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

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Cardiac
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Cardiac
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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
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First Edition published in 2008
Second Edition published in 2020
Impression: 1
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v
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 encom-

passed 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
vii
Preface
This latest edition of Cardiac Catheterization and Coronary Intervention ex-

pands 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 cath-
eterization, 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 com-
ponent of modern cardiac care. Since the first edition of this book, the
development of complementary cardiac imaging techniques such as car-
diac 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 inter-
ventional 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 cath-
eterization and coronary angiography.
ARJM
GLDM
AB
November 2019
ix
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 con-
tributed 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.
xi
Contents
Symbols and abbreviations xiii

Contributors xvii
References xix
1 Introduction 1
2 The team 25
3 Vascular access 43
4 Cardiac catheterization 71
5 Specific conditions 107
6 Coronary angiography 129
7 Coronary artery bypass graft angiography 165
8 Percutaneous coronary intervention 183
9 Additional procedures 253
10 Complications 277
11 Post procedure 315
Index 323
xiii
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
xiv S YMBOLS AND ABBREVIATIONS
INR international normalized ratio

IR(ME)R 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
S YMBOLS AND ABBREVIATIONS xv
SVG saphenous vein graft

SVR systemic vascular resistance
SVT supraventricular tachycardia
TAVI transcatheter aortic valve intervention
TLR target lesion revascularization
VF ventricular fibrillation
VSD ventricular septal defect
VT ventricular tachycardia
WHO World Health Organization
xvii
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
xix
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/
1
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
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 ref-
erence 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 3
History of cardiac catheterization
The first human heart catheterization studies were performed using a modi-
fied urinary catheter that was inserted via the internal jugular vein into the
right atrium. This work was initially performed on cadavers but, by per-
forming 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 angi-
ography in 1959. In 1977, Andreas Grüntzig performed the first coronary
angioplasty in Zurich on a severe proximal left anterior descending cor-
onary artery lesion in a 38-year-old man (% p.184). The first coronary ar-
tery 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.
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 mo-
dalities. This includes the evaluation of left ventricular function, the assess-
ment of valvular heart disease, pericardial disease, congenital heart disease,
and cardiomyopathies.
In general terms, the only absolute contraindication to cardiac catheter-
ization 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
Indications for coronary angiography
Coronary angiography is primarily used to determine the coronary
anatomy and to identify any luminal stenoses. It provides some infor-
mation 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 7
• 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 catheter-
ization 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.
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 evi-
dence 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 sig-
nificantly lower (<50% in some studies) and strongly influenced by technical
and patient-related factors.
When compared to invasive angiography, the diagnostic accuracy of car-
diac CT has been showed to be influenced by:
• Type of scanner (a 64-detector row scanner is the minimum standard).
• Pretest CAD probability.
• High coronary artery calcium score.
• High heart rate.
• High body mass index.
For this reason and because of the strong negative predictive value, car-
diac CT is currently indicated mainly to rule out CAD.
Currently, these are the main indications for cardiac CT

• Ruling out CAD in patients without established CAD who present
with typical or atypical angina or with non-anginal chest pain plus an
abnormal resting ECG.
• Ruling out stable CAD in patients with low to intermediate pretest
probability or after an inconclusive functional test.
• Ruling out coronary lesions in patients admitted with suspected acute
coronary syndrome and inconclusive ECG and cardiac-injury markers.
• Assessing patency of saphenous vein grafts (they are less mobile than
native vessels, are larger in size, and tend to not develop calcified
atherosclerosis and for this reason are well assessed by cardiac CT).
Cardiac CT or invasive angiography? 9
• Clarifying coronary anatomy, distal landing zone, and proximal cap

for optimal planning of revascularization in coronary chronic total
occlusions.
• Defining anomalous coronary origin and/or anatomy, including
arteriovenous fistula.
Cardiac CT should NOT usually be considered in
• Patients with high pretest probability of coronary disease.
• High coronary artery calcium score (>1000).
• Large body mass index.
• Previous coronary stenting (CT accuracy for instent restenosis
decreases with stent size <3 mm diameter and thick-strut stents—first
generation).
Cardiac CT in transcatheter aortic valve intervention
Cardiac CT is a key step in the decision- making and planning of
transcatheter aortic valve intervention (TAVI) for aortic stenosis, by pro-
viding details about:
• Size, tortuosity, and disease of femoral and axillary arteries in guiding
vascular access selection.
• Aortic annulus sizing (diameter, area, and perimeter) for selection of
TAVI valve size and type.
• Aortic root and sinotubular junction sizing (relevant for self-expandable
TAVI valve).
• Whole aorta anatomy definition with special regard for tortuosity,
atherosclerosis, and complex lesions (thrombus stratifications,
ulcerations).
• Degree of calcification of the aortic valve.
• Height of coronary artery ostia from the aortic annulus plane.
• Identification of angles for ideal angiographic working view.
Radiology equipment
The standard equipment to produce X-ray-based images in the catheter-
ization laboratory (CathLab) is based on the C-arm fluoroscopic system. It
consists of an X-ray generator and detector:
X-ray generator
(X-ray tube located on the lower part of the C-arm, thus under the patient.)
The X-ray generator or X-ray tube consists of:
• Cathode (negative charge).
• Anode (positive charge).
• Evacuated glass insert.
• Tube housing.
• Collimators.
The cathode usually consists of a coil of tungsten wire which emits electrons
when heated by the passage of electric current. The electrons are acceler-
ated towards the anode by a high potential difference (measured in kilo-
volts (kV)). The anode is a rotating saucer-shaped tungsten disc. When the
electrons emitted by the cathode interact with the anode, X-rays (photons)
are produced (plus heat). The anode rotates to dissipate the heat produced
and the whirring noise usually heard coming from the tube is actually pro-
duced by the rotating anode.
All these reactions take place within an evacuated glass insert containing
both the cathode and the anode. The glass insert itself is contained within a
tube housing with internal lead walls. This lead lining presents a small radio-
lucent window allowing the beam of X-ray to pass through. The housing
tube also presents collimators which are lead panels that can be moved in
by the radiographer to restrict the size of the X-ray beam, thus limiting ra-
diation exposure to the field of interest only.
The energy of the X-ray beam can be influenced by the operator/radi-
ographer acting on:
• Voltage (kV) applied between the anode and the cathode.
• Current (milliampere (mA)) flowing from the cathode to the anode.
• Filtration (aluminium or copper filter at the exit of the X-ray beam).
Increasing photon energy reduces radiation absorption (and thus radiation
dose) because photons are more ‘penetrating’. This, however, is associ-
ated with lower-quality images since, due to less absorption, more photons
reach the X-ray detector leading to lower image contrast. See Table 1.1.
Modern systems have an integrated dose rate control, aiming to modu-
late mA and kV in order to maintain a constant dose of radiation reaching
the detector, thus keeping the image quality steady when other settings (e.g.
projection angles) change.
Radiology equipment 11
Table 1.1 Effects of changing kV
Effect on number of Effect on photon

photons
Energy
Increase kV + +
Increase mA + =
Increase filtration − +
X-ray detector
(Located on the upper part of the C-arm, thus above the patient.)
The X-ray beam, generated by the X-ray generator, passes through the
patient’s body structures, interacting with them mainly by the phenomena
of absorption and scattering. The resulting X-ray beam, exiting from the
patient’s body, reaches the X-ray detector where the image is generated.
There are two types of X-ray detectors:
Image intensifier (old-generation X-ray detector)
Received X-rays are converted into light by an input phosphor and light is
then converted into electrodes by a photocathode. The electrons are then
focused and intensified to interact with an output phosphor which recon-
verts electrons back into light which is then picked by a camera.
Flat-panel detector (new-generation X-ray detector)
A phosphor screen converts X-rays into light, which is then converted into
electrons. These electrons form the digital image.
Fluoroscopy and acquisition
Optimization is the process of ‘getting an adequate diagnostic picture with
the lowest practicable dose’. There are multiples strategies to address
image optimization and they can be grouped as follows:
Equipment-based strategies:
• Dose rate control.
• Projection angles (shallow angles reduce exposure, since less patient
thickness and surface are exposed).
• kV and mA settings.
• Fluoroscopy (pulsed).
• Acquisition.
Technique-based strategies:
• Patient position.
• As distant as possible from the X-ray generator.
• As close as possible to the X-ray detector.
• Collimation.
Broadly, fluoroscopy is defined as the technique used to obtain real-time im-
ages of a body structure. During a CathLab procedure, two main modalities
are used to obtain images:
Fluoroscopy (or pulse fluoroscopy)
This provides real-time imaging. It offers the benefit of lower radiation ex-
posure for the patient and the CathLab team. This is achieved through auto-
mated switching on and off of the X-ray beam throughout the exposure.
In this way, a predefined number of images (frame) will be produced in a
time unit (second). The frame rate in pulse fluoroscopy is typically set at
7.5 frames per second (fps). Because of these settings, pulsed fluoroscopy
offers a lower image quality and it is ideal for scouting shots, wiring, and
balloon and stent delivery. Modern systems now allow storing of a few
seconds of fluoroscopy, eliminating the need to use acquisition purely to
store images.
The acquisition or ‘cine’ mode
This has a higher radiation dose and higher frame rate (usually from 12.5 to
30 fps (7.5 fps at the Oxford Heart Centre)). It is used to obtain a series
of high-resolution images with reduced image noise. These images have
higher resolution and contrast and are saved for recording/diagnosis pur-
poses. The number and length of acquisition or cine ‘runs’ is usually the
main source of patient radiation exposure in interventional cardiology pro-
cedures. This is why acquisition/cine mode should be used sparingly.
Fluoroscopy and acquisition 13
Radiation safety
All staff performing cardiac catheterization and coronary angiography must
be familiar with local radiation protection procedures. There will be a des-
ignated Radiation Protection Supervisor who will check some basic paper-
work and issue dose meters so that radiation exposure can be monitored.
An interventional cardiologist will receive an appreciable amount of radi-
ation that may span several decades. It is important that this is accurately
monitored. Appropriate protective devices (% p.15) should be worn and
all exposures must be ‘as low as reasonably achievable’ (ALARA) (% p.15).
Basic dosimetric quantities
• Most background radiation is received from natural sources (87%),
particularly from radon gas and from gamma rays.
• Medical sources account for at least 10% of ionizing radiation.
• The absorbed dose is the energy absorbed per unit mass and is
measured in grays (Gy; 1 Gy = 1 joule (J)/kg).
• The equivalent dose is the absorbed dose weighted by a radiation
quality factor and is measured in sieverts (Sv).
• The effective dose is that dose that would give the same level of risk if it
had been received uniformly over the whole body.
• Annual dose limits for an exposed worker aged over 18 years should be
less than 20 mSv (averaged over a 5-year period).
• Typical annual whole body doses for an interventional cardiologist are
up to 5 mSv and for a radiologist 0.5–1 mSv.
Biological effects
When ionizing radiation passes through tissue matter it undergoes inter-
actions and loses energy. The biological effects depend not only on the
total energy but also the type of radiation and how the energy is distrib-
uted. Some radiation is transmitted through the tissue and is attenuated
by the film to produce an image. Some radiation is scattered away from
the direction of the primary beam (scattered radiation). Some of the radi-
ation undergoes interactions within the tissue volume with the production
of ionized molecules and free radicals and with direct or indirect damage
to proteins, enzymes, and DNA. If enough cells in a tissue are killed or un-
able to function normally, there will be a loss of function of that tissue or
organ depending on the number of affected cells. These effects are called
deterministic effects and include cataracts, impaired fetal development, and
neurological and gut damage. In the cardiac CathLab, prolonged radiation
to a small area of skin may result in deterministic effects ranging from mild
erythema to skin ulceration. Damage to chromosomal DNA may lead to a
modified cell that can still reproduce, resulting in cancer. These effects are
called stochastic effects.
Radiation safety 15
Ionising Radiation (Medical Exposure) Regulations 2017

In the United Kingdom, the use of ionizing radiation is governed by
the Ionising Radiation (Medical Exposure) Regulations (IR(ME)R) 2017.
Hospitals must define and hold a register of referrers (those entitled
to request procedures—usually clinicians), practitioners (those respon-
sible for accepting requests (usually radiologists)), and operators (usually
radiographers). During cardiac catheterization, the cardiologist is often
the referrer, practitioner, and the operator. A clinical evaluation must be
recorded for all exposures, including fluoroscopy, and doses should be
audited. Hospitals are to be investigated regularly. If a radiation dose is
delivered that is greater than expected, the local radiation protection ad-
visor must be contacted. In cases of overexposure, plaintiffs could bring
an action under criminal (not civil) law.
Radiation protection
Most cardiac CathLabs will have viewing areas protected from the radiation
source by lead glass shields. There will also often be mobile shields for staff
and the operator. Lead gowns are usually one-piece aprons or a separate
top and skirt. The latter may be better suited to those with back problems.
The amount of protection given by lead gowns is described as lead equiva-
lent (LE) and is measured in mm LE. Most gowns are 0.25–0.35 mm LE.
The higher the LE, the heavier the gown. The amount of protection is also
dependent on the output of the radiation source. Lead rubber 0.35 mm LE
thyroid shields should be worn to protect the thyroid gland and lead glasses
to protect the eyes.
The inverse square law

The intensity of the radiation varies inversely to the square of the dis-
tance from the source, that is, stepping back from 1 m to 2 m away from
the source will reduce the radiation exposure by a factor of four.
ALARA
‘As low as reasonably achievable.’
There are two main modes of imaging in the cardiac CathLab: screening
and acquisition. X-rays pass through the patient from the X-ray source be-
neath the patient to the image intensifier. Screening uses low-energy X-ray
pulses to display a real-time image on the screen. Screening is generally used
for catheter and wire positioning and manipulation. Image acquisition uses
a higher X-ray dose and stores the images digitally to a hard disc (and often
to another medium such as a CD).
There are a number of ways in which the radiation dose can be minim-
ized and ALARA:
• Always think about radiation dose when putting your foot on the
screening pedal. Is screening absolutely necessary at this point?
• Ensure that the image intensifier has finished moving before screening.
• Keep the image intensifier as close as possible to the patient.

• Having the X-ray source (beneath the patient) further away from the
patient reduces the dose to the skin.
• Low frame-rate acquisitions may reduce dose at the expense of reduced
image quality—uses may include screening for long interventional
procedures or during pregnancy.
• Use of magnification increases the dose rate to the patient’s skin.
Risk estimates to the patient
An assessment of the probability of inducing a fatal cancer can be made
using data from the survivors of nuclear bombs and from nuclear workers.
The normal lifetime risk of developing cancer (about one in three) must be
taken into consideration with these figures. See Table 1.2.
Table 1.2 Risk estimates to the patient by examination
Examination Typical effective Equivalent Additional lifetime

dose (mSv) background risk of fatal cancer
radiation
Chest X-ray 0.02 3 days 1 in 1,000,000
Abdomen X-ray 0.7 4 months 1 in 30,000
Lumbar spine 1.3 7 months 1 in 15,000
CT head 2.3 1 year 1 in 10,000
Coronary angiogram 6 2.7 years 1 in 3500
Radionuclide cardiac 6 2.7 years 1 in 3500
study (Tc-99m)
Barium enema 7 3.2 years 1 in 3000
CT chest 8 3.6 years 1 in 2500
CT abdomen 10 4.5 years 1 in 2000
CT coronary angiogram 10 4.5 years 1 in 2000
Radiation safety 17
Dose excess
According to the IR(ME)R definition, an incident occurs when a patient re-
ceives an unintended radiation exposure or receives a radiation exposure
greater than intended.
• Near miss: an event which could have led to unintended exposure or
overexposure, which was promptly noted to allow preventative actions
to be put in place.
• Incident not requiring notification.
• Incident requiring notification.
In interventional cardiology, an overexposure is typically considered when
the total exposure is at least ten times greater than the intended dose. As
a general rule, the radiographer must warn the operator when 1 Gy of ra-
diation exposure has been reached. In these circumstances, the operator
is asked to record the degree of radiation exposure in the report and to
communicate it appropriately to the patient.
Radioprotection applies to CathLab staff and not only to patients.
Recommended limits of radiation exposure for CathLab staff are shown
in Table 1.3.
Table 1.3 Recommended limits of radiation exposure for CathLab staff
Effective dose Skin and Eye

extremities
Employee (mSv/year) 20 500 20
Trainee (<18 years old) 6 150 15
(mSv/year)
Dose limit for women of reproductive capacity is 13 mSv to the abdomen for any consecutive
3-month period.
Dose excess 19
Patient preparation
History
• Prior to any invasive cardiac procedure it is vital to have clear
documentation of the indication for the procedure and the cardiologist
responsible.
• It is also important to record if any medical events have happened or
symptoms have changed since that decision was made.
• Prior interventional procedures should be reviewed, paying attention to
vascular access sites, choice of catheters, complications, and outcomes.
• If the patient has had coronary artery bypass graft (CABG) surgery then
the operation note should be made available (% p.166).
• Echocardiography results should be noted.
• The patient’s drug history should be reviewed and allergies (or lack of )
recorded.
• Often this information is performed at a pre-admission clinic but can be
obtained on the morning of admission.
• The patient’s fasting status should be confirmed.
• After appropriate discussion of risks (% p.278) and benefits, consent for
the procedure should be obtained and documented according to local
guidelines.
• Both groins should be shaved if femoral cannulation is planned.
Investigations
• A brief physical examination should be performed, noting in particular:
• Pulse and blood pressure.
• The presence or absence of peripheral pulses.
• Any evidence of pulmonary congestion (i JVP, basal crackles).
• Results of recent blood tests should be available. As a minimum, this
should include a blood count, assessment of electrolytes, renal function,
and glucose.
• Lipid status should be documented.
• Anticoagulation status should be obtained in patients who have been
taking warfarin.
• A 12-lead ECG should be performed prior to cardiac catheterization (to
act as a baseline).
• Patients should have a venous cannula inserted for the administration of
sedation, intravenous (IV) fluids, and emergency drugs (preferably in the
left arm).
Special considerations
Antiplatelet therapy
Most patients undergoing coronary angiography will have suspected CAD
and will already be on antiplatelet therapy (with aspirin and/or clopidogrel).
Patients who are due or expected to undergo PCI are usually preloaded
with clopidogrel 300–600 mg according to local policy (% p.218).
Anticoagulation therapy
(% p.64.)
Patient preparation 21
Warfarin is typically withheld for 3–5 days prior to the procedure. Most

operators would be comfortable with an international normalized ratio
(INR) of less than 2. In patients who require continuous anticoagulation
(e.g. mechanical mitral valves), IV unfractionated heparin is recommended
and stopped 2 hours before the procedure. Patients on subcutaneous low-
molecular-weight heparin can have the dose omitted on the morning of
the procedure.
Impaired renal function
See % p.312 for detailed management. Patients with known renal impair-
ment (particularly patients with diabetes mellitus) should be well hydrated
prior to cardiac catheterization. Some cardiac centres also recommend
giving N-acetylcysteine. Contrast load should be minimized and consider-
ation made for non-ionic, hypo-or iso-osmolar contrast agents (% p.79).
Biplane imaging may reduce the number of contrast injections required.
Diabetes mellitus
Patients requiring insulin or oral hypoglycaemics should be placed early
on the procedure list. The morning dose of insulin and short-acting oral
hypoglycaemics can be withheld on the morning of the procedure. Close
monitoring of the capillary blood sugar level should be performed. The pa-
tient should be encouraged to eat and drink once recovered and return to
their usual medication regimen. Patients on metformin have a very low risk
of lactic acidosis if renal function is normal; however, it is recommended to
withhold metformin for the day prior to the procedure and for 2 days after.
Catheter laboratory preparation
Personnel
The cardiac CathLab personnel usually consist of a specialist nurse, a car-
diac physiologist, a radiographer, and a cardiologist. Each will have defined
roles in preparing the patient for cardiac catheterization. It is important that
the team understand these routines before commencing a case (e.g. who
would defibrillate in the event of ventricular fibrillation (VF)?). It is good
practice to observe a number of procedures in a cardiac CathLab when
changing hospital as routines vary from place to place. It is also important
to have an understanding of the local resuscitation guidelines in addition
to knowing the whereabouts of resuscitation equipment and emergency
drugs. Most centres would teach this as part of the induction process.
Patient
• The patient will need to be checked in by a member of the team and
correctly identified.
• The consent form should be checked and the signature confirmed with
the patient.
• Female patients of child-bearing age would need to confirm that they
are not pregnant.
• Before commencing the procedure, review the notes to ensure that the
investigation is still clinically indicated.
• Introduce yourself in a confident, professional manner and remember
the patient’s name.
Equipment
Once the patient is positioned on the table:
• Wear protective equipment (masks/hats) according to local policy.
• Ensure venous access has been obtained.
• Ensure a good-quality continuous ECG recording.
• Check the pulse oximetry trace and confirm adequate oxygenation
(SaO2 >96% on room air).
• Give supplemental oxygen to high-risk patients or those receiving high
doses of sedation (see ‘Pre-medication’).
• Wear lead protection (% p.15) and a sterile scrub suit.
• Prepare and drape the vascular access site using an aseptic technique.
Check with the nursing staff about local procedure.
• Check the pressure manifold has been adequately flushed (% p.76) and
that contrast has been run through (% p.76) without air bubbles.
• Ensure that the pressure transducer has been calibrated.
• Check the sterile trolley, ensuring that all necessary equipment is
present (% p.76 and p.77).
Catheter laboratory preparation 23
Pre-medication
Some patients are understandably anxious before cardiac catheteriza-
tion. Short-acting benzodiazepines are useful to alleviate anxiety (and the
associated hypertension) in the CathLab. Diazepam (given as Diazemuls
2–10 mg IV) or midazolam (0.5–2.5 mg IV) can be given as the patient
arrives on the table. Care should be taken in the elderly, in patients with
advanced airways disease, in patients with significant co-morbidity, and
in the obese. Additional sedation can be given with small aliquots of a
short-acting opioid (e.g. fentanyl 25–50 mcg).
25
Chapter 2
The team
The cardiologist 26
The nurse 32
The cardiac physiologist 38
The radiographer 42
26 Chapter 2 The team
The cardiologist
Roles
In coronary interventions, the cardiologist’s clinical duties extend from pre-
procedural care to post-procedural care. At every step, the cardiologist
must maintain self-awareness of his/her role as team leader and must act
and behave accordingly. Beside clinical care responsibilities, the cardiolo-
gist can also have educational/teaching duties towards medical students,
trainees, and CathLab team members. According to the individual job de-
scription, the cardiologist may be also involved in clinical research, with ad
hoc duties that research activities imply.
Pre-procedural care
• To assess the appropriateness of indications for coronary intervention
(% p.28).
• To admit the patient to the ward.
• To arrange for specific preliminary non-invasive investigations whenever
clinically required.
• To explain treatment options to patients and relatives.
• To consent the patient for the procedure.
• To appropriately plan the procedure.
• To discuss the case, when required, with the team.
• To verify team availability and the full working of all the equipment
required for the procedure.
• To attend and lead a briefing meeting discussing:
• The main details of the cases planned for the day.
• The intra-procedural and post-procedural care plan.
• Potential expected technical or staffing issues.
• Role of list coordinator.
• Roles of each team member in case of cardiac arrest or
complications.
• To appropriately plan the procedure.
• To be present at patient sign-in and World Health Organization (WHO)
checklist verification (% p.33).
• To lead the time out before the start of the procedure.
Intra-procedural care
• To perform the procedure guaranteeing and taking care of:
• Aseptic rules to ensure sterility of the operating field.
• Patient’s clinical conditions (ECG, O2 saturation, haemodynamics).
• Patient’s comfort (requesting sedation and/or pain relief as
appropriate).
• Monitoring radiation exposure and contrast volume (% p.98).
Appropriate treatment strategy and corresponding techniques are
•
adopted.
• Regular control of activated clotting time (ACT) to monitor
anticoagulation status.
• Verification that equipment (stents, balloons, etc.) provided by
circulating/scrubbed nurse is as requested.
The cardiologist 27
• To lead the management of cardiac arrest or complications, should they

