA) ECMO: one cannula into the femoral artery and one into the inferior vena cava (through femoral vein). VA ECMO is meant for providing oxygenation and circulatory support (combined lung and heart failure). • Veno-​venous (VV) ECMO: both cannulas are in the venous system. This form of ECMO is meant to supply only for impaired oxygenation (and not for both impaired oxygenation and circulation as VA ECMO). For this reason, it is usually considered for isolated lung failure.



Major contraindications for ECMO use • Moderate severe aortic regurgitation. • Significant peripheral vascular disease. • Contraindications to anticoagulation.



Possible ECMO-​related complications • Bleeding. • Limb ischaemia. • Vascular trauma. • Compartment syndrome. • Acute kidney injury. • Haemolysis. • Thrombus and air embolism. • Infection. • Neurological injury. Compared to other percutaneous MCS devices, ECMO offers both cardiac and pulmonary support, even though it does present some disadvantages: • Larger access site (surgical cut-​down is often required). • Need for continuous anticoagulation. • Higher risk of systemic thromboembolism. • Poor coronary perfusion. • Risk of ventricular distension. • More complex management. • Need of a dedicated and experienced staff (ECMO team).



Methods An external pump drains blood from a venous cannula (18–​21 F) towards an oxygenator. Oxygenated blood is then pumped into the aortic arch through the arterial cannula (14–​16 F). VA ECMO can guarantee from 3 to 7 L/​minute of cardiac output (vs max. 5 L/​minute for Impella® 5.0).



Chapter 0



Complications Risks of complications  278 Death  279 Myocardial infarction  280 Pulmonary oedema  281 Stroke  282 Hypotension  283 Cardiac tamponade  284 Contrast reaction  286 Vasovagal reaction  287 Arrhythmia  288 Vascular complications  294 Limb ischaemia  296 Coronary dissection  300 Left main stem dissection  302 Iatrogenic type A aortic dissection  304 Air embolism  306 Coronary perforation  308 Renal failure  310 Contrast nephropathy  312 Cholesterol embolization  314



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Risks of complications Cardiac catheterization is an invasive study that involves real risks to the patient. The risks increase with patient age and co-​morbidity. Though vascular complications (particularly haematoma formation) and vasovagal reactions are more common, the risk of serious complications from diagnostic cardiac catheterization and coronary angiography remains low: • Death (% p.279) 0.1%. • Myocardial infarction (% p.280) 0.1%. • Pulmonary oedema 0.1%. • Stroke (% p.282) 0.1%. • Cardiac tamponade (% p.284) 0.1%. • Contrast reaction (% p.286) 0.4%. • Vasovagal reaction (% p.287) 2–​3%. • Arrhythmia (% p.288) 0.4%. • Ventricular fibrillation (VF). • Ventricular tachycardia (VT). • Atrial fibrillation (AF). • Supraventricular tachycardia (SVT). • Heart block. • Vascular complications (% p.294) 1–​2%. • Haemorrhage. • Pseudoaneurysm. • Arteriovenous fistula. • Infection. • Coronary dissection (% p.300) 0.1%. • Air embolism (% p.306) 0.4%. • Renal failure 0.7%. • Cholesterol embolization 1.4%.



Death



Death Unfortunately, death remains a recognized complication of invasive cardiac procedures. It occurs infrequently during cardiac catheterization (1 in 1000 cases). The standard consent procedure prior to the investigation should include mention of mortality. The mortality risk from cardiac catheterization increases with: • Age. • Left main coronary stenosis. • Three-​vessel coronary disease. • Impaired ventricular function. • Class IV heart failure. • Aortic valve disease.



Unexpected death in the catheter lab Unexpected mortality is one of the most traumatic complications in the CathLab. Acute vessel occlusion, coronary dissection (% p.300; occasionally in patients with normal coronary arteries), massive air embolism (% p.306), intractable ventricular arrhythmias (% p.288), and pericardial tamponade (% p.284) are cited causes.



Relatives Make an effort to contact the deceased patient’s next of kin and/​or family and explain the course of events. Complaints and litigation can often be avoided with effective communication. If there has been an iatrogenic complication then speak to your unit manager and complete an adverse incident form according to local hospital policy. Let the family view the body if they wish to with suitable privacy. Be aware of any special religious requirements.



Reporting death The primary care physician should be notified at an early opportunity as they will be involved in bereavement counselling for the family. The case should also be discussed with the hospital coroner. If death is unexplained then a postmortem should be requested.



Documentation It is important for all staff to write clear, legible notes documenting the exact timing of events, the personnel present, equipment used, and the perceived mechanism of death. Document if the next of kin has been contacted and what has been said.