occur (% p.288).
• To verify integrity of kit used at the end of the case, ensuring that, apart
from the stent, no piece of equipment has been left inside the patient’s
circulation.
Post-procedural care
• To sign the patient out.
• To type a report, summarizing:
• Clinical history.
• Indication for the procedure.
• Details of coronary anatomy and pattern of disease.
• Procedural steps of interventions when performed.
• Details of equipment used, with particular specification of number,
type, size, and length of stents deployed.
• Details of complications if they occurred and management.
• Instructions about the post-procedural care plan.
• To provide clear management plan in terms of:
• Vascular haemostasis.
• Medications for primary and secondary prevention.
• Indication for cardiac rehabilitation when indicated.
• Discharge  plan.
• Future follow-up.
• To provide a detailed letter for the general practitioner to inform about
the patient’s in-hospital stay, procedural outcome, and future care plan.
• To inform and discuss with the department manager and the coroner in
case of intra-procedural death.
• To communicate the procedure outcome to the patient and to inform
the patient and family of possible incidents or complications that
occurred during the procedure in line with duty of candour.
• To monitor the patient post procedure, with special care for possible
early signs of complications or renal failure.
• To be in charge of the overall care of the patient until discharge.
• To debrief the CathLab team at the end of the day, especially in case
of complications or whenever important learning points should be
discussed and shared.
Training
Completion of general cardiology training is a fundamental prerequisite be-
fore considering a subspecialty training in interventional cardiology.
General cardiology training is quite standardized and consistent across
European countries, typically including:
• 1–2 years of general medicine.
• 3–4 years of cardiology training, with theoretical and practical exposure
to both invasive and non-invasive fields.
A structured and recognized formal training in interventional cardiology has
been missing for a long time. Over the last few years, a standardized core
curriculum has been proposed and approved by the European Association
of Percutaneous Cardiovascular Interventions (EAPCI) and followed by
national societies, in order to ensure high standards of quality care and clin-
ical excellence across European countries.
Main learning objectives of the core curriculum are:
• Ability to define appropriate indication and timing for PCI, ensuring an
optimal and cost-effective use of resources available.
• Ability to communicate/explain pros and cons of each
therapeutic option (medical, percutaneous revascularization,
surgical revascularization) to patients, family, and members of the
multidisciplinary team.
• Achievement of theoretical knowledge and practical skills to perform
PCIs as an independent first operator.
• Optimal pre-procedural, intra-procedural, and post-procedural
management with particular care regarding:
• Vascular access selection.
• Adjunctive pharmacology.
• Selection of adjunctive techniques when required.
• Complications management.
• Haemostasis techniques.
• Follow-up and secondary prevention.
Apprenticeship/fellowship
The subspecialty training should be based on two learning modalities:
• Apprenticeship/fellowship.
• Formal learning.
The apprenticeship/fellowship should ideally consist of a 2-year period
during which the trainee is called to become proficient in:
Pre-procedural care
• Patient’s admission.
• Consent.
• Arranging pre-PCI non-invasive tests.
• Pre-PCI drug therapy.
• Participation in heart team discussion/meetings.
Intra-procedural care
• Performing supervised procedures with increasing level of complexities
(minimum of 200 PCIs).
• Discuss cases with supervisor.
• Participate in primary PCI on-call rota.
• Expertise in intravascular imaging and invasive physiology.
Post-procedural care
• Procedure report.
• Monitor patient’s status post PCI.
• Discuss post-PCI drug therapy and follow up with supervisor.
Formal learning
All trainees are asked to:
• Attend accredited formal sessions locally, nationally, or abroad for a
minimum of 30 full days (240 hours) over 2 years.
• Be involved in research in interventional cardiology.
The cardiologist 29
The training programme should be assessed and evaluated according to:

• Documentation of attendance at accredited training courses.
• Procedures logbook.
• Skill assessment by an independent trainer.
• Skill assessment on a simulator.
• Appraisal by training programme director.
• Final examination:
• Theoretical section (100 multiple choice questions in 120 minutes).
• Case studies (50 questions on 10–20 case studies).
Requisites for a cardiac centre to offer accredited training
in interventional cardiology
• Independent interventional cardiology unit integrated with the
cardiology department.
• More than 800 coronary intervention procedures in a year.
• Electronic database for diagnostic and interventional procedures
regularly audited by the National Interventional Society.
• At least two supervisors available, with more than 1000 PCIs and over
5 years’ experience in interventional cardiology.
Logbook
The logbook is an important tool to track the record of cumulated experi-
ence in interventional cardiology and it is one of the main documents to
present for final accreditation or reaccreditation.
The logbook should follow the template of the Cardiology Audit and
Registration Data Standards (CARDS) data standards for interventional car-
diology, as recommended by the European Society of Cardiology.
The logbook should contain information about:
• Date of the procedure.
• Diagnostic versus intervention.
• First versus second operator.
• Vascular access.
• Clinical presentation:
• Elective (stable CAD).
• Urgent (acute coronary syndrome (ACS)).
• Emergent (primary PCI l shock).
• Procedural complexity:
• Bifurcation.
• Left main stem.
• Multivessel disease.
• Calcified lesion.
• Chronic total occlusion.
• Saphenous vein graft.
• Special techniques adopted:
• Invasive physiology.
• Intravascular imaging.
• Rotational atherectomy.
• Laser.
• Thrombus aspiration.
• Distal protection (filters).
• Complications and management:

• Coronary perforation.
• Coronary dissection.
• Kit loss.
For trainees, the logbook should be reviewed and signed off on a monthly
basis. For non-trainees, the logbook still represents an important element
for the annual appraisal and revalidation.
Certification and recertification
In 2018, the EAPCI launched the first programme for certification for inter-
ventional cardiologists, with the aim to ‘ensure comparable requirements
for EAPCI and certified specialists’.
The system is based on:
• Theoretical knowledge assessment (Part A).
• Practical skills assessment (Part B).
Part A consists of a written test with multiple choice questions covering the
EAPCI core curriculum. At the time this book was written, Part B was still
under development.
The requisites to have access to certification are:
• EAPCI membership.
• Doctors with national board certification in cardiology or doctors during
cardiology specialist training (fellows) as confirmed by their training
director (letter of confirmation).
The certification is granted to candidates who successfully pass Part A. The
certification has a validity of 5 years, after which recertification can be
considered.
Further reading
European Society of Cardiology. APCI certification. M https://www.escardio.org/Education/
Career-Development/Certification/Interventional-Cardiology
European Society of Cardiology. ESC WG 10. Curriculum for interventional cardiology training. M
https://www.escardio.org/static_file/Escardio/Subspecialty/EAPCI/Accredit_wg10_DiMario.
pdf
The cardiologist 31
The nurse
Roles
There are usually a minimum of two nurses within the CathLab setting.
However, over recent years, the volume of patients with complex anatomy
presenting for revascularization or complex valvular disease unsuitable
for surgery has steadily increased. The reasons for this are numerous and
mainly account for an increasing number of elderly and co-morbid patients
referred for coronary and/or structural procedures in the CathLab. To
meet this need, in many centres, including the Oxford Heart Centre, a third
nurse is asked to support CathLab procedures when staffing allows.
Two main roles are established for nurses working in the CathLab: ‘scrub
nurse’ and ‘circulating nurse’.
The role and responsibilities of the scrub nurse
• Punctual preparation of the equipment in an organized fashion, in
accordance with the manufacturer’s instructions and ensuring that all
adjuncts and medications are checked (with another nurse), labelled,
utilized, and stored correctly.
• To take part in team briefing meeting, sign in, WHO checklist (% p.33),
time out, and sign out for each patient attending the CathLab.
• To maintain the patient’s safety and sterility within the scrub field.
• To ensure that the procedure is done under the standardized aseptic
technique: from the initial hand washing, through the preparation of
the wound site with skin preparation solution, to the completion of
the case.
• To maintain field sterility and to encourage the rest of the CathLab team
to do so.
• To ensure that the relevant equipment and drugs are checked prior to
issuing them to the operator.
• To act as the patient’s advocate, alongside the circulating nurse by
complementing the circulating nurse’s role of monitoring the patient.
• To observe and monitor, in collaboration with the radiographer, the
contrast dose during the procedure and to ensure that the patient does
not receive any unnecessary dose.
• Post procedure, to establish access site haemostasis with the locally
preferred devices/technique (% p.178).
The role and responsibilities of the circulating nurse
• To verify that the CathLab environment has had all the relevant safety
checks and is kept tidy.
• To receive a detailed handover from the preparing nurse about the
relevant information concerning the patient (including clinical history
preceding the procedure, blood results, past medical history, relevant
drugs, dual antiplatelet doses if required, allergies, renal function, height
and weight, and any co-morbidities).
• To take part in the WHO checklist, verifying appropriate positive-
patient identification and consent.
• To ensure that all necessary adjuncts reach the scrub team in a safe and
timely manner.
The nurse 33
• To take clear and thorough documentation of the procedure and to

make records on the hospital’s chosen reporting platform.
• To inspect the integrity of all equipment.
• To constantly monitor the patient during the procedure, in collaboration
with the other team members, and to immediately communicate any
changes in the patient’s status to the operator.
• In anticipation of these changes, to be prepared and to have any
necessary equipment, adjuncts, and/or medications prepared in
advance.
• At the time of these events, to make notes and accurate documentation
of the procedure (ideally, this would be a task for a second circulating
nurse, if available, in collaboration with the other team members).
• To facilitate and support the timely measurement of ACT throughout
the case and to ensure that the team receives timely doses of heparin
whenever required (based on ACT results).
• To act as the patient’s advocate.
• At the appropriate intervals, to communicate with the patient (when
the operator is not using fluoroscopy) to assess any visual changes in
the patient’s condition and to offer comfort, safety, and emotional and
psychological support whenever it is needed.
• To regularly monitor blood glucose levels, and to act accordingly, in
diabetic patients.
Training
Training within a CathLab setting for nurses is part of a departmental pro-
gramme based on local rules and guidelines.
The achievement of competencies is based on a mixture of observation
in practice and theoretical knowledge. There is an emphasis on having the
basic knowledge about the procedure, its adjuncts, and about anticipation
and preparation for emergency situations when the needs of the patient
and of the whole CathLab team may rapidly change.
Any new recruit is provided with a supernumerary period (usually 10
weeks—depending on each member of staff ’s learning needs). Throughout
this time, the new starter can observe and learn both circulating and scrub
nurse skills required for each interventional procedure.
Locally designed workbooks can supplement this period in order to con-
solidate the learning process. Following completion of the supernumerary
period, the starter is observed in practice for each procedure and supple-
mented with questions on an assessment grid.
An achievement of 100% is required prior to being signed off and de-
clared as a competent CathLab nurse. This education is also supplemented
by access to educational events applicable to this field. This includes any
locally arranged sessions taught by the departmental educators on the rele-
vant subject or attendance at national or international meetings.
Patient checks and WHO checklist
The WHO checklist is a distinct tool utilized in all CathLabs that emphasizes
improving patients’ safety with the main aim of preventing ‘never events’.
Acknowledgement
A special thanks to Lauren MacPhee-Leech for the preparation of this chapter.
Firstly, all members of the team should be present at the beginning of

the CathLab session for the ‘briefing meeting’ where the following are
discussed:
• Work list.
• Main details about each case.
• Possible challenges expected for each case.
• Post-procedure destination for each patient (day-case unit, cardiology
ward, coronary care unit, other medical ward).
• Expected staffing or equipment issues.
• Each team member’s role in case of complications or cardiac arrest.
Each team member should also be present during sign in, when the patient
enters the CathLab. The sign-in procedure should be commenced prior to
sedation, general anaesthesia, or draping. The following checks are required
as part of the standard sign in and WHO checklist:
• Confirm the patient’s identity (includes date of birth and hospital
number), correct procedure, and consent form.
• Patient-related information and a checklist matching whiteboard to
record the following information:
• Haemoglobin.
• Creatinine.
• Height and weight.
• Site of IV access.
• Double antiplatelet therapy (maintenance dose and/or loading dose).
• Bleeding issues.
• Respiratory issues.
• Diabetes (with last blood glucose level).
• Drug allergies.
• Selected arterial site for the procedure.
Time out
At this stage the circulating nurse should sign the corresponding section of
the checklist (WHO) form and hand it over to the operator to complete
the ‘time out’ which would include the following steps:
• Operator to confirm that everyone is aware of the information
discussed during the team brief/sign in and that the case can proceed.
• Operator to confirm that the equipment required for the case is
checked and ready.
• IR(ME)R is authorized as per the standard operation protocol (for
IR(ME)R details see ‘Radiographer section’, % p.42).
Sign out
At the end of the case, the sign out should be completed by the scrub
nurse to formally summarize the procedure, outcome, and patient plan
for recovery and discharge. Specifically, the following points need to be
addressed:
• To confirm the accurate documentation of the procedure performed.
• To perform equipment check, sharp tools (needles, scalpels) count, and
to verify the integrity of wires.
• To record if equipment has been left in situ.
The nurse 35
• To record any unexpected issues that needs to be addressed.

• To record the need and duration of double antiplatelet therapy, in case
a stent or other device (e.g. TAVI valve) was inserted. To verify whether
a loading dose is recorded in the patient’s drug chart and to specify if a
loading dose has already been given in the CathLab or if it needs to be
administered when the patient arrives at the destination ward/unit.
• To highlight any key concerns regarding the post-procedure recovery
and patient management plan.
Until all sections are completed and acted on, the patient should not leave
the CathLab.
Sedation
Sedation is currently widely utilized in a number of cardiac procedures
including cardioversion, catheter ablation, transoesophageal echocardiog-
raphy, cardiac device implantation, as well as angiography, PCIs, and struc-
tural interventions.
Key components of nurse-led sedation
• Safe and appropriate IV cannulation.
• An understanding of the pharmacokinetics of the relevant drugs and
reversal agents.
• An understanding of the procedure and when sedation is appropriate.
• Ability to judge the patient’s needs for IV fluid, inotropic and other
blood pressure supportive therapy, with a knowledge of the patient’s
ejection fraction, cardiac structure, performance, and coronary patency.
• Safe intra-procedural monitoring using heart rate, blood pressure, and
pulse oximetry following drug administration.
• Autonomy to make adjustments to the oral request for relevant drugs
and allowing freedom to titrate the request doses to administer to
the patient (thus freeing the operator to concentrate on the technical
aspects of the case).
Post-procedure care
The aim of post-procedure care is to monitor patients to prevent, to
identify early, and to treat effectively any vascular access site or systemic
complications.
A full set of post-procedure care observations typically includes:
• Non-invasive blood pressure monitoring.
• Three-lead ECG monitoring (if stented).
• O2 saturations.
• Respiratory rate.
The frequency of parameter monitoring should be determined by each
patient’s condition, usually with 15-minute intervals for the first hour, half-
hourly for the second hour, and hourly thereafter (using nursing judgement).
Radial access monitoring includes:
• Verifying achievement of patent haemostasis.
• Wound site observations every 15 minutes until radial haemostasis
device has been removed, particularly looking for loss or changes in
forearm colour, sensation, temperature, shape, size, pulse, and pain.
• Managing bleeding and haematomas.

• In case of a lengthy hospital stay, to look for signs of infection.
Femoral access monitoring includes:
• Checking for femoral, popliteal, and pedal pulses of affected access site.
• Wound site observations every 15 minutes until mobile, particularly
looking for loss or changes in colour, sensation, temperature, shape,
size, pulse, and pain.
• Managing bleeding and haematomas.
• In case of a lengthy hospital stay, to look for signs of infection.
Any changes in haemodynamics should be alerted to the nurse in charge. If
the patient encounters chest pain (particularly after a PCI), then a 12-lead
ECG should be recorded in the first instance and the operator should be
alerted as it could be a sign of a procedural complication.
Patient self-care
It is important to interact with the patient asking for his/her input in
identifying possible issues or asking for cooperation to prevent possible
complications:
• Encourage the patient to report any chest pain or dizziness.
• Encourage the patient to rehydrate following the procedure.
• Discourage any activity that would put the access site at risk of bleeding
and explain how to apply pressure should they choose to.
• Emphasize the important of bed rest when femoral access is utilized.
• Educate the patient on the importance of double antiplatelet therapy
following a stent insertion and explain the risk of consequences of any
missed doses.
• Educate about the indication to avoid strenuous activity, alcohol, and
signing legal documents (if sedation given) for the first 48 hours.
• Provide instructions about driving restrictions after the procedure.
The nurse 37
The cardiac physiologist
Roles
The cardiac physiologist has specialist knowledge and skills regarding patient
care, cardiac physiology, and ECG interpretation to support diagnostic and
interventional procedures.
The main roles and responsibilities of the cardiac physiologist are as
follows:
• To attend briefing meetings and to be present at the patient’s sign in,
WHO checklist, time out, and the patient’s sign out.
• To set up appropriate equipment in preparation for each type of
procedure including resuscitation equipment where appropriate and
calibrate where necessary.
• The cardiac physiologist is responsible for checking that the ECG,
oxygen saturation probe, balloon pump, defibrillator, and temporary
pacing box are working and stocked.
• The resuscitation trolley must be checked daily with a checklist to
ensure all equipment is there. This list must not leave the vicinity of the
resuscitation equipment. The various equipment must also be checked
that it is in date and where necessary packaged and sterile.
• To select suitable technology for the procedure, choosing and adapting
the appropriate diagnostic technique, patient position, machine settings,
and transducer for each patient.
• To perform cardiac monitoring and make accurate pressure and
haemodynamic measurements appropriate for the procedure.
• To continuously monitor the physiological condition of the patient
and effectively communicate/act with the CathLab team (operator,
radiographer, scrub and circulating nurses) on any adverse changes.
• To analyse the results and contribute to the production of a factual
report, as required.
• To deliver shock in case of a shockable rhythm during the procedure
(this role is typically attributed to the cardiac physiologist during the
team briefing. Unless otherwise prespecified, the cardiac physiologist
should consider him/herself in charge of delivering shock when
instructed to do so by the operator).
• To cooperate with the operator in performing specific procedural
techniques such as:
• Rotational atherectomy.
• Pressure wire studies.
• To cooperate with the operator in establishing temporary pacing,
setting up:
• Pacing rate.
• Pacing threshold and amplitude.
• To cooperate with the operator in setting up balloon counterpulsation
or other form of left ventricular device if in use in the CathLab.
• To monitor the time interval from the last dose of heparin and/or last
ACT measure to inform the operator when ACT needs to be repeated
or heparin to be re-administered.
Electrocardiogram
The cardiac physiologist typically arranges the necessary equipment for
ECG recording and cooperates with the operator in monitoring the ECG
throughout the procedure.
The ECG equipment and electrode positions for ECG recording in cor-
onary/structural procedures are standard. Typically, radiolucent cables are
adopted.
The ECG is usually recorded at a standard speed of 25 mm/second and
a scale of 10 mm/mV. During ECG monitoring, typically three leads are
displayed simultaneously alongside pressure tracings. On the operator’s re-
quest, the cardiac physiologist might be asked to display standard a 12-lead
ECG recording.
During the procedure, the cardiac physiologist is called to monitor and
inform the operator about baseline heart rhythm and main changes to the
baseline ECG including:
• Changes of ST segment (depression/elevation).
• Supraventricular and ventricular ectopics (especially in case of bigeminy
or couplets/triplets).
• Significant bradyarrhythmias (first-or second-degree or complete
atrioventricular blocks or new development of bundle branch blocks).
• Minor tachyarrhythmias (atrial fibrillation (AF)/flutter, VT, VF).
Pressure tracings
Pressure recording addresses three main functions:
• Monitoring the patient’s haemodynamic and health status.
• Guiding the operator in catheter manipulation.
• Diagnostic purposes.
When setting the line for monitoring of pressure tracings, the patient
should be laid supine on the CathLab table with one pillow behind their
head. It is important that the transducer for pressure monitoring is placed
at the same height as the ECG V4 electrode and the level of the transducer
should be adjusted to reflect this. For a higher degree of accuracy, a ruler
should be used to confirm a good alignment between the height of V4 and
the pressure transducer itself.
Prior to the procedure, the pressure should be calibrated and ‘zeroed’,
although this can also be done during the procedure if the pressure mani-
fold is ‘opened to air’.
The monitored pressure is a direct measure of pressure at the tip of the
catheter and can be useful to monitor the patient’s haemodynamics during
the procedure and to provide the operator with an indication of the pos-
ition of the guiding catheter. The shape of the waveform can also indicate
where the tip of the catheter is.
Recording of pressure traces has a diagnostic role mainly in cases of:
• Valvular disease (for measurement of pressure gradients).
• Right heart catheter (for detection of pulmonary hypertension).
• Pressure wire studies (for detection of ischaemia in moderate coronary
stenosis).
Damping
From the shape of the waveform, the operator can understand whether the
tip of the guiding catheter is free in the aorta or is engaging the coronary
ostia in the appropriate way. A damping in the aortic pressure waveform
can indeed be a sign that the tip of the catheter:
• Is facing against the aortic vessel.
• Is too deeply engaged within the coronary artery ostium.
• Is facing against atherosclerotic plaque located at the ostium of the left
main stem or right coronary artery.
• Is engaging the conus branch in case of right coronary artery
cannulation.
When an aortic pressure waveform appears damped, the operator knows
that contrast should not be injected (or needs to be injected with very high
caution) because of the risk of aortic wall or coronary wall dissection. In
case of damping in pressure because of cannulation of the conus branch,
the operator knows that prolonged cannulation or contrast injection can
induce ischaemia of the atrioventricular node and of the right ventricle out-
flow tract (both supplied by the conus branch) with the consequent poten-
tial risk of inducing VF.
When to call
The cardiac physiologist is asked to inform and warn the operator and all
the other CathLab team members whenever an abnormal event occurs on
the ECG or pressure traces monitoring.
Here are the main events the cardiac physiologist should notify to
the team:
• Significant reduction in blood pressure compared to baseline (as a
general rule when systolic blood pressure <90 mmHg).
• Damping or ventricularization of the aortic pressure waveform.
• Changes in the ST segment on ECG (depression/elevation).
• Onset of significant bradycardia.
• Onset of new bundle branch block (especially if left).
• Onset of heart block (first degree, second degree, or complete).
• Onset of atrial flutter or AF.
• Onset of VT.
• Onset of accelerated idioventricular rhythm (useful in primary PCI).
• Onset of VF.
• Onset of asystole.
• 15–20-minute time warning for ACT check.
Recording and documentation
The cardiac physiologist is asked to produce an accurate recording of the
whole procedure. Printouts of baseline and final ECG and pressure tracings
should be included in the report along with all ECG and pressure tracings
relative to main events that occurred during the procedure.
A complete cardiac physiologist’s report should include:
• Patient’s name, identification number, and date of birth.
• Patient’s height and weight.
• Date and time of the procedure (start and end time).
• Arterial access.
• Venous access (for right heart catheterization or temporary pacing).
• Drugs administered and time of administration.
• Contrast volume.
• Equipment used (guiding catheters, wires, balloons, stents, pressure
wire, intravascular imaging, etc.).
• Timing of wiring (especially in primary PCI).
• Timing of balloon inflation/stent deployment.
• Pressure and duration of inflation for each balloon/stent.
• Value of fractional flow reserve (FFR)/instantaneous wave-free ratio
(iFR) if pressure wire study performed.
• Timing and values of ACT checks.
• Device used for arterial haemostasis.
• Total procedural time.
• Fluoroscopy time and radiation dose (dose area product).
• Timing and corresponding management of intra-procedural
complications if any.
• Settings of temporary pacing, aortic counterpulsation, or other
ventricular support devices if used.
The radiographer
Roles
The radiographer is the healthcare professional called to use his/her ex-
pertise and knowledge on patient care, physics, human anatomy, radiology,
and radioprotection to best support the execution of diagnostic and inter-
ventional procedures in the CathLab.
In accordance with prevailing legislation (e.g. IR(ME)R 2017, Ionising
Radiation Regulations 2017) and local protocols, the main responsibilities
of the radiographer are as follows:
• To provide optimal radiographic imaging across all types of cardiac
procedures that require X-ray guidance using image intensifiers.
• To keep patient radiation dose as low as reasonably practicable (ALARP
principle) while providing optimal image quality.
• To select and provide, on the operator’s request, specific acquired
views/images to be used as reference during the procedure.
• To take part in CathLab team briefings, sign-in, time out, WHO
checklist, and sign out.
• To be responsible for preparation, supply, and stocking of X-
ray contrast, and for quality assessment of personal protective
equipment (PPE).
• To check and document for pregnancy with all female patients of
childbearing age prior to imaging in line with local policy.
• To promote radiation protection for staff by recording and warning the
operator and other team members about:
• Screening time.
• Radiation doses.
• Distance from the intensifier.
• Appropriate shielding and PPE (apron, thyroid collar, etc.).
• Especially when high radiation doses are about to be reached, to advise
the operator on optimizing image quality to best demonstrate coronary
anatomy, prevent artefacts, and minimize patient dose by:
• Projections selection.
• Saving fluoroscopy to minimize need of cine acquisition.
• Collimation.
• Appropriate (low) acquisition rate.
• Avoiding zooming.
• Appropriate additional filtration.
• To take actions and cooperate with other team members during
complications or cardiac arrest (e.g. move C-arm to facilitate
cardiopulmonary resuscitation).
• To record patient radiation and contrast doses in line with local policy.
• To archive X-ray images according to the standards of exchanging,
forwarding, and storing digital data.
• To educate/reassure patients concerned about their radiation dose.
• To teach other healthcare professionals as required (radiation
protection best practice).
• To train new and junior radiographer colleagues.
• To audit as necessary.
43
Chapter 3
Vascular access
The Seldinger technique 44
Which arterial access route to use? 46
Trends in vascular access 48
Radial artery access 50
Femoral artery access 54
How to obtain venous access 58
Femoral vein access 59
Internal jugular vein access 60
Subclavian vein access 62
Anticoagulation issues 64
Compression devices 66
Arterial closure devices 68
44 Chapter 3 Vascular access
The Seldinger technique
• First developed by the Swedish radiologist Sven-Ivar Seldinger in 1953,
this technique was originally designed as a method to allow safe access
to blood vessels for arteriography.
• Use of the technique in modified form has been adapted to provide
access to veins, arteries, and hollow organs (e.g. chest drains,
percutaneous enterogastrostomy tubes).
The Seldinger technique is shown in Fig. 3.1.
THE SELDINGER TECHNIQUE 45
• Percutaneous puncture of the desired

vessel with a hollow bevelled needle.
• Passage of an atraumatic, curved-

tipped guide wire through the needle
into the vessel.
• Removal of the needle leaving the

guide wire within the vessel.
• Passage of an introducer sheath (with

or without dilator) over the guide
wire into the vessel.
• Removal of the guide wire, leaving the

sheath in the vessel. A haemostatic
valve provides access for the passage
of catheters or devices into the vessel
without blood loss.
Fig. 3.1 Seldinger technique

Further reading
Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique.
Acta Radiol 1953; 39: 368–76.
Which arterial access route to use?

Whichever approach the operator plans to use, knowledge of the spe-
cific anatomical landmarks (and of potential complications) is paramount.
• Most commonly, cardiac catheterization and selective coronary

angiography is performed via the radial route (% p.50), although some
operators may still opt for femoral access (% p.54).
• Specific catheter shapes have been developed for both access routes
and offer access to the coronary ostia and left ventricular cavity, taking
into account the curvature of the thoracic aortic arch.
• An alternative approach may be required when access is precluded for
any reason, or when it is not possible to adequately reach the desired
target vessel for anatomical or technical reasons.
• Typical reasons for choosing an alternative approach include the
following:
Coronary artery bypass grafts
(% p.166.)
• In patients with previous bypass grafting, catheterization is commonly
performed via the femoral artery or the left radial artery if the patient
has a left internal mammary artery (LIMA) graft (% p.166).
• Although selective engagement of the LIMA from the right radial
approach is possible, it is technically challenging and may result in injury
to the ostium of the LIMA.
• Vein grafts can also be challenging to engage from the right radial artery,
due to the natural shape of the catheter as it enters the ascending aorta
from the right brachiocephalic artery.
• Similarly, the right internal mammary artery (RIMA), when used for
grafting, may be difficult to selectively intubate from the left radial or
femoral route. Selective engagement may only be possible from the
right radial route.
Peripheral vascular disease
• Peripheral vascular disease is not a contraindication to catheterization
via the femoral route, but if neither femoral arterial pulse is palpable,
or only poorly palpable and cannot be accessed, a radial approach is
preferred.
• In the presence of peripheral grafts, close attention to the exact
anatomy is necessary: if an axillofemoral graft is present, the abdominal
aorta itself may be occluded, and therefore a femoral approach is
pointless even if the femoral pulse is palpable.
• Some operators will puncture peripheral Dacron grafts in order to
perform catheterization, but this may lead to post-procedural bleeding
complications and is generally not recommended.
Which arterial access route to use? 47
Abdominal aortic aneurysm
• Given the overlap in risk factors with coronary artery disease,
abdominal aortic aneurysms are common in patients undergoing
coronary angiography, but may not be diagnosed before the procedure.
• An undiagnosed abdominal aortic aneurysm should be suspected if the
guide wire or catheter loops back on itself or deviates laterally from its
usual course when passing through the descending aorta.
• Care should be taken when negotiating catheters through an aneurysm,
and exchanging over a guide wire is recommended to prevent catheter
dislodgement of thrombus or intimal disruption.
• There is no absolute level of enlargement of the abdominal aorta
that precludes femoral catheterization. Operators should weigh up a
risk:benefit analysis on an individual patient basis.
• The presence of thrombus seen on ultrasound is a contraindication to
the femoral approach. Although much of this may be organized, there
is a significant risk of distal embolization leading to renal failure, distal
ischaemia, and ‘trash foot’.
Coarctation of the aorta
(% p.105.)
• The commonest site for aortic coarctation is immediately distal to the
origin of the left subclavian artery.
• Depending on the magnitude of the trans-coarctation gradient (i.e.
severity), it may not be possible to advance catheters across the
coarctation from the femoral route.
• A radial approach should be considered for coronary angiography, or
simultaneous femoral and radial cannulation if an accurate pressure
gradient is required.
The anticoagulated patient
(% p.64.)
• Patients taking anticoagulant therapy are at increased risk of bleeding
complications when arterial puncture is undertaken for cardiac
catheterization.
• In patients where anticoagulation has not or cannot be stopped prior
to catheterization (% p.64), the radial route (% p.50) (where bleeding
complications are reduced) should be used.
• The femoral route should be reserved for emergency situations, such as
the insertion of an intra-aortic balloon pump (% p.268).
Trends in vascular access
• Over the last decade, radial access has replaced femoral access as the
favoured route for coronary catheterization and interventional cardiac
procedures.
• Radial access is now the most common route for vascular access in the
UK, Europe, and Asia, with uptake in North America increasing.
• The change in practice has been driven by randomized trial and registry
data demonstrating that radial access was associated with reduced
bleeding complications and reduced mortality.
• Although not proven, improvements in mortality were thought to derive
from the reduction in access-site bleeding complications.
Benefits of radial access
• Reduced rates of access-site bleeding complications.
• Reduced mortality rates.
• Quicker post-procedure mobilization.
• Improved levels of patient comfort and satisfaction.
• Reduced healthcare costs.
• Despite convincing data, uptake of radial access is highly variable and

affected by operator, institutional, and procedural factors.
• Radial access is technically more challenging for operators not
specifically radially trained. The learning curve is steep and many
operators will notice increased procedural duration and failure rates as
they cross over from femoral access.
• There has also been recent concern that radial access may result in a
higher operator radiation dose.
The radial access route has a few minor, but still relevant drawbacks:
• The risk of occlusion (relevant in patients with renal failure requiring
future dialysis, or patients requiring full arterial surgical coronary
revascularization).
• A potentially uncomfortable position for the patient who is asked to
maintain their arm in the supine position (relevant in patients with arm/
shoulder orthopaedic injury).
Trends in vascular access 49
Radial artery access
Anatomy
• The patient’s arm should be extended, supine (palm upwards), and
relaxed. The wrist should be hyperextended.
• Many operators choose to place a light strap or bandage across the
palm and onto an arm board to maintain correct positioning, with or
without a rolled towel or other support under the wrist and elbow.
• The radial artery is best palpated proximal to the flexor retinaculum,
using the index, middle, and ring fingers simultaneously, allowing
palpation of the entire distal course of the vessel in the wrist.
• The point of puncture should be approximately 1 cm proximal to the
radial styloid process (Fig. 3.2).
Procedural approach
• The forearm should be shaved and painted with antiseptic. Some
operators also prepare the right femoral artery in case of radial access
difficulties or when alternative access may be required during the
procedure (e.g. intra-aortic balloon pump insertion).
• Placement of intravenous cannulae should be avoided in the same arm,
and bracelets, watches, etc. removed.
• Local anaesthesia: 1–2 mL of 1% lidocaine should be infiltrated
subcutaneously, taking care not to puncture the artery.
• The skin should be superficially nicked with a blade over the site of the
intended puncture and the radial artery cannulated via the Seldinger
technique (% p.44).
• The sheath should be inserted gently (radial sheaths are generally 5 or
6 French (F) and may be short or long, sometimes with a hydrophilic
coating).
• It is common practice to inject a cocktail of spasmolytic and
anticoagulant agents into the radial artery prior to catheterization.
Various regimens may be used (e.g. heparin 2500 IU, verapamil 2.5 mg,
glyceryl trinitrate (GTN) 200–400 micrograms).
Angiography via the radial route
• A guide wire should always be passed into the aortic root before
advancing catheters through the brachial and subclavian arteries.
• If the guide wire persistently enters the descending aorta, a deep breath
as the wire is advanced out of the subclavian artery may help engage the
ascending aorta.
• Although a standard catheter may be used, specific radial shapes have
been developed, including the Tiger™ and Kimny™ catheters (Fig. 3.3).
Line removal
• Radial sheaths are almost always removed immediately after the
procedure is completed.
• Tourniquets were historically used to compress the puncture site, but
several compression devices are now available (% p.66).
Puncture
point
α: 30°–60°
Puncture
point α
Styloid
process
Fig. 3.2 Method of radial artery puncture. After determining the course of the distal portion of the artery, the puncture
should be made 1 cm proximal to the radial styloid. The introducer needle should be directed along the anatomical course of
the vessel
Radial artery access
51
Fig. 3.3 Selective coronary angiography via the radial artery. The Kimny™ (top) and
Tiger™ (bottom) catheters have been specifically designed to be used from the radial route
Complications
(% See also p.56.)
• Radial artery spasm: this is a common problem that can usually be
prevented through mild sedation of the patient prior to radial access
(e.g. with opiates and benzodiazepines). If spasm does occur, it may be
responsive to intra-arterial nitrates and verapamil delivered through the
sheath or catheter.
• Post-procedural loss of radial pulse: occurs in up to 5% of cases and is
frequently asymptomatic.
• Local haematoma: often develops proximally to the puncture site
immediately after placement of the compression device. This is easily
treatable by placement of a second external compression device
abutting the one already in situ.
• Forearm haematoma: occurs in up to 1% of radial cases and develops
slowly on the ward after sheath removal. Treatment is usually
conservative and consists of bandage compression of the forearm, ice to
reduce swelling, and elevation of the arm using a sling. The patient should
be carefully monitored for the development of compartment syndrome.
• Serious bleeding complications are very rare using the radial technique.
The Allen test
This bedside test examines the integrity of the ulnar artery supply to the
palmar arch; in the event of compromise of the radial artery, this is essen-
tial to prevent ischaemic damage and loss of hand function. Although not
universally applied, some operators will not perform radial access unless
the Allen test is normal.
• Both the ulnar and the radial arteries are simultaneously compressed
manually to occlude flow.
• The patient should be asked to open and close their hand into a fist
six or seven times (until the hand blanches).
• Pressure over the ulnar artery is released.
• If the colour of the palm returns to normal within 10 seconds, the test
is normal and it is safe to proceed with radial access.
• Some operators augment the sensitivity of this test by using a pulse
oximeter (plethysmography): the probe should be attached to one of
the fingers, and the return of the pulsatile waveform after ulnar artery
release indicates test normality.
• Be careful when just using the term ‘positive’ with this test. It can lead
to confusion. It may be safer to say ‘Allen test is normal’.
Radial artery access 53
Snuff box radial approach

This approach consists in accessing the radial artery during its course on the
dorsal side of the hand where the artery becomes palpable at the junction
of the intersection of the thumb and the index finger over the bony struc-
tures of the snuff box (Fig. 3.4).
After the sheath is placed, the arm can be pronated into a neutral and
comfortable position for both the patient and operator. Potential benefits
of the snuff box approach include:
• Easier left radial access for both the patient and the operator.
• Easier radial access in patients with limited arm (either left or right)
supination.
• Possible easier retrograde recanalization of the radial artery with a
lower risk of occlusion.
• Lower risk of forearm compartment syndrome.
• Shorter haemostasis time (more superficial position of radial artery).
Fig. 3.4 Example for location of distal radial artery in the snuff box approach.
Radial artery is highlighted by the line and the snuff box by the filled triangular area.
The dotted line circle points the site of puncture for distal radial puncture technique
Femoral artery access
Anatomy
• The patient’s leg should be abducted and the foot turned outwards.
• The femoral artery should be palpated at or above the groin crease.
• The point of puncture should be in the common femoral artery, above
the bifurcation into the superficial and deep femoral vessels, and below
the inguinal ligament (Figs. 3.5 and 3.6).
• Radiographically, the puncture should be at the level of the femoral
head, approximately 0.5–3 cm below the inguinal ligament. Consider the
use of fluoroscopy prior to femoral puncture to guide access, especially
in patients who are overweight.
Procedural approach
• The groin area should be shaved and painted with antiseptic.
• Local anaesthesia is infiltrated: such as 10 mL of 1% lidocaine, taking
care not to puncture the vein or artery.
• The skin should be incised with a blade and the superficial skin layers
dissected open with forceps.
• The Seldinger approach (% p.44) is used to cannulate the femoral
artery.
• The needle should approach the vessel, bevel up, at an angle of 30–45°
to the skin surface and should be advanced until arterial blood is seen to
pulse and flow freely out of the needle’s hub.
• The arterial sheath is inserted and the sidearm flushed with heparinized
saline to prevent thrombus formation.
• 6 F arterial sheaths are typically used (% p.82); 4 or 5 F may be used
for diagnostic angiography, and 7 or 8 F for complex intervention
procedures.
Anterior
spine
Inguinal
ligament
Skin
crease
3 cm
Common
femoral
artery
Profunda
Saphenous vein
Superficial Femoral
femoral artery vein
Fig. 3.5 Anatomy of the inguinal canal. Ideal puncture site of femoral artery is
between skin crease and inguinal ligament
Common
femoral artery Arterial
sheath
Superficial
femoral artery
Profunda
Fig. 3.6 Angiogram highlighting femoral artery anatomy. Contrast injected through

arterial sheath: note puncture site ideally sited in common femoral artery
Angiography via the femoral route

• Most catheter shapes (% pp. 82–4) are designed for use from the
femoral route.
Line removal
• Haemostasis after femoral artery cannulation is generally achieved by
digital compression.
• When heparin has been administered, sheath removal should be
delayed until either the activated clotting time (ACT) is less than 150–
200 seconds, or 3–4 hours have passed (depending on local protocol).
• Before removing the sheath, firm pressure should be applied with two
or more fingers 1 cm above the point of vessel puncture.
• The sheath is removed briskly and pressure applied continually for
approximately 8–10 minutes until haemostasis is obtained.
• After 3 hours of bed rest, the patient may usually be mobilized (% p.317).
• Alternatives to digital compression include the use of vascular
closure devices (% p.68), external compression devices (% p.66), and
procoagulant patches.
• Hypertensive patients may require administration of antihypertensive
medication (e.g. 5–10 mg of nifedipine sublingually) to facilitate
haemostasis after line removal.
Complications
• Local haematoma (% p.294): complicates up to 25% of procedures.
• Vasovagal reactions at puncture or on sheath removal (% p.287).
• Femoral artery tear/dissection: uncommon in non-diseased/calcified
iliofemoral arteries.
• Retroperitoneal haemorrhage (% p.294): may occur after high puncture
(above inguinal ligament).
• Femoral artery pseudoaneurysm (% p.294).
• Distal embolization of thrombus from sheath.
How to obtain venous access

• Venous access may be required during cardiac catheterization
procedures for purposes including:
• Right heart pressure/saturation measurements.
• Cardiac output measurements.
• Shunt estimation.
• Pulmonary angiography.
• Myocardial biopsy.
• The route of access chosen may be determined by the nature of the
procedure, patient factors, and operator expertise.
Femoral vein access 59
Femoral vein access
Anatomy
• The femoral vein usually lies medial to the femoral artery in the inguinal
canal (% Fig. 3.5, p.54).
• Anatomical relations may be remembered by the acronym
‘NAVY’: structures lateral to medial are (femoral) Nerve, Artery, Vein,
Y-fronts!
Procedural approach
• The groin area should be shaved and painted with antiseptic.
• Local anaesthesia: 5–10 mL of 1% lidocaine.
• The artery should be palpated and protected laterally with fingers of the
left hand, with the needle held in the right hand.
• The vein is cannulated via the Seldinger approach (% p.44): the needle,
mounted on a syringe containing heparinized saline, should be advanced
as for arterial cannulation, with negative pressure gently applied to the
plunger of the syringe.
• When venous blood (dark) flows freely into the syringe, it should be
gently disconnected and the guide wire inserted into the vessel.
• The skin may be incised with a blade before or after vessel puncture.
• The venous sheath (usually 5 or 6 F) is inserted and the sidearm flushed
to prevent thrombus formation.
Indications
• This is the route most commonly used when performing routine left and
right heart catheterization (% p.90).
• It may be used for insertion of temporary pacing wires and central
venous cannulae in patients on anticoagulants or with clotting
abnormalities (low risk of complications).
Complications
• Inadvertent arterial puncture.
• Local haematoma.
• Infection (if line not removed at end of procedure).
Internal jugular vein access