Handling staff (including yourself ) A death in the cardiac CathLab often involves a prolonged attempt at cardiac resuscitation and a large number of staff. It is physically and psychologically demanding. Following a mortality case, the cardiologist in charge of the case should ensure that the staff have time to talk about the case and, if necessary, should cancel or postpone further procedures. Some hospitals offer a counselling service to deal with involvement in death.



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Myocardial infarction The incidence of STEMI during cardiac catheterization is low (0.1%) and is related to vessel occlusion due to dissection, emboli of air (% p.306), thrombus, or of atherosclerotic debris. The definition of MI is under constant review. With the regular measurement of cardiac enzymes (particularly creatine kinase-​MB isoenzyme and cardiac troponins) following PCI, small enzymatic events are being recognized and diagnosed as a periprocedural MI. These are usually silent events with no abnormalities on the ECG but are associated with an increased future risk of death or MI.



Diagnosis and presentation • The diagnosis of vessel occlusion is usually quickly apparent on angiography. • Patients often complain of chest pain with signs of pallor and sweating. • Hypotension, bradycardia (% p.291), and ventricular tachyarrhythmias (% p.288) are common. • With vessel occlusion, the ECG usually shows ST-​segment elevation in the affected territory (Fig. 10.1).



Management • Ensure a patent airway and give 100% O2. • Immediate revascularization using PCI is the gold standard. • If cardiogenic shock ensues then insert an IABP (% p.268) if available. • If revascularization is not an option then patients can be managed conservatively using supportive measures (such as inotropes). • Thrombolysis in this situation is not usually recommended. • In hospitals without on-​site interventional support, consider urgent transfer for revascularization.



Fig. 10.1 STEMI



Pulmonary oedema



Pulmonary oedema Pulmonary oedema usually occurs in patients during cardiac catheterization as a result of the administration of large volumes of contrast in: • Patients with LV impairment. • Patients with elevated LVEDP (% p.89). • In patients with severe aortic (% p.108) and mitral (% p.112) stenosis. • Patients with dialysis-​dependent renal failure. Pulmonary oedema may also occur as part of a contrast reaction (% p.286) or due to myocardial ischaemia (% p.280).



Management • Administer high-​flow O2. • Sit the patient up if possible. • Administer an IV loop diuretic (e.g. furosemide 80–​100 mg). • If systolic blood pressure is greater than 100 mmHg, consider an infusion of IV nitrates (e.g. isosorbide dinitrate 2–​10 mg/​hour). • Continuous positive airways pressure-​assisted ventilation can be extremely effective in acute pulmonary oedema. • Consider intra-​aortic balloon pumping (% p.268). • Admit for close monitoring and further treatment.



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Stroke Stroke during cardiac catheterization (1 in 1000 cases) usually occurs due to mechanical dislodgement of atherosclerotic material from the aortic wall (% p.306) or due to embolus of thrombus. The risk of stroke is higher in elderly patients with known atheroma or prior stroke and in patients with diabetes mellitus, renal failure, hypertension, and aortic valve disease. Other causes of stroke include: • Emboli of air (% p.306). • Dissection of a carotid or vertebral artery (particularly during LIMA cannulation % p.178). • Thromboembolism from existing thrombi (e.g. LV thrombus % p.101) or from clot formation on catheters and wires. • Intracranial haemorrhage.



Avoiding stroke Before starting a procedure, carefully inspect all tubing, manifold, and syringes for air bubbles. Flush all catheters and clean the guide wires before use with heparinized saline (% p.76). Changing catheters over a guide wire reduces the risk of atherosclerotic plaque disruption. Consider systemic anticoagulation in high-​risk cases and monitor the coagulation time (% p.218).



Diagnosis and presentation • Patients may be only mildly symptomatic but can develop severe symptoms including hemiparesis, aphasia, and coma. • The commonest symptoms include visual disturbance, weakness, aphasia, and altered mental state. • Vertebrobasilar insufficiency occurs in almost half of cases. • Symptoms may develop hours after the study due to late embolization.



Management • Ensure: Airway, Breathing, Circulation and treat accordingly. • Abandon the case and remove any catheters. • Perform a full neurological examination and document findings in the medical records. • Think about the patient’s anticoagulation status. Is this a haemorrhagic or an embolic event? • Arrange CT to exclude haemorrhage. • There have been case reports describing the successful use of systemic and local thrombolysis for extensive embolic stroke. • Many neurological events completely resolve clinically within 24 hours. • Enlist expert neurological input for rehabilitation (e.g. stroke unit).