Anatomy
• The internal jugular vein lies lateral and anterior/superficial to the
carotid artery inside the carotid sheath; it runs between the two heads
of the sternocleidomastoid muscle immediately above the clavicle and
drains into the subclavian vein behind the clavicle, medial to the anterior
scalene muscle in the base of the neck.
• Handheld ultrasound may help identify jugular vein location.
Procedural approach
• The neck area should be painted with antiseptic; some operators also
sterilize and drape the subclavian area in case of access problems.
• There are three different approaches to cannulation of the internal
jugular: high, mid, and low/supraclavicular. The low approach carries
a high risk of pneumothorax due to proximity to the apical pleura; it
should only be performed by experienced operators.
• Local anaesthesia: 5–10 mL of 1% lidocaine infiltrated subcutaneously.
• A small incision with a blade will aid successful cannulation; attempting
to puncture through the skin may lead to anatomical distortion.
• The needle should be mounted on a syringe containing heparinized
saline and gently aspirated whenever the needle is being advanced.
• When the vein is punctured, the guide wire should be passed into the
vessel and the vein cannulated via the Seldinger technique (Fig. 3.7).
Carotid artery Internal jugular vein
Sternal head of Clavicular head of

sternomastoid sternomastoid
Insert needle at 45°

to skin, aiming for
the right nipple in
men or the right
anterior superior
iliac spine in women
Fig. 3.7 Cannulation of the internal jugular vein. The vein lies superficially between
the two heads of the sternocleidomastoid muscle, lateral to the carotid artery
Internal jugular vein access 61
High approach
• Turn the patient’s head away from the side of the intended puncture.
• The carotid artery should be palpated at the level of the thyroid
cartilage, between the two heads of the sternocleidomastoid muscle
and protected medially with the fingers of the left hand.
• The needle should be inserted into the skin, lateral to the carotid artery,
at 45°.
• The needle should be advanced aiming for the ipsilateral nipple in men,
or the anterior superior iliac spine in women.
• If the vein is not entered, further attempts should be made, aiming
slightly more medially.
Mid approach
• The patient should look directly ahead with their neck slightly extended.
• The carotid artery should be palpated midway between the mastoid
process and the sternal notch and protected medially with the fingers of
the left hand.
• The needle should enter the skin immediately lateral to the carotid
artery and be advanced downwards at approximately 45–60° until the
vein is entered.
Indications
• Pulmonary artery catheterization (% p.90).
• Myocardial biopsy (% p.258).
• Used for central venous access in patients with clotting abnormalities
or on anticoagulants, and in patients for whom pneumothorax would
be particularly dangerous (e.g. chronic obstructive pulmonary disease,
respiratory failure).
• Pulmonary angiography in patients with thrombus in the inferior vena
cava (or other obstruction, e.g. caval filter in situ).
Complications
• Inadvertent arterial puncture.
• Local haematoma.
• Infection.
• Cervical nerve root trauma.
• (Pneumothorax/haemothorax with low approach, chylothorax with left-
sided approach.)
Tips for cannulation of internal jugular/subclavian veins

• If the vein is not entered at the first pass, withdraw the needle slowly
in case it has transfixed the vessel; when venous blood enters the
syringe, the guide wire may be passed.
• If no venous blood may be aspirated at all, consider:
• Flushing the needle.
• 10–30° of head-down tilt.
• Intravenous filling (especially if the patient is volume depleted or on
high doses of diuretics).
Subclavian vein access
Anatomy
• The subclavian vein begins at the lateral border of the first rib, being the
continuation of the axillary vein. It ends after 3–4 cm, at the junction
with the ipsilateral internal jugular vein, from where it becomes the
brachiocephalic vein (posterior to the sternoclavicular joint).
• Immediately posterior to the vein lies the anterior scalene muscle, and
behind this, the subclavian artery and brachial plexus. More medially,
the phrenic nerve and internal mammary artery (and, on the left, the
thoracic duct) may be located deep to the vein.
• Venous ultrasound may help identify the subclavian vein location.
Procedural approach
• A rolled towel or litre bag of intravenous fluid can be placed between
the patient’s shoulder blades to expand the chest.
• The neck area should be painted with antiseptic.
• Local anaesthesia: 5–10 mL of 1% lidocaine infiltrated subcutaneously
from 2 cm below the medial third of the clavicle up to and just under
the clavicle itself.
• A small incision with a blade should be made.
• The needle, mounted on a syringe containing heparinized saline, should
be advanced to the clavicle and moved downwards until just below it.
• The needle should now be rotated through 30–45° and advanced
towards the suprasternal notch (placing a finger in the notch may aid
visualization of the target area).
• Care should be taken to keep the needle parallel to the bed in order to
avoid arterial or pleural puncture.
• When the vein is punctured, the Seldinger technique (% p.44) may be
used (Fig. 3.8).
Indications
• This is the route most commonly used when inserting permanent pacing
systems or indwelling central venous catheters for long-term use.
• Pulmonary artery catheterization.
Complications
• Arterial puncture.
• Pneumothorax.
• Haemothorax.
• Infection.
Subclavian vein access 63
Fig. 3.8 Cannulation of the subclavian vein. The vein passes under the medial third
of the clavicle; it may be cannulated by rotating and advancing the needle towards the
sternal notch once the tip is just below the edge of the clavicle
Anticoagulation issues
• Clearly, when any decision is made to stop long-term anticoagulation
prior to invasive procedures involving vascular puncture, the risks of not
continuing anticoagulant therapy must be weighed against the potential
bleeding risks of arterial puncture on an individual patient basis.
• The following are guidelines only, and local policies/protocols should be
adhered to.
Cardiac catheterization in the anticoagulated patient
• There is not always time to make requisite arrangements prior to
angiography (e.g. in the case of emergency).
• Fully anticoagulated patients should be catheterized via radial routes,
where bleeding complications are reduced.
• Operator preference may vary, but catheterization is generally safer
from the femoral route if the INR is less than 2.0 while on warfarin.
• If the femoral route is used in anticoagulated patients, consider the use
of fluoroscopy and ultrasound to guide arterial puncture. Bleeding risk
may be attenuated following the procedure by using compression or
closure devices (% p.66).
When to stop warfarin
Warfarin may be stopped 3–5 days before elective procedures, and the INR
checked on the morning of the planned procedure in the case of:
• Atrial fibrillation in low-risk patients (normal left ventricular function, no
previous history of stroke).
• Impaired left ventricular function with laminar apical thrombus (avoid
passing catheters into left ventricle).
• Recurrent deep vein thrombosis/pulmonary emboli.
• Impossible arterial access from any arm site.
Warfarin may be recommenced the evening after the procedure providing
there are no bleeding complications.
When not to stop warfarin
Warfarin should either be continued, or patients admitted and switched
to unfractionated intravenous heparin (which may be stopped immediately
prior to the procedure and restarted immediately afterwards) in the case of:
• Atrial fibrillation in moderate/high-risk patients (poor left ventricular
function, history of stroke, diabetes mellitus).
• Prosthetic cardiac valves (particularly metal valves).
• Rheumatic mitral valve disease.
• Known non-laminar intracardiac thrombus.
Anticoagulation issues 65
Direct oral anticoagulants (DOACs)

• DOACs should generally be withheld for 24 hours prior to elective
catheterization or PCI. The exception to this rule is for patients taking
dabigatran with renal impairment, where the dabigatran should be held
for 72 hours.
• DOACs can usually be restarted the evening following the procedure,
especially if there was no evidence of any bleeding complications or if
radial access was used.
Compression devices
External compression devices have been developed to aid femoral and ra-
dial sheath removal; both types rely on the availability of a bony landmark
to compress the punctured vessel against.
Femoral compression devices
• These devices act by using an external frame which applies pressure at,
or just above, the puncture site.
• Femoral compression devices may be used if bleeding is difficult to
control manually, especially in hypertensive and obese patients.
• Available devices include:
• FemoStop® (RADI Medical Systems): a clamp system that is attached
to the patient via a belt passing under the buttocks. The puncture site
is compressed by a sterile dome that may be inflated/deflated by a
manual pressure gauge (Fig. 3.9).
• CompressAR™ (Advanced Vascular Dynamics): a clamp akin to a
carpenter’s ‘G-clamp’ that may be attached to the patient’s bed to
provide direct downward compression of the puncture site.
Radial compression devices
• Radial compression bands generally work like a tourniquet, applying
pressure to compress the artery against the radius.
• These are compact devices that allow early patient ambulation.
• Available devices include:
• RadiStop® (RADI Medical Systems): a plastic wrist splint is attached
to the arm by Velcro® straps across the palm and wrist. The radial
Fig. 3.9 Use of the FemoStop® device. The FemoStop® is attached by a belt passing
under the patient’s buttocks, positioning the inflatable dome over the puncture site.
The dome is inflated above systolic blood pressure initially but then gradually reduced
until haemostasis is achieved. Picture courtesy of RADI Medical Systems
Compression devices 67
puncture site is compressed by further Velcro® straps attached to a

compressive pad (Fig. 3.10).
• TR-band™ (Terumo): a transparent wrist band that fits snugly around
the wrist incorporating a bladder that is inflated with air via a valve to
compress the puncture site.
Fig. 3.10 Radial compression devices. The RadiStop® (top panel) consists of a

compression pad attached to a wrist board by Velcro® straps. The TR-band™
(bottom panel) is a clear plastic wrist band with an inflatable compression bladder,
positioned over the puncture site. Pictures courtesy of RADI Medical Systems and
Terumo Europe Interventional Systems
Arterial closure devices
• With the advent of arterial closure devices, the need for (often painful)
digital compression has been reduced and patients may be mobilized
and discharged earlier, even if angiography has been performed via the
femoral route.
• A meta-analysis raised some concern over effectiveness of first-
generation closure devices and suggested an increased tendency
to haematoma (% p.294) and possibly pseudoaneurysm (% p.294)
formation.
• Strict adherence to aseptic technique, device datasheets, and indications
for use is advised when using these devices.
Collagen plug closure devices
• These devices utilize a collagen plug deployed over the site of vessel
puncture in the artery which is tamped down to achieve haemostasis.
The collagen is then absorbed after approximately 3 months, leaving no
foreign material behind.
• Devices of this type include Angio-Seal® (St. Jude Medical) and are
generally the most straightforward to use (Fig. 3.11).
Vascular suture devices
• This closure method relies on sheath-based delivery of small needles
carrying suture material to the vessel puncture site; the needles are
deployed by a plunger and a surgical knot is tied by a ‘clincher’ before
sheath withdrawal.
• An example of this type of device is Perclose ProGlide® (Abbott
Vascular).
Vascular clip devices
• This method deploys a nitinol clip outside the vessel, encircling the
rim of the puncture site and thus achieving haemostasis. As the clip is
outside the vessel, the apposition of native tissues promotes healing.
Pharmacological procoagulant patches
• A variety of procoagulant-impregnated patches are available; the active
agent is activated by contact with blood. These are, strictly speaking,
aids to digital compression rather than closure devices, although they
have been shown to reduce time to haemostasis.
Arterial closure devices 69
Introducer sheath
Collagen plug
Anchor
Fig. 3.11 Angio-Seal™ closure device. A bioabsorbable anchor is deployed via an

introducer sheath into the vessel lumen, and the collagen plug tamped down against
the vascular wall. The plug is reabsorbed within 3 months. Picture courtesy of St.
Jude Medical
Further reading
Koreny M, Riedmuller E, Nikfardjam M, et al. Arterial puncture closing devices compared with
standard manual compression after cardiac catheterization: systematic review and meta-analysis.
JAMA 2004; 291: 350–57.
71
Chapter 4
Cardiac catheterization
Cardiac catheterization 72
Pressure waveforms 74
Equipment 76
Catheters 82
Accessing the left heart 86
Left heart pressures and waveforms 88
Accessing the right heart 90
Right heart pressures and waveforms 92
Calculations 94
Ventriculography 96
Aortography 104
72 Chapter 4 Cardiac catheterization
Cardiac catheterization
Cardiac catheterization allows the invasive acquisition of haemodynamic
data using direct and indirect pressure measurements and oxygen satur-
ations, and provides anatomical information using contrast angiography.
Right heart catheterization used to be a routine part of an invasive cardiac
study. The increased accessibility and accuracy of non-invasive imaging (in
particular, echocardiography and Doppler techniques), however, has re-
duced the need to perform right heart catheterization. Always review non-
invasive imaging prior to performing an invasive study and confirm that the
test remains indicated.
Principal uses
Left heart catheterization
• Coronary angiography (% p.2).
• Assessment of left ventricular function (% p.100).
• To assess the severity of valvular dysfunction (% p.86).
• To measure and record left heart pressures (% p.88).
• As part of a simultaneous left and right heart study.
Right heart catheterization
• During interventional procedures (including pacemaker electrode
introduction, electrophysiological studies, congenital heart disease,
intervention for pulmonary embolism, and myocardial biopsy).
• In the assessment of suspected pulmonary hypertension.
• To measure and record right heart pressures (% p.92).
• To estimate cardiac output (CO) indirectly (% p.94).
• As part of a simultaneous left and right heart study.
Simultaneous left and right heart catheterization
• The assessment of intracardiac shunt (% p.95).
• The assessment of mitral valve disease (% p.112).
• Suspected pericardial constriction (% p.122).
• To measure systemic and pulmonary vascular resistances (% p.94).
• During intervention procedures (particularly congenital heart disease).
Cardiac catheterization 73
Pressure waveforms
Cardiac catheterization allows pressure measurement within the heart using
a fluid-filled catheter connected via a manifold to a pressure transducer.
The transducer converts the pressure waveform into an electrical signal
that is viewed on a monitor and recorded. The long distance between the
catheter tip and the pressure transducer can result in a timing delay and
some damping of the pressure signal. Fitting a transducer to the catheter
tip would result in more accurate measurements; however, this technique
is impractical and expensive. Artefacts can also occur due to interference
from high-velocity jets (end-pressure artefact), direct contact with the
vessel wall or valve (catheter impact artefact), or due to motion of the
catheter within the chamber (catheter whip artefact).
Aortic and cardiac waveforms
An understanding of pressure waveforms and timings is an important part
of interpreting cardiac catheterization data. A simplified diagram (Fig. 4.1)
helps illustrates some of these timings.
Pressure waveforms 75
AV
closes
aortic
pressure
dicrotic
notch
AV
opens left ventricular
pressure
MV
closes MV
left atrial
opens
pressure
end-diastolic
volume
left
ventricular
volume
end-systolic
volume
ECG
Fig. 4.1 Pressure waveforms and timings. AV, aortic valve; MV, mitral valve
Equipment
Manifolds
Pressure manifolds usually have three to five selectable ports (Fig. 4.2). The
proximal port is connected directly to the cardiac catheter, one port is con-
nected to pressure via a flush infusion (% p.76), one port is connected to
the contrast solution (% p.76), and a syringe is connected to the distal end
of the manifold. The pressure transducer is zeroed by opening the distal
port to air at the level of the patient’s mid-chest. It is vital that the system is
carefully flushed to avoid entrapment of air that may embolize during injec-
tions. In some hospitals, an assistant may help set up the manifold. Check it
carefully before injection.
Guide wires
Most guide wires are composed of a central core, a distal spring coil, and an
outer coating. They vary in length from short wires (30–45 cm) to facilitate
arterial access, to long exchange wires (250–300 cm) for catheter exchange.
Guidewires also vary in diameter with smaller calibres (0.025 inch) used for
access from the arm. The tips of the wires are flexible and either straight
or J tipped. The usual guide wires for diagnostic cardiac catheterization are
0.03–0.038 inch J-tipped  wires.
Hydrophilic guide wires (e.g. Terumo) are extremely useful when vessels
are tortuous or narrow. Once access has been obtained they can be ex-
changed for a conventional guide wire if required. These guide wires can be
slightly more fragile than conventional guide wires and they should not be
manipulated through an introducer needle.
Flush infusion
This varies according to hospital protocol. Heparinized saline is typically
used (e.g. heparin 1000 IU injected into a 500 mL bag of 0.9% saline).
Pressure injector
Pressure injectors are powered angiographic devices that allow a precise
bolus of contrast to be injected at an exact infusion rate (Fig. 4.3). They
are used for imaging cardiac chambers and for large vessel angiography.
Contrast agent is preloaded into the reservoir on the injector. Air must
be expelled from the reservoir before connecting to the catheter. Check
that the catheter is tightly secured to the injector as the high pressures can
result in catheter disarticulation. The injector operator then aspirates on
the injector to ensure there are no air bubbles in the system. Control of
the injection is directed by personnel according to local policy (usually the
physician or radiographer). During injection, closely watch the image and
be prepared to stop the injection if complications occur (catheter displace-
ment/myocardial staining; % p.284).
Mechanical injector pumps are also available for coronary angiography
(% p.138). These allow controlled injections of contrast using a hand con-
troller and may improve image quality and reduce contrast dose.
Equipment 77
to catheter to syringe
pressure contrast
Fig. 4.2 Pressure manifold
Fig. 4.3 Medrad® injector. Image courtesy of Bayer

Contrast media
See Fig. 4.4.
Why are contrast agents needed?
• Radiographic contrast media are agents used to improve the visibility of
internal structures such as blood vessels during X-ray examinations.
• Different body structures attenuate and reflect the X-ray beam to
different extents, determined primarily by density, thickness, and atomic
weight. X-rays may visualize the outline of large arteries (e.g. the aorta),
but give little other detail.
• Blood vessels may be opacified by filling them with a liquid of higher
atomic weight than surrounding tissues. Contrast media are therefore
suspensions that contain high atomic number/weight elements.
• Angiographic/intravascular contrast agents usually contain iodine, which
is soluble and has relatively low toxicity.
• Angiographic contrast agents are renally excreted.
Fig. 4.4 Summary characteristics of commonly used angiographic contrast agents

Equipment 79
Characteristics of contrast media
• Different contrast agent characteristics may alter ease of injection,
patient tolerability, and the likelihood of side effects/complications.
Osmolality
• Osmolality is determined by the concentration of dissolved particles and
is expressed as milliosmoles/kilogram of water (mOsm/kg H2O).
• Agents with higher osmolality than blood will opacify vessels better, but
tend to draw water from adjacent tissues by osmotic pressure.
• High osmolality-associated side effects include the sensation of heat or
discomfort after injection, and potentially toxic effects on the kidneys
and blood–brain barrier. The closer an agent’s osmolality is to blood/
bodily fluids, the better it is tolerated.
Viscosity
• Contrast agent viscosity determines ease and speed of injection; highly
viscous agents may be difficult to inject through low-gauge catheters and
may be sluggish in filling vessels.
Ionic versus non-ionic agents
• Early contrast agents were based on a single benzoic acid ring with
three iodine atoms, attached to a cation (sodium/meglumine) which
dissociated from the anionic ring on dissolving. This produces a high
osmolality, ionic contrast medium.
• Joining two rings together produced increased iodine concentration
(six atoms) which still ionized in solution, but reduced osmolality. Such
agents are termed ionic dimers.
• An alternative solution was found in replacing the cation with a non-
dissociating organic chain to form a non-ionic contrast agent. Osmolality
of these agents is substantially lower than that of ionic agents due to the
non-dissociation in solution.
• In general, non-ionic compounds have superior side effect profiles but at
greater cost.
Side effects of contrast media
Side effects of contrast agents may be idiosyncratic or predictable (i.e. dose
dependent).
Idiosyncratic reactions
• Anaphylactoid reactions (% p.286) vary in severity and, although similar
in presentation to immunoglobulin E-mediated anaphylaxis, occur via an
unknown mechanism.
Dose-dependent reactions
• Include patient sensations of heat, flushing, localized discomfort (e.g. in
the arm during internal mammary artery angiography), vasodilatation,
hypotension, and depression of myocardial contractility.
• High doses of contrast are potentially nephrotoxic, and may lead to
contrast-induced nephropathy (% p.312), especially in patients with
diabetes mellitus and reduced baseline creatinine clearance.
• It is good practice not to exceed 5–7 mL/kg of patient (depending

on exact agent used) to avoid side effects including contrast-induced
nephropathy.
Physiological response
Response to contrast agents varies according to the preparation and volume
used. Haemodynamic responses include vasodilatation, myocardial depres-
sion, and an increase in left ventricular end-diastolic pressure (LVEDP) and
are more pronounced with high-osmolality preparations. For this reason,
patients with severe left ventricular impairment, severe coronary disease,
and severe valvular disease should be considered for non-ionic compounds.
Contrast reactions are rare (for management, see % p.286). Transient renal
dysfunction (% p.310) is more common in patients with pre-existing renal
failure.
ECG changes
Injection of a contrast agent can result in transient bradycardia (% p.291).
This usually resolves within a few seconds. Transient ST segment changes
and widening of the QRS complex are commonly seen during coronary
angiography. Ventricular arrhythmias are uncommon but can be induced
during coronary injection (% p.288).
Equipment 81
Catheters
There are a large number of catheter sizes and shapes (commonly used
ones are shown in Figs. 4.6–4.11). Catheters are preselected according
to the procedure being performed. The choice of catheters for specific
procedures are discussed in individual chapters but choice is particularly
important for coronary angiography (% p.132) and coronary bypass angiog-
raphy (% p.168). Cardiac catheters are sized according to their outer diam-
eter using the French (F) catheter scale with smaller numbers representing
smaller catheters (Fig. 4.5).
Catheters are usually in the range of 4–8 F (typically 6 F) and most are
100 cm long. There is a Luer-Lok connector at the distal end of the catheter
for attaching to the manifold.
Prior cardiac catheterization

If a patient has had a prior cardiac catheter study performed, then check
to see which catheters were used and identify any problems that may
have arisen with catheter selection.
Fig. 4.5 French (F) catheter scale
Fig. 4.6 Judkins left and right catheters

Catheters 83
Fig. 4.7 Pigtail and Amplatz left catheters
Fig. 4.8 Pigtail right and Williams catheters
Fig. 4.9 Modified Amplatz and Sones catheters

Fig. 4.10 Multipurpose and National Institutes of Health (NIH) catheters
Fig. 4.11 Bypass graft catheters

Catheters 85
Accessing the left heart
Left heart catheterization is usually performed retrogradely using ac-
cess from the arterial system (e.g. femoral, radial, or brachial; % p.46).
Left heart catheterization can also be performed using a transseptal ap-
proach from the right atrium into the left atrium. This may be across a
patent foramen ovale, atrial septal defect (ASD; % p.120), or through a
transseptal puncture. It can also be achieved through a ventricular septal
defect (VSD; % p.121).
Choice of catheter
The pigtail catheter (% p.83) is the catheter of choice to access the as-
cending aorta and left ventricle from the femoral artery. The multipurpose
catheter (% p.84) is an alternative and is occasionally used when accessing
from the arm. A 0.035-inch J guide wire (% p.76) is usually recommended
to help catheter positioning.
Catheter manipulation
• Advance the catheter over the guide wire until the tip is positioned just
above the aortic valve.
• Withdraw the guide wire and connect the catheter to pressure.
• The image position can then be optimized for aortography (% p.104) if
required.
• To cross the aortic valve, image in an anteroposterior (AP) or right
anterior oblique (RAO) view and advance the catheter so that it loops
into a slight ‘U’ shape (Fig. 4.12).
• With gentle pressure, this is usually sufficient to allow the catheter to
cross the valve into the left ventricle.
• The image position can then be optimized for left ventriculography and
pressure measurements (% p.96).
Fig. 4.12 Crossing the aortic valve

Accessing the left heart 87
The ‘difficult aortic valve’

There will be times when crossing the aortic valve proves difficult:
• First check the notes to ensure that the patient does not have
significant aortic stenosis (% p.108).
• The guide wire can be reintroduced into the diagnostic catheter and
used to ‘stiffen’ the catheter to facilitate passage across the valve.
• If this fails, then the guide wire can be used to directly cross the valve
using the catheter tip to direct the angle of approach.
• Changing the catheter to a Judkins right 4 or a left Amplatz catheter
(% pp.82–3) can help with guide wire direction.
• A straight-tipped or hydrophilic wire (% p.76) may help cross
the valve.
• Once the guide wire is across the valve, the catheter is advanced over
the wire, the guide wire is withdrawn, and the catheter is connected
to pressure.
• If left ventriculography is planned then the catheter can be exchanged
over a long guide wire to a pigtail catheter (Fig. 4.13).
Fig. 4.13 Directed guide wire across the aortic valve

Left heart pressures and waveforms

See Figs. 4.14 and 4.15.
Ao
Fig. 4.14 Normal pressure values (in mmHg) for an adult male. Left atrium (LA),
left ventricle (LV), aorta (Ao). Typical pressure waveforms are shown in Fig. 4.15
Fig. 4.15 Left heart pressure waveforms

Left heart pressures and waveforms 89
The left atrial pressure wave has three peaks: the a wave is due to atrial
systole (following the P wave on the ECG), the c wave is due to pressure
from the closed mitral valve on the left atrium, and the v wave is due to left
ventricular systole. The v wave is usually slightly higher than the a wave. The
x descent follows the a wave and represents relaxation of the atrium. The
y descent follows the v wave and represents left atrial emptying. The left
ventricular pressure trace shows an a wave just prior to ventricular systole
(due to left atrial contraction).
The aortic pressure wave form is characterized by a dicrotic notch (in-
cisura) in the down slope due to aortic valve closure. It is used as a timing
marker to indicate when inflation of an intra-aortic balloon pump should
start (% p.268).
Left ventricular filling pressure

The LVEDP is an important measurement of left ventricular filling
and volume status. It is measured on the left ventricular waveform at
the end of diastole just after the a wave (the C-point) or coinciding
with the R wave on the ECG. Normal values are 3–12 mmHg. When
LVEDP rises to greater than 30 mmHg, pulmonary oedema is likely.
If the LVEDP is high then contrast doses should be minimized and left
ventriculography avoided (% p.96). An indirect measurement of left
ventricular filling can be made using the pulmonary capillary wedge
pressure (PCWP; % p.92).
Accessing the right heart
Right heart catheterization can be performed using a number of approaches
from the venous circulation (% p.58). During left and right heart proced-
ures, it is usual to access the heart from the right femoral vein though there
may be circumstances when approaches from the superior vena cava are
preferred.
Choice of catheter
There are a number of different catheters that are used for accessing the
right heart. These vary from short catheters that measure right atrial pres-
sure to balloon flotation catheters that can be wedged in the pulmonary
arterial circulation. For most diagnostic right heart studies, a multipurpose
catheter (% p.84) can be used.
• The right heart catheter is usually connected to a pressure tracing to
help identify catheter positioning.
• Flush it well before inserting the catheter.
• It is then relatively easy to access the right atrium from either the
superior or inferior vena cava.
• Occasionally, the catheter can lodge in venous side branches when
approaching from the femoral vein.
• Gently withdrawing and rotating the catheter under screening will help
access the heart.
• To cross into the right ventricle, the catheter sometimes passes directly
through the valve but often requires the formation of a loop in the right
atrium that prolapses into the right ventricle (similar to the technique
used for pacing leads).
• Use of a guide wire can help stiffen the catheter and provide torque
to steer.
• Ventricular ectopy will indicate that the catheter has passed into the
right ventricle.
• To reach the pulmonary artery, it is often necessary to pull back gently
on the catheter to take it away from the right ventricular apex.
• Rotate the catheter so that the tip points cranially and advance into the
main pulmonary artery.
• Use of a guide wire can help in difficult cases.
• Selective left and right pulmonary arteries can be accessed by rotating
and advancing gently under screening.
• To obtain a PCWP tracing, the catheter is advanced as the patient
inhales to a position where gentle resistance is felt.
The ‘difficult right heart’
There will be times when it is difficult to access the right ventricle and pul-
monary artery.
• Forming a loop of catheter in the right atrium may facilitate prolapse of
the catheter through the tricuspid valve.
• Gently withdrawing and rotating the catheter may then bring the
catheter tip into the correct position.
Accessing the right heart 91
• A soft-tipped J guide wire (% p.76) can be introduced into the

diagnostic catheter and used to ‘stiffen’ it to facilitate passage across the
tricuspid valve.
• Asking the patient to take a deep breath can help guide the catheter into
the pulmonary artery (PA) and obtain a clearer PCWP.
• Vigorous manipulation in the right ventricle can result in ventricular
arrhythmias (% p.288) (Fig. 4.16).
Catheter knotting
This may occur due to vigorous and prolonged catheter manipulation.
If knotting is suspected then immediately ask for expert help. Do not
pull the catheter tight. Occasionally the knot can be underdone; care-
fully advancing the guide wire can help. If this fails then the catheter can
be pulled tight to make the knot as small as possible, pulled back to the
introducer sheath and the entire system removed. This can result in sig-
nificant bleeding and surgical repair of the vessel may be required. Other
percutaneous techniques involve the use of snares and forceps. Surgical
removal of knotted catheters is well reported.
Fig. 4.16 Accessing the right heart from the inferior vena cava

Right heart pressures and waveforms

See Fig. 4.17 and Table 4.1.
Fig. 4.17 Right heart and pulmonary waveforms
Table 4.1 Normal ranges
RA 0–8 mmHg
RV Systolic 20–25 mmHg Diastolic 6–12 mmHg
PA Systolic 20–25 mmHg Diastolic 4–8 mmHg
PCWP 6–12 mmHg
Right heart pressures and waveforms 93
Respiratory variation
During spontaneous inhalation, right atrial pressure falls as intrathoracic
pressure falls. During exhalation, right atrial pressure rises as intrathoracic
pressure increases. The reverse is seen during mechanical ventilation. See
Figs. 4.18 and 4.19.
Right atrium Right ventricle

30 30
20 20
10 10 a
a c v
y
x
0 0
Fig. 4.18 The right atrial pressure wave form is similar to that of the left atrium
(% p.88). The a wave represents right atrial systole following the P wave on the
ECG, the c wave represents tricuspid valve closure, and the v wave represents right
ventricular contraction. The pressure in the right atrium is slightly lower than the left
atrium and the v wave is usually slightly smaller than the a wave. The peak of the a
wave represents maximum filling of the right ventricle. In atrial fibrillation, there is
loss of the a wave; in complete heart block and junctional rhythm, cannon waves
are seen (large a waves due to the right atrium contracting against a closed tricuspid
valve); in tricuspid regurgitation (% p.117), large c and v waves are seen with loss
of the x descent; in tricuspid stenosis (% p.117), prominent a waves are seen with
a muted y descent. In the right ventricular trace, the a wave represents right atrial
contraction
Pulmonary artery Pulmonary capillary wedge

30 30
20 20 a v
x y
10 10
0 0
Fig. 4.19 The pulmonary capillary wedge pressure (PCWP) is usually a slightly

damped version of the left atrial pressure (% p.89). In normal physiology, the mean
PCWP is similar to the pulmonary artery diastolic pressure and the right atrial mean
pressure
Calculations
Cardiac output
CO can be estimated with left ventriculography (% p.96) or measured
using either the thermodilution or Fick methods. These invasive techniques
are inaccurate and rarely (if ever) performed for clinical purposes. A basic
understanding (if just for historical purposes) is still probably important.
CO is usually normalized for body surface area to generate the cardiac
index (CI). This is typically 2.5–3.5 L/min/m2:
CO (L/min)
(
CI L/min/m2 = )
( )
body surface area m2
Thermodilution method
This involves injection of a bolus of liquid into the proximal port of a right
heart catheter (e.g. Swan–Ganz). A thermistor mounted in the distal end of
the catheter records a change in temperature. Rapid computerized analysis
then produces a CO.
Fick method
This technique assesses the CO by determining the rate of oxygen con-
sumption and the difference between systemic and arterial oxygen
concentrations:
02consumption (mL/min)
CO (l/min) =
Ao-PA O2content (ml/100 mL ) X10
As O2 consumption is difficult to measure, the indirect Fick method can
be applied assuming oxygen consumption based on sex, age, and body
surface area.
Vascular resistance
Vascular resistance is calculated by the ratio of pressure gradient across a
vascular bed divided by the flow through that bed. It is measured in Wood
units (mmHg/L/min) or dynes/s/cm5 with 1 Wood = 80 dynes/s/cm5.
Systemic vascular resistance (SVR; normal 800–1400 dynes/s/cm5) can be
useful in determining the cause of hypotension; typically low in sepsis and
elevated in cardiogenic shock. Pulmonary vascular resistance (PVR; normal
25–125 dynes/s/cm5) is often measured during assessment for cardiac
transplantation.
Systemic vascular resistance
80 (aortic mean pressure − RA mean (mmhg ))

SVR =
cardiac output (L/min)
where RA = right atrial.
Calculations 95
Pulmonary vascular resistance

80 (PA mean pressure − mean LA or PCwP (mmhg ))
PVR =
cardiac output (L/min)
where PA = pulmonary arterial and LA = left atrial.
Shunt quantification
• Usually performed using oximetry from multiple venous and arterial
samples.
• Errors occur due to streaming and inaccurate catheter positioning.
• Commonest use is to determine the ratio of a shunt from left to right
(pulmonary to systemic flow ratio).
• Samples are taken in the superior vena cava (SVC), the inferior vena
cava (IVC), PA, and aorta.
• As the saturation in the SVC is lower than the IVC, the mixed venous
saturation is calculated as:
3 × SVC (% ) + IVC ( % )
mixed venous sat ( % ) =
4
• The pulmonary to systemic flow ratio is then calculated as:
pulmonary flow aorta ( % ) − mixed venous ( % )

=
systemic flow PV (or 98% ) − PA (% )
• If pulmonary vein (PV) sampling is not possible then substitute 98%.
• A ratio of less than 1.5 suggests a small left-to-right shunt.
• A ratio of over 2 signifies a large shunt.
Gorlin formula
Rarely used now in clinical practice. The equation depends on forward flow
through the valve; it overestimates the valve area at high COs and under-
estimates it at low outputs.
Aortic valve area
CO
=
44.3 (systolic ejection period)(hR ) (root mean gradient )
mitral valve area

CO
=
37.7 (diastolic filling period)(hR ) (root mean gradient )
Ventriculography
Left ventriculography
Left ventriculography has traditionally been a routine part of a diagnostic
cardiac catheterization. In addition to providing information on left ven-
tricular contraction and function, left ventriculography identifies and quan-
tifies abnormal wall motion, left ventricular aneurysms, left ventricular
thrombi, VSDs, and valvular regurgitation.
Indications
• Left ventricular function in patients with known or suspected coronary
artery disease.
• Left ventricular function in patients with valvular heart disease.
• Quantification of mitral regurgitation (MR) (% p.114).
• Localization of VSDs (% p.121).
Relative contraindications
• Critical aortic stenosis.
• Severe left main stem stenosis (risk of hypotension).
• Elevated LVEDP greater than 35 mmHg.
• Pulmonary oedema.
• Left ventricular systolic hypertension.
• Left ventricular thrombus.
Complications
• Cardiac arrhythmias (VT/VF) (% p.288).
• Air or thrombus embolization (% p.306).
• Contrast reactions and nephropathy (% p.312).
• Intramyocardial injection (usually benign but tamponade (% p.284) may
occur).
• Complications related to vascular access (% p.294).
Ventriculography versus echocardiography
Advances in echocardiography techniques (e.g. harmonic imaging and con-
trast) have reduced the need for left ventriculography. Echocardiography
obviates the radiation dose and contrast load to the patient. If a good-
quality echocardiogram is available then this should provide all (and
more) of the information that a typical left ventriculogram provides.
Right ventriculography
Not commonly performed but is occasionally used in the assessment of:
• Tricuspid regurgitation.
• Right-to-left shunts.
• Right ventricular cardiomyopathies.
• Abnormalities of the right ventricular outflow tract.
See Fig. 4.20.
Ventriculography 97
Fig. 4.20 Right ventriculography in the AP projection. The catheter tip is sited in the
right ventricle (RV). The tricuspid valve (TV) and pulmonary arteries (PA) are well
demonstrated
Procedure
Left ventriculography is usually performed using a pig-tailed catheter with
side holes (% p.83). Alternatives catheters are discussed elsewhere (% p. 86 ).
Vascular access is obtained according to operator preference and patient co-
morbidity. The catheter is advanced into the left ventricle with or without the
guide wire as described (% p.86).
Catheter position
• Position the catheter tip in the left ventricular cavity so that ventricular
ectopy is minimized and the catheter avoids contact with the mitral
valve apparatus. This usually means placing the tip in the mid-cavity
(% p.98).
• Care should be taken in patients with known or suspected left
ventricular aneurysm (% p.101) to avoid dislodgment of unseen mural
thrombi.
• Connect the catheter to pressure, confirm a left ventricular pressure
tracing, and note the LVEDP (% p.89).
• Connect the pressure injector (% p.76) to the catheter (occasionally an
extension connector is required).
• Contrast should be slowly expelled from the injector during connection
to eliminate air.
• Ensure that connections are secure as high pressures may result in
equipment separation.
Contrast injection
• Care must be taken to avoid inadvertent injection of air.
• The pressure injector is used to deliver a preset volume of contrast
over a programmed period of time.
• Typical contrast volumes are 30–35 mL at 10–15 mL/second.
• Some operators choose to use a linear rise (rise/fall time) of between
0.1 and 0.5 seconds. This provides a step up to the peak flow rate to try
and prevent catheter whip. Typical values are 1/100th of the flow rate,
that is, if the flow rate is 10 mL/sec, use a rise/fall time of 0.1 seconds.
• In patients with impaired left ventricular function or elevated LVEDP
(>25 mmHg), contrast volume and rate of injection should be reduced
(e.g. to 30 mL at 10 mL/second).
• Patients should be warned of a widespread ‘warm flush’ sensation and
feeling of micturition that can result from contrast vasodilatation.
• Ask the patient to inspire deeply and hold it to line up the image. Repeat
and acquire the image.
• Inject the contrast a few frames after the start of acquisition (a
radiographer will often do this) and continue to acquire until a
satisfactory cardiac cycle has been obtained.
• During contrast injection the catheter may need to be withdrawn
rapidly if complications occur.
• Following injection reconnect to the pressure transducer.
Difficulties with left ventriculography

• The catheter tip may get caught up in the papillary muscles (particularly
with pigtail catheters). Gentle rotation in either direction and catheter
withdrawal is usually sufficient to safely extract it.
• Ventricular ectopy is common during catheter manipulation, particularly
with very apically positioned catheters. Try gently withdrawing and
repositioning the catheter.
• Keep acquiring the image until a satisfactory (and ectopic-free) cardiac
cycle has been seen. There is often a short period of ectopy at the start
of the injection before normal systolic function returns.
• Try to avoid injecting contrast directly into a left ventricular aneurysm
(% p.101). If in doubt about position, then try a test injection by hand
of 10 mL.
• Warn the patient before administering contrast. The flush sensation that
some patients experience can be alarming if unexpected.
Left ventricular views
• Left ventriculography is usually performed using a 30° RAO projection.
This visualizes the anterior, apical, and inferior walls. See Fig. 4.21.
• The 60° left anterior oblique (LAO), 20° cranial view identifies the
posterolateral and septal walls. It is also particularly useful for localizing
VSDs. See Fig. 4.22.
• In facilities where biplane ventriculography is available, both views
can be obtained from a single contrast injection. It does, however,
increase the radiation dose and may take additional time to position the
equipment.
Ventriculography 99
aorta
anterior
inferior apical
Fig. 4.21 Schematic of RAO view
aorta
septum
postero-
lateral
Fig. 4.22 Schematic of LAO view
• MR is usually seen in a 30° RAO projection with the radiographer

panning across to the left atrium (% p.115). The 60° LAO, 20° cranial
view can also be used.
• Frame rates are typically 30–60 fps.
• Once imaging has been acquired, connect the catheter to pressure,
again being careful to avoid air entering the circuit.
• Ensure that imaging is of diagnostic quality. Occasionally, left
ventriculography may need to be repeated if opacification or the
catheter position is unsatisfactory.
• When the technician indicates that the pressure is being recorded,
pull the catheter back from the left ventricle to the aorta to record
an estimate of the gradient through the left ventricular outflow tract
(% p.108).
• Remove the catheter over the guide wire to complete the procedure.
• See Figs. 4.23 and 4.24.
Image interpretation
Fig. 4.23 RAO projection of the left ventricle showing a pigtail catheter in the mid-
left ventricular cavity
Fig. 4.24 LAO projection of the left ventricle during contrast injection
Global left ventricular function

See Fig. 4.25.
An overall assessment of left ventricular function can be made by ‘eye-
balling’ the left ventriculogram. This is a technique based largely on ex-
perience. Left ventricular function is typically described as normal, mildly
impaired, moderately impaired, or severely impaired. Quantitative analysis
Ventriculography 101
Fig. 4.25 RAO projection left ventriculography showing end-diastole (left), systole

(centre), end-systole (right). There is very good left ventricular function with cavity
obliteration during systole
of left ventricular function can be made by dedicated software from stored

cine ventriculography. Ejection fraction (EF) is calculated from the end-
systolic volume (ESV) and end-diastolic volume (EDV):
EDV − ESV
EF (% ) = (stroke volume)
EDV
Regional wall motion
Regional left ventricular wall motion can be described from standard left
ventriculography views. Myocardial function is described as:
• Normal—uniform, concentric motion during systole.
• Hypokinetic—reduced systolic function.
• Akinetic—absent systolic function.
• Dyskinetic—paradoxical systolic function.
Left ventricular thrombus
See Figs. 4.26 and 4.27.
Thrombus in the left ventricle may be identified during left ventriculog-
raphy, particularly in patients with poor left ventricular function and/or left
ventricular aneurysm. Appearances are of a filling defect (lack of contrast
opacification), usually located at the left ventricular apex (% p.102). Left
ventricular thrombi may occasionally be laminar.
thrombus
Fig. 4.26 Left ventriculogram revealing a well-circumscribed filling defect at the left

ventricular apex in keeping with a thrombus
aneurysm
left ventricle
Fig. 4.27 Left ventriculogram demonstrating a large anterior wall pseudoaneurysm

of the left ventricle
Ventriculography 103
Aortography
Indications
The principal uses of ascending aortography during cardiac catheterization
studies are to:
• Assess the severity of aortic regurgitation (Fig. 4.28).
• Assess aortic pathology (aneurysm/dissection (rarely)/coarctation)
(Fig. 4.29).
• Identify the origin and patency or coronary artery bypass grafts
(% p.166).
LCA
RCA
AR
Fig. 4.28 Aortogram demonstrating the origins of the left (LCA) and right (RCA)
coronary arteries. There is mild central aortic regurgitation (AR)
Fig. 4.29 Aortogram demonstrating significant enlargement of the ascending aorta