Hypotension



Hypotension Hypotension is a common pre-​, peri-​, and post-​cardiac catheterization complication. Patients are often mildly dehydrated due to fasting and may be on a combination of hypotensive cardiac medications. Often a slow IV infusion of fluids is all that is required. Hypotension can also occur due to a number of other reversible causes, some of which are life-​threatening if left untreated: • Pericardial tamponade (% p.284). • Contrast reaction (% p.286). • Vasovagal reaction (% p.287). • Bleeding (% p.294). • Myocardial ischaemia (% p.280).



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Cardiac tamponade Cardiac tamponade is a potentially catastrophic complication of cardiac catheterization. It is recognized during: • PCI, usually as a result of coronary perforation (% p.308). • Left ventriculography, due to intramyocardial injection (Fig. 10.2). • Manipulation of catheters and pacing wires in the right ventricle (as the right ventricle is relatively thin walled).



Diagnosis and presentation • Clinical deterioration can be rapid with tachycardia, hypotension, and syncope occurring within minutes. • During angiography, contrast can often be seen collecting around the heart in the pericardial space. • Echocardiography will confirm the diagnosis (% p.123) but if there is a high clinical suspicion then perform immediate pericardiocentesis (% p. 254).



Management • Early recognition is important. • Perform pericardiocentesis (% p.254) and leave the drain in until bleeding has stopped (this may be a few days). • Think about the patient’s anticoagulation status and consider reversing heparin with protamine (% p.285), and administering platelets and clotting factors. • Treat the cause if possible (e.g. seal of coronary perforation using covered stents or coils % p.308).



Fig. 10.2  Pericardial effusion complicating left ventriculography. The catheter position in the left ventricle (LV) resulted in intramyocardial injection of contrast and extravasation into the pericardium (arrowed)



Cardiac tamponade



Protamine sulphate This is used to reverse the effects of heparin. In high doses it has an anticoagulant effect. It is given as an IV infusion over 10 minutes (maximum 50 mg): 1 mg neutralizes 80–​100 units of heparin (when given within 15 minutes of heparin). Heparin is rapidly excreted (half-​life around 60–​90 minutes) so use lower doses if longer than 15 minutes has elapsed. Allergic reactions are reported, particularly in patients with diabetes who have received isophane insulin.



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Contrast reaction Anaphylactoid reactions to contrast material are becoming less common during coronary angiography (0.4%) due to the use of non-​iodinated hypo-​ osmolar agents. Nevertheless, patients can rapidly deteriorate with profound hypotension and airway obstruction. Reactions are usually type 1 immunoglobulin E-​mediated hypersensitivity.



Avoiding a contrast reaction • Patients with a prior history of anaphylaxis, contrast reaction, atopy, and asthma are at the highest risk. • In patients with prior contrast reactions, administer chlorpheniramine 10 mg (or similar antihistamine) and hydrocortisone 100 mg intravenously 1 hour before the procedure.



Diagnosis and presentation • Symptoms usually start within 15 minutes of the first injection. • Signs and symptoms include pruritus, flushing, cyanosis, rash, wheezing, and angio-​oedema. • Tachycardia and hypotension can occur.



Management • Early recognition is important. • Ensure a patent airway and give 100% O2. • Administer IV hydrocortisone 200 mg and an antihistamine (e.g. chlorpheniramine 10 mg). • Give epinephrine 0.5 mg IM (0.5 mL of 1:1000). • Give nebulized bronchodilators (salbutamol 5 mg) for bronchospasm. • Commence IV fluids with 0.9% saline. • Blood test for serum tryptase will show elevated levels if there has been mast cell degranulation. Anaphylaxis In severe anaphylaxis, patients consider epinephrine 100 micrograms intravenously (1 mL of 1:10,000). Patients can become rapidly pulseless with profound hypotension. In this instance, then treat for pulseless electrical activity (% p.289) with chest compressions and ventilation.



Vasovagal reaction



Vasovagal reaction Faints are common in patients undergoing cardiac catheterization (2–​3%). High emotional states, dehydration, mild starvation, and an anticipated painful stimulus render patients susceptible to neurocardiogenic syncope (combined cardioinhibitory and vasodepressor). Young, anxious males seem particularly affected. Attacks often occur on the ward prior to the procedure especially during venesection and cannulation. Vasovagal reactions are also seen at the time of arterial puncture or during compression haemostasis.



Diagnosis and presentation Patients often complain of feeling non-​specifically unwell, fatigued, nauseated, and sweaty. The heart rate will usually start to slow before the blood pressure drops. The patient may become pale, syncopal, apnoeic, and appear dead. Ensure that the diagnosis is correct. Tamponade can present similarly and just as quickly but usually is associated with tachycardia. If there is any uncertainty, arrange immediate echocardiography.