Aortography 105
Procedure
• Aortography is typically performed using a pigtail catheter with side
holes (% p.83).
• Advance the catheter under screening to the proximal ascending aorta
using a guide wire.
• Make sure the catheter is not interfering with aortic valve leaflet opening
or closing.
• Remove the guide wire, aspirate the catheter, and connect to a pressure
injector (% p.76).
• The image is then acquired during a breath hold using an injection
volume of 40–60 mL at 20 mL/second in an LAO projection.
• For imaging coronary artery bypass grafts (% p.166), the end of
the catheter is usually positioned slightly higher up the aorta with a
prolonged acquisition phase to trace the origin, location, and direction
of the grafts.
Coarctation of the aorta
In patients with known or suspected aortic coarctation, cardiac cath-
eterization can determine the pressure gradient through the coarctation.
Aortography will help identify the size and site of the obstruction and any
coexisting aortic pathology. A pressure gradient of greater than 50 mmHg
through the obstruction is considered an indication for intervention. Imaging
for aortic coarctation (arrowed in Fig. 4.30) is usually performed using an
RAO projection.
Fig. 4.30 Aortogram demonstrating aortic coarctation

107
Chapter 5
Specific conditions
Aortic stenosis 108
TAVI work-up 110
Aortic regurgitation 111
Mitral stenosis 112
Mitral regurgitation 114
Pulmonary valve 116
Tricuspid valve 117
Pulmonary embolism 118
Pulmonary angiography 119
Atrial septal defect 120
Ventricular septal defect 121
Constrictive pericarditis 122
Pericardial tamponade 123
Cardiomyopathy 124
Myocardial infarction with non-obstructed coronary arteries 126
108 Chapter 5 Specific conditions
Aortic stenosis
Prior to cardiac catheterization, data from non-invasive studies should have
provided a mean and peak gradient, in addition to an estimate of aortic
valve area (Table 5.1). Nevertheless, there will be occasions when direct
haemodynamic assessment of aortic stenosis severity is required during a
catheter study. Coronary angiography is often performed during the study
(% p.6).
Pressure gradient
The most accurate method of determining the pressure gradient across the
aortic valve is to have simultaneous measurements from within the left ven-
tricle and the aorta. This either requires two catheters or a double-lumen
catheter into the left ventricle. Less accurate assessments can be made by
recording the pressure from the femoral artery.
In practice, the aortic valve gradient is usually obtained in cardiac cath-
eterization studies by performing a left ventricular pull-back measurement
and recording the peak-to-peak pressure gradient (% p.109). This technique
is limited by the time differences between the two peak measurements and
by direct errors from the catheter interfering with the aortic valve opening
and closure.
See Fig. 5.1.
Valve area
An assessment of aortic valve area can be made using the Gorlin formula
(% p.95). This requires knowledge of the cardiac output, the mean pressure
gradient, and the systolic ejection time. There are a number of inaccuracies
and practical limitations with the technique that have led to its extinction
from routine practice.
Crossing the aortic valve in severe aortic stenosis

This is now rarely performed for diagnostic reasons as the additional
data rarely changes patient management and is hazardous. It has been
shown that attempts to cross the valve frequently result in silent (and not
so silent) emboli on brain magnetic resonance imaging (MRI). Accurate
non-invasive testing (especially echocardiography) should be considered
the gold standard for the majority of patients.
When there is a need to cross the aortic valve, for example, a discrep-
ancy between clinical symptoms and non-invasive testing or during TAVI
work-up (% p.110), this can be performed using a 5 F AL1 diagnostic
catheter and a hydrophilic straight-tipped guidewire. Once the catheter
is advanced into the ventricle, it can then be swapped for a pigtail cath-
eter using an exchange length J wire. Great care must be taken to ensure
the wire is manipulated in a controlled manner. Aortography may assist
if identifying the point of leaflet opening (‘Prussian helmet sign’; Fig. 5.2).
Aortic stenosis 109
Table 5.1 Data to obtain prior to cardiac catheterization
Valve area (cm2) Peak (mmHg) Mean (mmHg)

Mild stenosis >1.4 <35 <20
Moderate stenosis 1.0–1.4 35–65 20–40
Severe stenosis <1.0 >65 >40
150
LV
100
50 Ao
Fig. 5.1 Simultaneous left ventricular (LV) and aortic (Ao) pressure traces in aortic
stenosis. Mean aortic gradient (shaded area) and peak-to-peak (arrows) gradient
are shown
(a) (b) (c) (d)
Fig. 5.2 The Prussian helmet sign on aortography (arrow) provides a useful visual
landmark when there is a clinical need to cross the valve in aortic stenosis
TAVI work-up
Transcatheter aortic valve implantation (TAVI) is rapidly becoming an estab-
lished treatment option for patient with severe symptomatic aortic stenosis.
Standard TAVI work-up angiography involves a systematic assessment of
the coronary (% p.110), aortic, and peripheral arteries. Aortography should
always be performed to assess the angulation between the valve and the
ascending aorta. Detailed haemodynamic assessment may not always be
required depending on the reliability of non-invasive studies but can include
transvalvular pressure gradients and right heart catheterization.
Access route evaluation
Transfemoral access is the commonest and most preferable approach for
TAVI and a detailed assessment of size, tortuosity, and degree of calcifica-
tion of the peripheral vasculature is required. Some of this information can
be gathered non-invasively through CT angiography, but invasive angiog-
raphy allows identification of the puncture site and will provide valuable in-
formation on whether tortuous iliac or femoral arteries can be straightened
with an extra stiff guide wire (e.g. Amplatz extra stiff 0.032). If marked
iliofemoral disease is present, then angiography can also be performed on
the axillary and subclavian arteries to identify alternate access sites.
Iliofemoral angiography
This is typically performed using a graded pigtail catheter that is posi-
tioned just above the distal aortic bifurcation. Ensure the table height is
elevated to maximize the field of view. Before performing the acquisition,
make sure the table can pan to the femoral head on both sides. A pump
injection is usually required for full opacification (e.g. 20 mL contrast at
20 mL/second). Grading on the pigtail catheter allows for accurate meas-
urement of vessel diameter after the procedure.
Aortic regurgitation 111
Aortic regurgitation
Qualitative estimation of aortic regurgitation can be made by observing the
degree of left ventricular opacification during aortography (% p.104). The
estimate depends on the regurgitant volume in addition to the function of
the left ventricle:
• Grade I—minimal regurgitation. Clears rapidly with each beat.
• Grade II—opacification of left ventricle is less than aorta.
• Grade III—opacification of left ventricle becoming equal to the left
ventricle.
• Grade IV—intense opacification of left ventricle greater than the aorta.
Opacification often persists during subsequent beats.
Mitral stenosis
Cardiac catheterization for the assessment of mitral stenosis typically in-
volves simultaneous left and right heart catheterization. Coronary angi-
ography is usually performed during the procedure if the patient is being
considered for mitral valve surgery (% p.6).
• Insert a right heart catheter (e.g. MPA2 or Swan–Ganz; % p.84) into the
main PA (% p.90) to measure the PA systolic pressure (% p.118).
• Advance the catheter to obtain a PCWP (% p.92) to act as a surrogate
for left atrial pressure.
• Insert a pigtail catheter into the body of the left ventricle (% p.100) to
record the LVEDP (% p.89).
• The mean mitral valve gradient is the area between the PCWP curve
and the left ventricular pressure curve during diastole. See Fig. 5.3.
• The PCWP, however, probably overestimates the left atrial pressure by
2–3 mmHg in mitral stenosis.
• Mean gradients are influenced by heart rate, particularly if the rhythm is
AF so an average of at least 10 beats should be used.
• Left ventriculography is occasionally performed at the procedure end to
examine mitral valve calcification, leaflet motion, and degree of mitral
regurgitation (% p.115).
See Table 5.2.
Mitral valve area can be calculated using the Gorlin equation (% p.95) but
as previously mentioned, this technique is prone to a degree of error and
is now rarely performed.
150
LV
100
50
PCW
Fig. 5.3 Simultaneous left ventricular (LV) and pulmonary capillary wedge (PCW)
pressure traces in mitral stenosis. Mean mitral valve gradient (shaded area) is shown
Mitral stenosis 113
Table 5.2 Values for different forms of mitral stenosis
Valve area (cm2) Mean gradient (mmHg)

Normal 4–6 N/A
Mild stenosis >1.5 <5
Moderate stenosis 1.0–1.5 Variable
Severe stenosis <1.0 >10
Mitral regurgitation
Right heart catheterization in patients with MR will reveal large v waves in
the PCWP trace. These are transmitted left ventricular pressure waves and
occur during the down-slope of the left ventricular pressure trace (Fig. 5.4).
Large v waves are not specific for MR as they can occur in other conditions
that elevate left atrial pressure (e.g. VSD, infiltrative myocardial disease).
Qualitative estimation of MR can be made by observing the degree of
left atrial opacification during left ventriculography (Fig. 5.5). The estimate
depends on the regurgitant volume in addition to the function of the left
ventricle:
• Grade I—minimal regurgitation. Clears rapidly with each beat.
• Grade II—moderate opacification of left atrium. Clears with
subsequent beats.
• Grade III—intense opacification of left atrium becoming equal to the left
ventricle.
• Grade IV—intense opacification of left atrium becoming greater than
the left ventricle. Opacification often persists during subsequent beats.
It is important to ensure that reported MR is not the result of catheter
pressure on the mitral valve apparatus (catheter-induced MR) or ventricular
ectopics. It may also be possible to identify the cause of MR from the left
angiogram (e.g. flail leaflet or annular calcification).
150
LV
100
V wave
PCW
50
Fig. 5.4 Simultaneous left ventricular (LV) and pulmonary capillary wedge

(PCW) pressure traces in mitral regurgitation. A large v wave is seen representing
transmitted left ventricular pressure waves
Mitral regurgitation 115
Fig. 5.5 Grade IV severe mitral regurgitation. The left atrium opacifies quickly and
becomes darker than the left ventricle
Pulmonary valve
Pulmonary stenosis
The degree of pulmonary stenosis can be measured by advancing a right
heart catheter through the valve into the main PA and performing a ‘pull-
back’ with continuous pressure recordings (% p.92).
Pulmonary regurgitation
Pulmonary regurgitation can be assessed by pulmonary angiography
(% p.119). This will also determine any degree of PA dilatation (Fig. 5.6).
PA
Fig. 5.6 Pulmonary angiogram (posteroanterior view) in a patient with complex

congenital heart disease. The main pulmonary artery (PA) is dilated and there is
significant pulmonary regurgitation
Tricuspid valve 117
Tricuspid valve
Tricuspid stenosis
Tricuspid stenosis is uncommon and usually occurs in combination with mi-
tral valve disease. Cardiac catheterization is rarely used alone to diagnose
tricuspid stenosis. Small (5 mmHg) gradients can lead to significant symp-
toms and for this reason, accurate recordings using two matched catheters
(one in the right atrium and one in the right ventricle) should be used.
Tricuspid regurgitation
Right heart catheterization in tricuspid regurgitation will reveal large v waves
in the right atrial trace as blood is forced into the right atrium during systole
(% p.93).
Pulmonary embolism
Invasive pulmonary angiography for the investigation of suspected pul-
monary embolism has largely been replaced by CT pulmonary angiog-
raphy. There are, however, occasions when cardiac catheterization may
be performed in the patient with proven or suspected pulmonary emboli,
for example, in massive pulmonary embolism when embolectomy is being
considered.
The venous access site should be carefully considered as femoral venous
access may dislodge an iliofemoral clot. PA and systemic arterial pressures
should be continuously recorded. A PA systolic pressure of greater than
60 mmHg is considered a contraindication to pulmonary angiography unless
in very experienced hands.
Pulmonary angiography 119
Pulmonary angiography
Imaging of the pulmonary vascular tree is usually performed in an AP pro-
jection with a pigtail catheter sited in the main pulmonary artery. A con-
trast rate of 30–40 mL at 12–20 mL/second is used if PA pressures are
normal. Digital subtraction angiography is used if the patient is compliant
with breath-holding. Selective PA branch hand injections of 10 mL of con-
trast may identify filling defects (Fig. 5.7).
PA
Fig. 5.7 Selective pulmonary angiography of the right pulmonary artery (PA)

demonstrating filling defects (arrowed) in keeping with multiple pulmonary emboli
Atrial septal defect
An ASD is one of the commonest congenital cardiac defects seen in adults.
Patients often present with symptoms of breathlessness or palpitation re-
lated to right heart failure and pulmonary hypertension. The diagnosis will
usually have been supported using transthoracic and transoesophageal
echocardiography.
During cardiac catheterization, a right heart study will be performed to
evaluate intracardiac pressures, to examine for pulmonary hypertension,
to quantify the intracardiac shunt, and to exclude anomalous pulmonary
venous drainage. A typical examination would involve:
• Right heart catheterization and recording of the PA pressure (% p.92).
• Right heart pullback (% p.93).
• An attempt to cross the ASD and record left atrial saturation.
• Quantification of the shunt (% p.95).
Secundum ASDs are now commonly closed using a percutaneous approach
and closure is often planned at the same time as the cardiac catheteriza-
tion study. If required, the procedure can be imaged and guided using
transoesophageal or intracardiac echocardiography (Fig. 5.8).
Fig. 5.8 Transoesophageal echocardiography demonstrating large atrial septal

defect (left panel), which was successfully closed percutaneously using a septal
occluder (right panel)
Ventricular septal defect 121
Ventricular septal defect
Usually the diagnosis of a VSD has been confirmed on echocardiography.
Cardiac catheterization can be useful to identify the location and size of the
defect and to calculate any intracardiac shunt (% p.95). Cardiac catheteriza-
tion for the evaluation of a VSD in adults is usually performed during or just
prior to a corrective procedure.
• Simultaneous left and right ventricular pressure measurements will
determine the pressure gradient through the defect (% p.92).
• Oximetry will allow the degree of shunt to be measured (% p.95).
• Left ventriculography (% p.96) using the LAO cranial view allows
visualization of the ventricular septum (Fig. 5.9).
VSD
LV
RV
Fig. 5.9 Left ventriculography using a pigtail catheter in a patient during

percutaneous closure of a ventricular septal defect (VSD). Contrast is seen to pass
from the left ventricle (LV) to the right ventricle (RV) through the VSD
Constrictive pericarditis
Characteristic haemodynamic responses in constrictive pericarditis are:
• Hypotension.
• Tachycardia.
• An inspiratory rise in right atrial pressure (Kussmaul’s sign).
• An M or W configuration in the right atrial pressure trace (steep Y
descent and smaller X descent).
• A dip and plateau of early rapid diastolic filling followed by abrupt
cessation due to pericardial constraint.
• Elevation and equalization of the diastolic pressures in all cardiac
chambers.
• Matching of left ventricular and right ventricular diastolic pressures
during respiration (Fig. 5.10).
LV
RV
Fig. 5.10 Simultaneous left (LV) and right (RV) ventricular traces in a patient with
pericardial constriction. The diastolic pressures match with a ‘dip and plateau’ phase
and a ‘square-root sign’ appearance
Pericardial tamponade 123
Pericardial tamponade
Echocardiography will give the diagnosis instantly. There are similar haemo-
dynamic findings to pericardial constriction at cardiac catheterization. There
is usually a fall in systemic pressure with inspiration (pulsus paradoxus) of
greater than 10 mmHg. The right atrial pressure is generally elevated and
blunted in tamponade (Fig. 5.11).
See also % p.284 for causes and management and % p.254 for
pericardiocentesis.
Fig. 5.11 Transthoracic echocardiography (apical four-chamber view)

demonstrating a large pericardial effusion surrounding the heart. The right ventricle
(RV) and right atrium (RA) are small with collapse of the RA (arrowed). LA, left
atrium; LV, left ventricle
Cardiomyopathy
Hypertrophic cardiomyopathy
In patients with hypertrophic cardiomyopathy and a left ventricular outflow
obstruction, cardiac catheterization will reveal a dynamic gradient between
the left ventricle and the aorta. A pigtail catheter is sited in the body of
the left ventricle (% p.98) and slowly withdrawn while continuous pressure
recordings are made. Ideally, a second arterial catheter will be sited in the
aorta for beat-to-beat comparison. In obstructive hypertrophic cardiomy-
opathy, a gradient will be seen from the apex to the outflow tract. As the
catheter is withdrawn, the pressure will fall just before crossing the valve
(Fig. 5.12).
The gradient can be accentuated by asking the patient to perform
the Valsalva manoeuvre or by administrating vasodilator therapy (e.g.
sublingual GTN).
Restrictive cardiomyopathy
Infiltrative or restrictive cardiomyopathies have similar haemodynamic
findings to constrictive pericarditis (% p.122) at cardiac catheterization.
One discriminator is the respiratory variation that occurs between the left
and right ventricular pressure traces. This does not occur in constrictive
pericarditis.
LV LVOT AO
Fig. 5.12 Pullback trace from left ventricle (LV) through left ventricular outflow tract
(LVOT) to aorta (AO) in patient with hypertrophic cardiomyopathy
Cardiomyopathy 125
Brockenbrough sign
After a premature ventricular complex (PVC), the pressure across the
aortic valve increases in aortic stenosis with an increase in systemic pres-
sure for the sinus beat after the ectopic (Fig. 5.13). This is in contrast to
obstructive hypertrophic cardiomyopathy, where the systemic pressure
of the beat following the ectopic is usually lower than that of the beat
before.
PVC
AO
LV
Fig. 5.13 Brockenbrough sign. AO, aorta, LV, left ventricle, PVC, premature
ventricular complex
Myocardial infarction with non-

obstructed coronary arteries
Myocardial infarction with non-obstructive coronary arteries (MINOCA) is
an increasingly recognized condition. It is estimated to affect around 5–10%
of patients presenting with myocardial infarction (MI). These patients pre-
sent somewhat of a quandary, as the underlying mechanism for myocardial
damage is often not immediately apparent. A systematic and thorough diag-
nostic strategy is required to elucidate the cause, often involving both inva-
sive and non-invasive testing. Establishing a final diagnosis is important as it
has direct implications for patient management and prognosis.
Plaque rupture
The majority of MIs are due to rupture of an atherosclerotic plaque, al-
though plaque erosion is more common in women and smokers. Not all
plaques that rupture are obstructive on invasive angiography, as there may
be outward growth of the vessel to accommodate plaque growth (posi-
tive remodelling). Intravascular imaging can confirm plaque rupture or the
presence of laminated thrombus in the artery and should be considered in
patients presenting with MINOCA, especially for those with one or more
established cardiovascular risk factors and localizing ECG changes.
Coronary artery spasm
Severe vasoconstriction of the coronary arteries can result in almost com-
plete occlusion of the vessel, producing MI or even sudden cardiac death.
Spasm often occurs in regions of mild plaque growth but can also occur
in completely normal arteries following exposure to vasoactive substances
(e.g. cocaine, epinephrine, chemotherapeutic agents, etc.). Patients with
spasm do not always have traditional cardiovascular risk factors. The diag-
nosis can be confirmed through provocation testing with intracoronary ad-
ministration of ergonovine or acetylcholine. Treatment is pharmacological
and calcium channel blockers are a first-line therapy, although other vaso-
dilatory agents can also be considered.
Paradoxical embolus
The presence of an abnormal connection between the pulmonary and sys-
temic circulation can lead to MI through a paradoxical embolus. At cath-
eterization, there is often an abrupt terminal branch occlusion, but in some
cases there may be no evidence of embolus. Clinical suspicion of paradox-
ical embolus should be heighted in young patients with no cardiovascular
risk factors and ECG changes that suggest either right atrial or right ven-
tricular pathology. Transthoracic or transoesophageal echocardiography is
required to identify the presence of an intracardiac communication.
Myocarditis
This can present with symptoms, signs, and ECG changes that closely mimic
MI. Fulminant myocarditis is also associated with acute heart failure and
even circulatory collapse in extreme circumstances. Cardiac catheteriza-
tion is generally normal, but an elevated left ventricular diastolic pressure
MYOCARDIAL INFARCTION 127
portends a worse prognosis. The diagnosis can be confirmed on cardiac

MRI, with endomyocardial biopsy now rarely performed. Acute treatment is
generally supportive and subsequently dependent on the underlying cause.
Structural myocardial dysfunction
The MINOCA syndrome is often related to cardiomyopathies, including
stress-
induced (takotsubo), hypertrophic, or dilated cardiomyopathy.
Each distinct condition has important management strategies and ther-
apies that can influence patient outcomes. Non-invasive imaging via either
echocardiography or cardiac MRI remains the cornerstone of diagnosis.
Given the high rates of myocardial pathology in patients presenting with
MINOCA, some argue that cardiac MRI should now be offered as a routine
investigation.
Takotsubo cardiomyopathy
This mysterious condition presents with symptoms of chest pain that are
typically triggered by emotional or physical stress (although not always).
The condition is more common in women who are postmenopausal.
The ECG changes can be pronounced, including gross ST-segment eleva-
tion in keeping with ST-segment elevation myocardial infarction (STEMI)
(% p.227). However, coronary angiography always demonstrates unob-
structed arteries and the appearances on left ventricular angiography are
classical (Fig. 5.14). Left ventricular function often recovers with the passage
of time, but recurrence is possible.
Fig. 5.14 Left ventricular angiography of a patient with takotsubo cardiomyopathy

demonstrating classical apical ballooning
129
Chapter 6
Coronary angiography
Coronary anatomy 130
Choice of catheters 132
Catheter manipulation 134
Imaging the coronaries 138
Left coronary artery 140
Right coronary artery 148
Use of nitrates 152
Quantification of stenoses 154
Tips for interpretation 158
Common pitfalls 159
Unusual coronary anatomy 160
130 Chapter 6 Coronary angiography
Coronary anatomy
Left coronary artery
The left main stem (LMS) coronary artery originates from the left aortic
sinus of Valsalva. It then bifurcates into the left anterior descending (LAD)
and left circumflex (Cx) coronary arteries. Occasionally, the LMS trifur-
cates, sending off an intermediate branch between the LAD and Cx. The
LAD travels down the interventricular grove of the heart supplying blood
to the anterior wall of the left ventricle. It has diagonal branches that supply
the anterolateral wall and septal branches that supply the anterior two-
thirds of the left ventricular septum and the left bundle. The terminal LAD
supplies the apex of the left ventricle and often wraps around to supply
part of the inferior wall. The left Cx travels posteriorly down the left atrio-
ventricular groove supplying the posterior wall of the left ventricle. It has
obtuse marginal branches supplying the lateral wall of the left ventricle.
Right coronary artery
The right coronary artery (RCA) originates from the right aortic sinus of
Valsalva. It travels down the right atrioventricular groove towards the in-
ferior aspect of the heart. It has acute marginal branches (that supply the
right ventricle), a conus branch (that supplies the right ventricular outflow
tract), an atrioventricular node branch, and usually (60% of individuals) a
sinus node branch. The RCA terminates after the crux into the posterior
ventricular branch and the posterior descending artery (PDA) that supplies
the inferior wall of the left ventricle and inferior one-third of the ventricular
septum (Fig. 6.1).
Determining dominance
Coronary dominance is determined by the vessel that supplies the PDA. In
85% of individuals this is the RCA, in 8% the left Cx is dominant, and in 7%
there is co-dominance or a balanced circulation.
Coronary anatomy 131
Ascending aorta
Left main stem
Circumflex coronary
artery
Right coronary
artery
Diagonal branches
(of the LAD)
Left anterior
Posterior descending artery
descending artery
Septal branches
(of the LAD)
Fig. 6.1 Coronary anatomy

Choice of catheters
For routine diagnostic coronary angiography, catheters ranging in size from
4 to 6 F are used. Smaller catheters require more force to inject and to
obtain satisfactory opacification. Autoinjectors may help achieve satisfac-
tory flow. Smaller catheters also have the advantage of smaller sheaths and
puncture sites, allowing earlier mobilization and reduced vascular compli-
cations. Smaller thin-walled catheters, however, are more floppy and have
reduced torque.
See % p.82 for a list and diagrams of commonly used catheters.
• For routine diagnostic coronary angiography from the femoral route or
from the arm, the Judkins catheters are normally used.
• The Judkins left (JL) catheters have a 90° primary curve, a 180°
secondary curve, and various arm lengths.
• For routine femoral or left radial cases a JL4 is used, while the smaller
arm JL3.5 is used for procedures from the right radial.
• Smaller arm lengths (JL3.5) are also used in shorter patients, in those
with small aortic roots, in cases where the LMS coronary artery arises
superiorly, or in patients in whom the LAD coronary artery originates
from a separate origin.
• In patients with a dilated aortic root or in very tall patients, a longer arm
catheter (JL5 or JL6) can be helpful.
• In patients with dilated aortic sinuses, or if the coronary ostia is in an
unusual position, the left Amplatz (AL) catheters can help.
• The standard catheter for accessing the RCA via the femoral or radial
route is the Judkins right 4.0 (JR4) catheter.
• Alternatives are the Williams (3DRC) and modified Amplatz right (AR
MOD) catheters.
Prior study
If a patient has had a prior coronary angiography study then check to
see which catheters were used and identify any problems that may have
arisen before starting the case. For this reason it is important to clearly
document what catheters you use.
Choice of catheters 133
Engaging the left main stem coronary artery
The LMS coronary artery can usually be accessed using a JL4 (femoral or
left radial) or JL3.5 (right radial) catheters. The JL catheters are designed so
that minimal manipulation is required to engage the artery. Imaging is usually
performed in a posteroanterior (PA) or LAO projection.
• A guide wire is advanced through the aortic arch to the ascending aorta.
• The catheter is advanced over the wire so that the tip is sitting in the
aortic root.
• The guide wire is gently withdrawn under screening.
• Aspirate on the catheter to ensure free flow of blood and connect the
catheter to pressure.
• Occasionally, withdrawal of the wire results in immediate engagement
of the LMS ostium. Watch for this and keep an eye on the aortic
pressure trace looking for damping (% p.135).
• If you cannot aspirate on the catheter then the tip may be up against the
aortic wall or tightly engaged in the LMS. Gently pull the catheter back
until blood flows easily. Injection of contrast without doing this risks air
embolism (% p.306).
• Little manipulation of the JL catheter is usually needed but slow
withdrawal of the catheter may be required to select the LMS.
Occasionally, gentle clockwise (posterior) or anticlockwise (anterior)
rotation is required.
• Asking the patient to inhale deeply may help engage the artery,
particularly if accessing via the right radial route.
• Test injections of contrast may help identify anomalous origins (% p.160)
and unusual vessel take-off.
• If the LMS is not visualized easily then consider changing to a different
size or type of catheter (% p.82).
Damping
This may occur when the catheter is the same size or smaller than the
vessel selected. A dip in the systolic pressure with ventricularization of
diastolic pressures is seen. There is a pre-systolic deflection with a slower
upstroke and steeper downstroke than aortic pressure. ‘A’ waves may
be seen (Fig. 6.2).
Damping can occur with proximal vessel stenosis or deeper cannu-
lation of branches. Damping during LMS intubation is usually the result
of a LMS stenosis, catheter tip angulation up into the vessel wall, vessel
spasm (% p.159), or selective intubation of the LAD or Cx with a short
LMS. In addition, damping during RCA intubation can be due to selective
cannulation of the conus branch (% p.136) or intubation of a small non-
dominant vessel. Damping during intermediate vessel cannulation can re-
sult in ventricular arrhythmias.
200
100
Fig. 6.2 Pressure damping. There is a pressure drop with diastolic upsloping of the

pressure trace and visible A waves
Engaging the right coronary artery

The RCA can usually be intubated using a JR4 catheter. The JR catheters
require rotation and withdrawal to engage the ostium. Imaging is typically
performed in an LAO projection.
• A guide wire is advanced past the aortic arch to the ascending aorta.
• The catheter is advanced over the wire so that the tip is sitting in the
aortic root.
aortic wall or engaged in the coronary ostium. Gently pull the catheter
back until blood flows easily. Injection of contrast without doing this
risks air embolism (% p.306).
• With a JR4 catheter, the right coronary ostium is engaged by gentle
withdrawal on the catheter while applying clockwise torque.
• The catheter tip may suddenly ‘dive’ into the artery, particularly in
large dominant vessels. Keep an eye on the pressure tracing. Careful
withdrawal of the catheter or anticlockwise rotation may be required
to ensure the catheter tip is sitting in a stable position at the vessel
entrance.
• Occasionally, the catheter may selectively engage the conus branch of
the RCA (% p.136). Be careful, as contrast injection into this can induce
arrhythmia.
• Confirm catheter positioning before starting image acquisition.
Occasionally, the catheter can pull out of the artery if there is too much
torque on it.
• Ostial lesions can be missed if the catheter tip is too far into the artery.
If in doubt, try an injection of contrast with image acquisition in the right
coronary sinus.
• The RCA occasionally comes with a steep vertical take-off (termed
‘shepherd’s crook’). Changing to an AR MOD, 3DRC, or IMA catheter
can help.
Conus branch
The conus branch is the first branch of the RCA (% p.130) and sup-
plies blood to the right ventricular outflow tract. It can be easily cannu-
lated during catheter manipulation in the RCA ostium. Pressure often
damps rapidly. Injection of contrast into the conus branch can result in
rapid accumulation of blood in the myocardium resulting in a myocardial
blush. This can result in ventricular fibrillation and a cardiologist blush! If
conus cannulation is suspected, quickly and gently withdraw the cath-
eter. Gentle rotation and angulation is required to access the main RCA.
Occasionally, a different catheter is needed.
Radial catheters
Following the establishment of radial access for coronary angiography and
PCI, specialist catheters have been designed to allow operators to select-
ively engage both the left and right coronary arteries. This precludes the
need for catheter exchange and may reduce the incidence of radial spasm
and procedural fluoroscopy time.
The most commonly available radial catheter is the Tiger catheter (TIG),
which is designed with a unique set of curves that allow engagement of both
left and right coronary arteries. The catheter also has a side hole located
just distal to the tip that acts to minimize pressure dampening on intubation.
For selective engagement, imaging is usually done in the PA (for left cor-
onary artery) and LAO (for RCA).
• A guide wire is advanced from the right radial into the ascending aorta.
• The catheter is advanced over the wire so that the tip is sitting free in
the aortic root.
aortic wall or engaged in the coronary ostium. Gently pull the catheter
back until blood flows easily. Injection of contrast without doing this
risks air embolism (% p.306).
• With the TIG catheter, the left coronary ostium is engaged by
placing the tip of the catheter in the left coronary sinus and providing
anticlockwise rotation. The catheter may need to also be withdrawn
slightly. When the tip of the catheter is engaged, apply gentle
clockwise rotation to fully engage the left coronary.
Once imaging of the left coronary is complete, the TIG catheter can
•
be disengaged by either gentle withdrawal of the catheter.
• The RCA is then engaged in a similar method to a JR4 catheter, using
clockwise torque combined with gentle withdrawal. Care should be
taken when engaging the RCA, as the TIG catheter has a tendency to
dive down the vessel and has potential for dissection. If this happens,
apply gentle anticlockwise torque with withdrawal of the catheter to
seat it at the ostium of the RCA.
There are occasions where the TIG catheter cannot selectively
•
engage one (or both) arteries due to anatomical variability. If this
occurs, consider using a standard Judkins catheter.
Imaging the coronaries
With the increased use of PCI for revascularization, imaging coronary
stenosis has become lesion specific, so that a series of ‘standard images’
is performed less frequently (% p.188). Nevertheless, some cardiac cath-
eter laboratories will have a set routine of images for examining coronary
anatomy during diagnostic cases (see example, % p.139). Most operators
will also have a series of views that they are familiar with for confirming
normal coronary arteries.
Contrast injection
• Ensure that there is no air in the contrast syringe or tubing before
injecting.
• Tilting the distal end of the syringe up will reduce the risk of
embolization.
• Small test injections of a few millilitres of contrast will confirm correct
radiographic positioning before image acquisition.
• Some departments have automatic pressure injectors for injecting
contrast.
• The volume and rate on injection will vary according to the coronary
artery size, the patient size, and coexisting pathology (e.g. aortic valve
disease).
• Only a tiny amount of contrast is required for small-non dominant
vessels and occluded arteries.
• Injection of contrast should be made with the patient at deep inspiration
to pull the diaphragm down and keep the heart as still as possible.
• Some views (e.g. LAO cranial for distal RCA visualization) are optimized
at end expiration.
• The radiographer should ‘pan’ the field of view to follow the distal
vessels.
• If there is a particular point of interest then keep the focus there.
• Prolonged acquisition should be used to examine collaterals and for
grading of myocardial blush.
Storing the unexpected
The majority of X-ray systems allow screening loops to be stored digi-
tally. If something is seen while screening that may be clinically important
(e.g. embolization of an air bubble), ask the radiographer to store the
loop before depressing the screening pedal again.
Image planes
As a rough guide, the following image planes (Table 6.1; see also Figs.
6.3–6.14) are useful to examine the coronary arteries. See also % p.139.
Proximal vessels are generally visualized with a caudal projection and distal
vessels with a cranial projection.
Imaging the coronaries 139
Table 6.1 Rough guide to imaging planes useful for examining the coronary

arteries
Ostium Main and distal vessel

LMS PA, LAO, LAO caudal PA, LAO, LAO caudal
LAD RAO caudal, PA caudal, LAO RAO cranial, lateral
diagonal cranial
Cx intermediate, RAO cranial, RAO caudal, LAO caudal
obtuse marginal LAO caudal, RAO caudal,
LAO caudal
RCA LAO, RAO PA cranial, LAO cranial
Oxford University Hospitals imaging sequence

• Intubate in PA and acquire in:
• RAO shallow caudal (−30°/−10°).
• Right lateral (−90°/0°).
• RAO cranial (−45°/20°).
• RAO steep caudal (−45°/−20°).
• LAO cranial (50°/20°).
• LAO caudal (40°/−30°).
• Intubate in LAO and acquire in:
• LAO (45°/0°).
• RAO (−45°/0°).
• Right lateral (−90°/0°).
• LAO cranial (50° /20°).
See Figs. 6.3–6.10.
PA (0°/0°)
Fig. 6.3 PA—useful for examining the proximal LMS and LAD. OM, obtuse marginal
PA cranial (0°/40°)
Fig. 6.4 PA cranial—mid and distal portions of the LAD are usually well visualized
PA caudal (0°/−30°)
Fig. 6.5 PA caudal—allows visualization of the Cx, while also showing the ostium
and body of the LMA and proximal LAD
LAO cranial (50°/20°)
Fig. 6.6 LAO cranial—useful for separating the LAD from diagonals

LAO caudal—‘spider view’ (400/−30°)
Fig. 6.7 LAO caudal—visualizes proximal vessels particularly LMS, proximal LAD,

intermediate, proximal Cx
Left lateral (90°/0°)
Fig. 6.8 Left lateral—mid LAD/left internal mammary artery (LIMA) anastomosis,

distal LAD
RAO caudal (−30°/−20°)
Fig. 6.9 RAO caudal—proximal Cx, LMS. AV Cx, atrioventricular circumflex

RAO cranial (−45°/20°)
Fig. 6.10 RAO cranial—main LAD

See Figs. 6.11–6.14.
LAO (45°/0°)
Fig. 6.11 LAO—proximal, mid, and distal RCA

RAO (−45°/0°)
Fig. 6.12 RAO—proximal and mid RCA

LAO cranial (50°/20°)
Fig. 6.13 LAO cranial—distal RCA/PDA

PA cranial (0°/40°)
Fig. 6.14 PA cranial—distal RCA/PDA

Use of nitrates
Rationale
• Administration of nitrate agents may be useful or necessary during
coronary angiographic procedures to induce coronary vasodilatation.
• Nitrates may be given regardless of whether the patient is already
taking an oral preparation; in patients on IV infusions, the vasodilatory
response may be blunted.
• Administration of nitrates may help to differentiate between coronary
spasm and obstructive lesions (particularly in ostial locations), and
enable more accurate estimation of true vessel luminal diameter (useful
in angioplasty/PCI for stent sizing).
Indications
Routine administration
• Some operators administer nitrates routinely to all patients undergoing
angiography, to produce angiographic images in a state of maximal
vasodilatation.
• In this scenario, nitrate spray is often administered sublingually or a
nitrate infusion commenced prior to the procedure.
Intraoperative administration
• Nitrates are often given to treat and/or exclude coronary spasm
(% p.152 ) (Fig. 6.15).
Nitrate administration
• Glyceryl trinitrate (GTN) or isosorbide dinitrate (ISDN) may be
administered as repeated intracoronary boluses (100–250 micrograms);
maximal vasodilatation may take 1–2 minutes to develop.
• GTN spray may also be administered sublingually (1–2 puffs).
• More potent nitrate agents such as sodium nitroprusside are rarely used
except in the management of the no-reflow phenomenon (% p.246), or
sometimes in cases of intractable spasm in addition to calcium channel
blocking agents such as verapamil.
Coronary spasm
• Coronary spasm may occur during angiography as a result of the
patient’s underlying disease process, or be related to the procedure
itself.
• ‘Catheter-tip’ spasm most commonly occurs after ostial engagement
of the target vessel. Typically, the pressure waveform ventricularizes
(indicating vessel obstruction) and then falls, rising only after catheter
withdrawal or disengagement. This is commonest in non-dominant right
coronary arteries and in vessels with a native calibre similar to that of
the catheter being used (commoner in shorter patients with low body
weight) (Fig. 6.16).
• Administration of intracoronary nitrates after careful re-engagement will
help discriminate between spasm and ostial disease.
Use of nitrates 153
Fig. 6.15 Response to GTN. Mid-RCA spasm seen in patient presenting with

inferior myocardial infarction following ingestion of cocaine (left panel); following
administration of intracoronary GTN (right panel), non-obstructive plaque identified
at site of maximal spasm
Fig. 6.16 Coronary spasm—catheter tip spasm at the ostium of the RCA
• Spasm may also occur during PCI procedures, especially when relatively
stiff coronary guide wires are used that effectively ‘straighten out’ the
coronary anatomy.
• Other causes of spasm include ingestion of cocaine or amphetamine
derivatives (may cause refractory spasm also requiring intracoronary
verapamil).
• Rarely, coronary spasm and hypotension may occur as a consequence
of a contrast reaction (% p.286).
• It is important to recognize coronary spasm as it can mimic a severe
stenosis. If in doubt, a trial of intracoronary nitrate should be used.
• Catheter withdrawal may be required to relieve spasm.
• Acquire an image to document relief of spasm.
Quantification of stenoses
It is important to understand some principles of imaging that will allow the
operator to determine extra views to delineate difficult anatomy. For ex-
ample, an oval stenotic lesion may appear angiographically severe in one
projection but normal in another (Fig. 6.17). More than one image projec-
tion is therefore vital in assessing disease severity and separating overlapping
vessels. Reviewing the pictures after the case (% p.318) is also essential to
exclude abnormalities that may have been missed during the procedure.
Imaging the lesion
• For accurate quantification of obstructive coronary lesions, the area of
interest must be adequately imaged during coronary angiography.
• The lesion should be imaged in at least two different projections,
preferably at 90° (orthogonal views), especially for eccentric stenoses.
• Selected projections should avoid foreshortening and demonstrate the
lesion, free from overlap with other vessels, side branches, or other
obscuring structures.
Limitations of coronary angiography

• Inter-and intra-observer variability in interpretation.
• May underestimate disease severity—by up to 50% in extreme cases;
this may be due to incomplete views and/or lesion eccentricity.
• Angiographic appearance (‘luminology’) may not correlate with the
physiological effect of the stenosis.
• Interpretation of severity requires comparison with a ‘normal’ segment;
atherosclerosis is a diffuse process (making the vessel appear smaller
than it is), and vascular remodelling may occur (making the vessel appear
larger than it is).
• Limited spatial resolution (ability to discriminate small adjacent objects)
of approximately 0.2 mm only.
Quantifying lesion severity
• Most operators quantify lesion severity visually, as the % reduction in
luminal diameter observed (with reference to adjacent segments of
normal vessel).
• Given the dynamic nature of angiographic images, it is of no surprise
that this may be relatively inaccurate: assessment of mild and severe
lesions is most accurate, with inter-observer variability of around ±20%
in lesions of moderate severity.
• Haemodynamically important lesions are generally accepted to be those
with luminal diameter stenosis greater than 70%, correlating to area
stenosis of approximately 90%, in epicardial vessels, or luminal stenosis
greater than 50% in LMS lesions (Fig. 6.18).
• Given inherent inaccuracies in accurate visual estimation of diameter
stenosis, operators may choose to grade lesions as simply mild (≤30%),
moderate (30–70%), or severe (>70%).
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
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.
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 159
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.
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.
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.
Single coronary artery
• Very rare (<0.1%); different forms of this anomaly exist:
• L-I: LCA supplies the whole heart; effectively no RCA.
• L-II: RCA arises from LCA.
• R-I: RCA supplies the whole heart.
• R-II: LCA arises from RCA.
• R-III: separate LAD, Cx origins from RCA.
Fistulae
• Usually occur between a coronary artery and a pulmonary artery or,
less commonly, a cardiac chamber.
• Shunt size is rarely sufficient to be haemodynamically important.
Myocardial bridging
• Myocardial bridging occurs when a segment of a coronary vessel passes
intramyocardially for a short distance. This is commonest in the mid-
LAD and may result in functional compression of the coronary lumen
during ventricular systole.
• There is no good evidence that such bridging results in downstream
myocardial ischaemia, and correct treatment involves administration
of agents to reduce left ventricular hypertrophy and aid myocardial
relaxation (e.g. beta blockers, calcium channel blockers).
165
Chapter 7
Coronary artery bypass

graft angiography
Types of operation 166
Procedure 168
Saphenous vein grafts 170
Competitive filling 176
Collateral filling 177
Arterial grafts 178
166 Chapter 7 Coronary artery bypass graft angiography
Types of operation
Most patients undergoing CABG in the last decade will have had a combin-
ation of arterial grafts and saphenous vein grafts (SVGs) or received total
arterial revascularization. This is because conduit patency for mammary ar-
terial grafts has been shown to be substantially higher than that of vein
grafts. Within 3 months of CABG surgery, 8% of grafts will have obstructed;
at 5 years, up to 20% of SVGs will have obstructed; and at 10 years, only
half remain patent. Over 90% of left internal mammary artery (LIMA) to
LAD anastomoses, however, are patent 10–20 years postoperatively and
significant stenoses are uncommon. Patency rates are shown in Table 7.1.
One of the commonest operations currently performed for patients with
three-vessel coronary disease is to graft the LIMA to the LAD and SVGs to
the left Cx and RCA (Fig. 7.1). Bilateral internal mammary arteries are often
used in total arterial revascularization. The right internal mammary artery
(RIMA) is then usually grafted to the RCA. Radial artery grafts (% p.180)
have variable patency rates, particularly when the stenosis being bypassed
is less than 70%.
Aortography
See % p.104.
This may be performed before attempts at graft localization. It is
helpful in cases when it is unclear which grafts have been surgically per-
formed, if a graft is occluded, and to locate graft origin. Aortography is
usually performed in an LAO projection (Fig. 7.2). Once acquired, care-
fully loop through the images and freeze the frame on the clearest image.
This can then act as a road map for graft cannulation, providing that the
same angiographic projection is used. Sternal sutures and ribs spaces act
as X-ray markers.
Table 7.1 Patency rates
Conduit 1-year patency Late patency rate

Long saphenous vein 80–90% 60% at 10 years
Left internal mammary 98% 90% at 10 years
artery
Right internal mammary 96% to LAD 75% to Cx/ 90% at 5 years
artery RCA
Radial artery Highly dependent on target
vessel
Types of operation 167
Fig. 7.1 Two-vessel coronary artery bypass with saphenous vein graft (SVG) to the
RCA and left internal mammary artery (LIMA) graft to the LAD
Fig. 7.2 Aortography showing the vein graft to the LAD