Management • Early recognition may abort syncope. • Lie the patient down and elevate the patient’s legs (if possible). • Connect an ECG monitor and commence regular haemodynamic monitoring. • Administer atropine 0.5–​1.0 mg intravenously. • Start a rapid infusion of 0.9% saline. • Symptoms should improve within a few minutes. If not, then reconsider the diagnosis and exclude other causes of hypotension (e.g. MI, cardiac tamponade, or retroperitoneal bleed).



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Arrhythmia Transient benign arrhythmias are frequently seen during cardiac catheterization, particular supraventricular and ventricular ectopics and sinus bradycardia. More sinister arrhythmias are discussed in this section.



Ventricular fibrillation See Fig. 10.3. • Often a result of catheter manipulation near the ostium of a stenosed coronary artery, plugging of a coronary artery (e.g. intermediate vessel), injection in the conus branch of the right coronary artery (% p.135), or due to other complications resulting in coronary ischaemia (e.g. coronary dissection (% p.300) or air embolus (% p.306)). • VF needs immediate defibrillation (% p.260) using standard Advanced Life Support algorithms. • If VF is resistant to attempts at defibrillation then consider giving amiodarone 300 mg IV and using a different defibrillator. • Treat reversible causes—​correct K+, Mg2+.



Ventricular tachycardia See Fig. 10.4. • Precipitants are similar to those of VF. VT can also be induced during right heart catheter manipulation (particularly in the RV outflow tract % p.90) and during LV catheterization (% p.86). • Haemodynamically poorly tolerated VT needs immediate cardioversion using synchronized direct current (DC) shock under sedation/​general anaesthesia (200–​360 J or equivalent biphasic energy). • If VT is reasonably tolerated then consider giving a beta-​blocker (e.g. bolus metoprolol 5 mg IV) or amiodarone 150 mg IV over 10 minutes through a large vein. Both can be repeated. • Monitor for hypotension, inform an anaesthetist, and prepare for DC cardioversion.



Fig. 10.3  Ventricular fibrillation



Fig. 10.4  A regular, wide-​complex tachycardia. The QRS shape is constant although may be distorted if there is visible AV dissociation (arrowed)



Arrhythmia



• If blood pressure remains stable, consider lidocaine 50 mg IV over 2 minutes, repeated every 5 minutes until a maximum of 200 mg is given. • Stable monomorphic VT may respond to overdrive pacing (% p.289). • If VT persists, perform synchronized DC shock under sedation/​general anaesthesia (200–​360 J or equivalent biphasic energy).



Overdrive pacing • Sustained monomorphic VT may be terminated painlessly by antitachycardia pacing in 80–​90% of cases. • After positioning a transvenous pacing wire in the right ventricle (% p.256), pacing is performed at a rate 15–​20 bpm faster than the VT. • On many temporary pacing boxes there is a ‘×3’ setting on the rate for this reason. • A high output (5–​10 V) may be required. • Capture of the VT is indicated by a change in QRS morphology and an increase in heart rate on the monitor to the pacing rate. • Pacing is abruptly terminated after 5–​10 seconds of ventricular capture. • There is a risk that acceleration of the VT may occur with degeneration to pulseless VT or VF so operators must be prepared for immediate defibrillation. • Once sinus rhythm has been restored, constant background pacing at 90–​110 bpm may be performed to prevent recurrent attacks. This is particularly useful if VT occurs in the setting of pauses or bradycardia.



Atrial fibrillation See Fig. 10.5. • During cardiac catheterization it can be precipitated by atrial irritation during right heart catheterization, by cardiac ischaemia, or by pericarditis. • Patients may be asymptomatic or symptoms and signs ranging from palpitation, chest pain, dyspnoea, and presyncope to syncope and frank pulmonary oedema. • The majority of induced AF episodes will spontaneously terminate without treatment. • If AF results in severe haemodynamic compromise (ventricular rate >150 bpm, hypotension and hypoperfusion, reduced conscious level, pulmonary oedema, cardiac ischaemia) then: • Administer high-​flow O2. • Give heparin 5000–​10,000 IU IV.



Fig. 10.5  An irregular rhythm with no obvious discrete P-​wave activity



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• Perform immediate cardioversion using a synchronized DC shock under sedation/​general anaesthesia (360 J monophasic or 200 J biphasic energy). • If AF is only minimally symptomatic with mild–​moderate haemodynamic compromise (ventricular rate