Procedure
Prior to angiography it is important to check the previous coronary angio-
gram report (and view the films if possible) and examine the surgical op-
eration records to identify the type of grafts used and the location of the
proximal and distal anastomoses. Check the patient’s history to ensure that
invasive assessment is justified.
Bypass graft angiography is usually performed after a thorough evaluation
of native coronary anatomy. It is important to carefully examine all three
main coronary territories for collateral formation (% p.177) and for com-
petitive filling (% p.176) from grafts. This information gives clues about graft
patency.
Examine the left coronary artery (% p.134) and then the right coronary
artery (% p.135). This will usually leave you with a JR4 catheter in situ to
start looking for grafts.
Choice of catheters
The JR4 is the catheter that is usually used to look for SVGs and occasionally
for the LIMA. Often a complete study (including native coronaries) can be
performed using just the JL4 and JR4. Vein grafts to the RCA occasionally
come off at an acute angle, in which case a multipurpose catheter (MPA1
or MPA2) can be useful (% p.84). The left coronary bypass (LCB) and
right coronary bypass (RCB) catheters (% p.84) can help graft localization.
Occasionally, an Amplatz left (AL) catheter (% p.83) is required, particularly
for left-sided vein grafts.
Location of grafts
Most SVGs have their proximal anastomosis on the anterior wall of the
ascending aorta just above the aortic sinuses (% p.169). The exact location
varies according to individual surgeon but grafts to the left Cx are usually
most superior with grafts to the RCA most inferior (Fig. 7.3). Occasionally,
you may come across a patient in whom the surgeon has left markers to
indicate the ostium of the graft. This practice has been largely abandoned
now. Surgical clips may also give clues.
• Catheter manipulation should be slow and purposeful.
• Engagement of the ostium is usually indicated by resistance to passage
or by a slight jump of the catheter tip.
• Check the pressure waveform to ensure that it is not damped
(% p.134). Slow withdrawal and rotation of the catheter may be
required if it is.
• A slow injection of contrast will indicate the correct catheter position.
• Occluded grafts will be identified as a small indention of the graft
‘stump’ (% p.169) on the aortic wall. Record an image to demonstrate
you have identified it (Fig. 7.4).
• There is an increased risk of inducing VF (% p.288) with vein graft
cannulation. Be careful.
Procedure 169
Fig. 7.3 Typical location for saphenous vein grafts (SVG) to the left coronary
artery (LCA), right coronary artery (RCA), circumflex vessel (Cx), and left anterior
descending coronary artery (LAD)
Fig. 7.4 A ‘stump’ representing right coronary vein graft occlusion

Saphenous vein grafts
Left anterior descending coronary artery grafts
• Grafts to the left coronary system are usually visualized and cannulated
in an LAO projection, although the RAO view may also be useful to
determine whether the catheter is directed anteriorly.
• Grafts to the LAD and diagonal usually originate just above the ostium
of the left coronary artery.
• Gently rotate the catheter clockwise to engage the graft.
• At least two views should be acquired of each vein graft.
• Ensure that the entire length of the graft, ostium, and insertion are
imaged.
• The radiographer should also pan across to enable visualization of the
distal ongoing vessel and assess any collateralization.
• Images can be acquired in the LAO and RAO projection (to view the
ostium and body) and LAO cranial and lateral projection (to view the
distal anastomosis and native LAD coronary artery; Fig. 7.5).
Fig. 7.5 Left lateral (left) and RAO (right) selective angiogram revealing narrowing
of the left anterior descending (LAD) coronary artery after the insertion of a large
saphenous vein graft (SVG)
Circumflex coronary artery grafts

• SVGs to the left Cx coronary artery are usually the most cranially
located grafts.
• They can be visualized and cannulated in an LAO or RAO projection.
• Pull the catheter tip back above the level of the other grafts and gently
rotate clockwise to find the ostium.
• In the RAO view, the catheter tip should point away from the spine.
• Images can be acquired in the LAO and RAO projection (to view
the ostium and body) and RAO caudal projection (to view the distal
anastomosis and native Cx coronary artery; Fig. 7.6).
Fig. 7.6 Selective saphenous vein graft (SVG) to the circumflex coronary artery
(Cx) in the RAO (left) and RAO caudal (right) projections. There is a stenosis at the
origin of the vein graft
Right coronary artery grafts

• Grafts to the RCA are usually cannulated in an LAO projection.
• The ostium of the graft usually lies just above and anterior to the
native RCA.
• To selectively cannulate the graft, withdrawing slightly from the RCA
ostium is often all that is required.
• Gentle clockwise rotation just above the RCA may also facilitate
cannulation if simple withdrawal is not successful.
• Some RCA vein grafts leave the aorta at an acute angle that is not
suitable for a JR4 catheter. Changing to a catheter with a steeper distal
tip makes engagement easier.
• Imaging is usually acquired in an LAO and RAO projection (to view the
graft) and in LAO cranial (to view the distal anastomosis; Fig. 7.7).
Fig. 7.7 Selective saphenous vein graft (SVG) angiography in the LAO (left) and
RAO (right) projections. The occluded right coronary artery (RCA) can be seen to
backfill
Long-term patency
• Vein grafts remain the most commonly used surgical conduits due to
their high availability, suitable length, and as they are not influenced by
vasospasm.
• Short-term patency rates for SVGs are high, with around 98% of grafts
patent immediately after surgery. At 1 month, patency rates drop to
less than 88% due to acute graft thrombosis, which may or may not be
clinically relevant.
• Long-term patency rates though are poor, with only 50–60% of SVGs
patent after 10 years.
• Causes of SVG failure include excessive intimal hyperplasia,
development of atherosclerosis within the graft, and graft thrombosis
due to plaque rupture.
• Aneurysmal dilatation of SVGs may also occur after time (usually
>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.

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).
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 competi-
tive 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 177
Collateral filling
Each of the three main coronary territories has the ability to develop col-
lateral 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
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, ei-
ther 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 179
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.
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 occa-
sionally 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 181
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
183
Chapter 8
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
184 Chapter 8 Percutaneous coronary intervention
History
The first percutaneous transluminal coronary angioplasty (PTCA) in a con-
scious 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 by-
pass 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 bal-
loon 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 ad-
junctive therapeutic and imaging techniques, many of which will be dis-
cussed 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 scaf-
fold 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 185
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
Indications for PCI
PCI is generally indicated for the relief of symptoms of angina; at the pre-
sent 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 187
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 pro-
vide further anatomical or functional information (e.g. intravascular ultra-
sound (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 189
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.
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 <60% respectively). Multivariate
predictors of procedural failure include chronic total occlusion (CTO),
unprotected bifurcation lesions, long lesions, and obvious thrombus
present.
• The risk of major adverse cardiovascular events remains generally
low: less than 1% in type A, 2–5% in type B, and 5–7% in type C lesions.
The SCAI classification
• This classification published in 2000 by the Society for Cardiovascular
Angiography and Interventions (SCAI), provides a more simplified
version of the ACC/AHA classification and is a more reliable correlate
of procedural outcomes and complications.
• The SCAI classification divides lesions by ACC/AHA type C criteria and
target vessel patency (Table 8.3).
• Current data suggest procedural success varies between 98.3% for
SCAI type I lesions to 80.2% for type IV lesions; complications occur in
approximately 2.3% of type I and over 10% of type IV lesions.
Lesion classification 191
Table 8.2 The ACC/AHA lesion classification system
Type A Type B Type C

Discrete (<10 mm Tubular (10–20 mm Diffuse (>20 mm length)
length) length)
Concentric Eccentric Excessive tortuosity
Readily accessible Moderate tortuosity Extremely angulated
segment (>90°)
Non-angulated segment Moderately angulated Occlusion >3 months old
segment (45–90°)
Smooth contour Irregular contour Bifurcation with
unprotected side branch
Light or no calcification Moderate or heavy Degenerate saphenous
calcification vein graft
No side branches Occlusion <3 months old Heavy thrombus burden
adjacent
No thrombus present Ostial location
Bifurcation with protected
side branch
Some thrombus present
Source: data from Ryan T et al. Guideline for percutaneous transluminal coronary angioplasty.
Circulation 1988; 78(2): 486–502.
Table 8.3 SCAI lesion classification system
Type I Type II Type III Type IV

Meets ACC/AHA type No Yes No Yes
C criteria
Target vessel patency Patent Patent Occluded Occluded
Further reading
Krone RJ, Shaw RE, Klein LW, et al. Evaluation of the American College of Cardiology/American
Heart Association and the Society for Coronary Angiography and Interventions Lesion
Classification System in the current “stent era” of coronary interventions (from the ACC-National
Cardiovascular Data Registry). Am J Cardiol 2003; 92: 389–94.
Guiding catheters
Although similar in many respects to diagnostic coronary angiography
catheters (% p.82), guiding catheters for PCI are different in function and
design:
• Diagnostic catheters are designed to allow injection of contrast to image
vessels.
• Guiding catheters need to support passage of relatively stiff and
bulky devices such as balloon and stent catheters beyond high-grade
obstructive lesions in vessels that may be tortuous, angulated, and rigid
due to calcification.
Technological improvements
Early catheters were of large calibre (10 F or 11 F) and handled poorly in
terms of torque and retention of shape; these problems led to the develop-
ment of multilayer bonded guiding catheters, consisting of:
• Outer polyurethane coat to maintain catheter shape.
• Middle woven mesh layer for stiffness.
• Inner Teflon® layer to reduce friction.
• Atraumatic soft catheter tip to prevent iatrogenic coronary dissection.
• Reduction in wall thickness means that 6 F guides may have an internal
diameter up to 0.71 mm, which may accommodate two balloon or stent
catheters simultaneously.
• Routine use of ever-decreasing catheter calibre (routine use of 6 F
guides is commonplace and 5 F, especially via the radial route, not
uncommon) has resulted in improved handling characteristics and
reduction in access site complications.
• A wide range of diagnostic catheter shapes are available as guiding
catheters (% p.82), and several shapes dedicated to PCI have been
designed to deliver improved support, including extra-support shapes to
deliver further guiding catheter stability (EBU/XB shapes) (Fig. 8.3).
Fig. 8.3 Schematic of left coronary extra-support catheter. This guiding catheter shape
delivers extra support by buttressing against the contralateral aortic wall. Examples of
this type of catheter include the EBU, XB (extra back-up), and Voda left shapes
Guiding catheters 193
Guiding catheter selection
Selection of an appropriate guiding catheter is paramount; poor catheter
support can make even the simplest PCI difficult, and conversely, good
backup may make complex procedures straightforward. Guiding catheters
should be selected on the basis of the degree of support, which is in turn
dependent on correct shape and appropriate calibre.
Guiding catheter support
• Guiding catheter support or back-up refers to the ability of the
positioned guiding catheter to maintain its position while antegrade
force is applied in order to position guide wires and balloon/stent
catheters within coronary arteries.
• When coronary anatomy is particularly tortuous and/or calcified,
increased amounts of support are required, as forward movement
of devices exerts a friction-based retrograde force which will tend to
disengage the guiding catheter from the coronary ostium; this makes
visualization of anatomy impossible and may lead to retrograde
expulsion of all PCI equipment from the target vessel.
Catheter shape
• Similar catheter shapes are utilized for PCI as are used in diagnostic
angiography. However, where increased support is required, some
catheter shapes offer distinct advantages, usually via buttressing against
the contralateral wall of the ascending aorta (Fig. 8.3).
• Operators will develop personal preferences for particular guide shapes,
but Table 8.4 outlines typically used guides for PCI in native coronary
arteries and their relative degrees of support.
Catheter calibre/size
• In general, larger calibre catheters (8 F >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.
Angioplasty guide wires
Following positioning of the guiding catheter, a guide wire must be posi-
tioned distally in the coronary bed to allow tracking of balloon/stent cath-
eters 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 sup-
port 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 dif-
ferent 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 195
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 sup-
port at the lesion when attempting to cross with balloon/stent catheters.
Distal positioning also reduces the chance of the wire becoming dis-
placed 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)
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 com-
ponent of the device (the balloon itself ) to the target lesion, using the angio-
plasty 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 ex-
change’ 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 197
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 pres-
sure 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 per-
forate 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
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 199
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.
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 201
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
Drug-eluting stents
History
With virtual elimination of immediate elastic recoil and late negative remod-
elling 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 203
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 <10%) and reduce MACE,
albeit in highly selected trial populations. That said, similar although
not as striking reductions in MACE and TLR have been demonstrated
for more complex lesions in ‘real-world’ patients in both large
registries and smaller randomized studies.
• While clinical endpoints in studies comparing SESs and PESs are
hitherto no different, there are differences in rates of restenosis
assessed by angiography and/or IVUS.
• One of the key surrogate measures used to assess DES efficacy is late
lumen loss (LLL), the distance in mm that a vessel renarrows between
the postprocedural and follow-up angiograms. In studies where DESs
were compared with BMSs, LLL predicted both angiographic and
clinical restenosis with consequent events. Whether the apparent
superiority in LLL of SESs over PESs demonstrated in randomized
studies will translate into any clinical differences remains to be seen.
Further reading
Morice M-C, Serruys PW, Sousa JE, et al. A randomized comparison of a sirolimus-eluting stent with
a standard stent for coronary revascularization. N Engl J Med 2002; 346: 1173–80.
Park JS, Shim WH, Ho DS, et al. A paclitaxel-eluting stent for the prevention of coronary restenosis.
N Engl J Med 2003; 348: 1537–45.
Bioresorbable scaffolds
The main limitations of metallic stents are all related to the permanent pres-
ence of a foreign body within the coronary artery wall, and they are typic-
ally the following:
• Vessel stiffness and loss of compliance.
• Vessel straightening.
• Vessel inflammation.
• Disruption of vasoregulation.
• Disruption of vessel remodelling.
By offering temporary vessel scaffolding (to prevent post-angioplasty re-
coil and restenosis) just for the time necessary and then disappearing,
bioresorbable scaffolds (BRSs) could overcome the limitations of metallic
stents and potentially offering a wide range of benefits, which include:
• Minimizing risk of stent failure.
• Keeping open future alternative revascularization options.
• Allowing future coronary investigations with computed tomography
(metallic stents are source of artefacts).
Polymer-based BRS: the Absorb® experience
The Absorb® BVS 1.0 (Abbott Vascular, Santa Clara, CA, USA) was the first
BRS to be largely tested and investigated in humans after nearly 30 years of
uncertain results from research on BRS technology. The Absorb® BVS 1.0
consisted of a platform of poly-l-lactic acid (PLLA) polymer, covered by a
poly-d,l-lactic acid (PDLLA) polymer. Everolimus was the antiproliferative
drug. The strut thickness was 150 μm and the crossing profile was 1.2 mm.
The reabsorption process is supposed to happen over a time interval of
36 months. The reabsorption phenomenon is associated with loss in mass
and radial support of the scaffold.
Magnesium-based BRS: the Magmaris® experience
These scaffolds are still made of metal thus offering higher mechanical
resistance. The magnesium is, however, resorbable at a lower rate com-
pared to polymers. Also, in this case the reabsorption process is based on
hydrolysis.
The Magmaris® (Biotronik) is currently the main magnesium-based BRS.
It has a strut thickness of 150 μm and is covered by PLLA polymer to an-
chor the antiproliferative drug (sirolimus).
Present and future of BRS
At present, although a number of devices have received approval both in
Europe and the USA, in the light of the randomized data, the 2018 European
guidelines on myocardial revascularization do not recommend BRS for clin-
ical care outside clinical studies.
Ongoing research is trying to address the current main limitations of first-
generation BRS (mechanical integrity, low tensile strength, late structural
discontinuity during reabsorption, high struts thickness).
Bioresorbable scaffolds 205
Alongside this, a careful and meticulous deployment technique, based

on intravascular imaging and on the PSP (pre-dilate–sizing–post-dilate) ap-
proach, is advocated as essential for positive results from BRS adoption.
Further reading
Katagir Y, Stone GW, Onuma Y, et al. State of the art: the inception, advent and future of fully
bioresorbable scaffolds. EuroIntervention 2017; 13: 734–750.
Neumann FJ, Sousa- Uva M, Ahlsson A, et al. 2018 ESC/ EACTS Guidelines on myocardial
revascularization. Eur Heart J 2019; 40: 87–165.
Stent thrombosis
The sword of Damocles for PCI with DESs?
Definition
• Formation of thrombus within a deployed coronary stent (Fig. 8.12).
Pathophysiology
• No clear evidence as to a single specific pathophysiology: many factors
may be important.
• Recent concern has arisen over stent thrombosis occurring very late
after DES implantation, sometimes despite ongoing/prolonged dual
antiplatelet therapy (% p.218).
• One potential explanation for this is the prevention of restenosis by
DES and therefore also of re-endothelialization which may protect
stents against adherent thrombus.
• Ongoing large-scale DES studies with prolonged follow-up may give
further information.
Factors predisposing to stent thrombosis
• Premature discontinuation of dual antiplatelet therapy, or clopidogrel
alone (especially for DESs).
• Stent malapposition or undersizing.
• DESs in complex lesions including bifurcations (% p.206).
• PCI in acute MI (% p.208).
• Renal dysfunction.
Epidemiology of stent thrombosis
• Stent thrombosis is uncommon but potentially catastrophic.
• Stent thrombosis is not a problem unique to DESs, and also occurs
in BMSs.
• Frequency of stent thrombosis has been difficult to assess, due to
inconsistent definitions and limited follow-up in randomized stent trials.
• The Academic Research Council decided on new universal definitions
for stent thrombosis following a meeting in Dublin in 2006 (Table 8.5).
• Recent data suggest incidence in BMSs is less than 1% up to 4 years after
stent implantation, and approximately 1.2–1.3% for DESs over the same
time period, when used in non-complex (‘on-label’) lesions.
Prevention of stent thrombosis
• Strict attention to PCI technique, including correct stent sizing and
optimal expansion at deployment is important; use of IVUS (% p.210) to
prevent stent malapposition may be beneficial.
• Adherence to dual antiplatelet therapy is crucial.
• There is no evidence that patients undergoing elective or emergency
surgery requiring discontinuation of antiplatelet therapy receive any
protection from heparin or low-molecular-weight heparin.
Stent thrombosis 207
Fig. 8.12 Stent thrombosis. This patient presented with an anterior STEMI 7 months
after undergoing PCI with drug-eluting stent implantation to the proximal LAD. He
had continued dual antiplatelet therapy. Thrombus is seen within the stented segment
of the LAD in the LAO 50° cranial 30° (left) and lateral (right) projections
Table 8.5 Academic Research Consortium or ‘Dublin’ definitions of stent

thrombosis (2006)
Definition
Definite/confirmed Acute coronary syndrome
And
Either angiographic confirmation of thrombus/occlusion
Or pathological confirmation of acute thrombosis
Probable Unexplained death within 30 days
Or
Target vessel MI
(even without angiographic confirmation of thrombosis
or other identified culprit lesion)
Possible Unexplained death after 30 days
Timing
Early Within 30 days
Late 30 days to 1 year
Very late After 1 year
Further reading
Mauri L, Hsieh WH, Massaro JM, et al. Stent thrombosis in randomized clinical trials of drug-eluting
stents. N Engl J Med 2007; 356: 1020–29.
Stone GW, Moses JW, Ellis SG, et al. Safety and efficacy of sirolimus-and paclitaxel-eluting stents. N
Engl J Med 2007; 356: 998–1008.
The PCI procedure
Patient selection and preparation
• Most problems during PCI procedures can be averted by careful patient
selection and appropriate preparation for the procedure.
• Preparation for the procedure should include careful review of specific
patient factors (e.g. diabetes mellitus, renal dysfunction, presence of
peripheral vascular disease) and of angiographic features/need for
particular equipment and pharmacological treatment/pre-treatment.
• Remember the five P’s of the SAS (Special Air Service): Preparation
Prevents Piss-Poor Performance (!).
Consent
• All patients undergoing PCI should be fully appraised of the estimated
chances of procedural success, and of the patient-specific risks.
• Patients should be consented using operator-or centre-specific risks of
complications (% p.278); approximate risks are as follows:
• Vascular complications (haematoma, false aneurysm) 3–5%.
• Stroke 0.1%.
• MI (Q wave and non-Q wave) 0.5–1.0%.
• Emergency CABG 0.2%.
• Death 0.5–0.8%.
• Risks of contrast reaction and renal failure are patient dependent.
• Assessment of risk should be on an individual patient basis, and although
several risk scoring systems exist, no single one has achieved widespread
acceptance.
Getting to the lesion
• Following arterial access (% p.46), an appropriate guiding catheter
should be chosen (% p.192) and passed into the ascending aorta.
• Trainees in PCI will quickly realize that guiding catheters do not always
behave in an identical fashion to their diagnostic counterparts, principally
due to thinner walls and thus different handling characteristics.
• A stable coaxial position is particularly important for PCI.
Lesion preparation
• For the majority of lesions, no preparation is required other than
balloon pre-dilation, although some operators will skip even this,
preferring to deploy a stent immediately (‘direct’ or ‘primary’ stenting).
• Lesion preparation aims to ensure that the stent catheter reaches the
target lesion with ease and without causing complications, and that
when the stent balloon is deployed, vessel compliance is such that full
expansion may be achieved. Preparation is particularly important for
calcified and thrombus-bearing lesions.
• Depending on lesion appearance and characteristics, adjunctive
techniques may be required, including rotational atherectomy (% p.248),
cutting balloon angioplasty (% p.197), use of distal protection (% p.244)
or thrombectomy devices, or additional information gleaned from IVUS
(% p.210) or pressure wire interrogation (% p.212).
The PCI procedure 209
Stent deployment
• Correct stent positioning is key: radio-opaque markers indicate the ends
of the stent on the balloon catheter.
• The stent should be deployed at a pressure not less than its nominal
deployment pressure, and preferably at a pressure sufficient to fully
expand the whole body of the device. It is customary to acquire a short
imaging run with the stent catheter fully expanded to demonstrate this
(Fig. 8.13).
• If the stent is not fully deployed, post-dilation may be required with a
semi-or non-compliant balloon (% p.196). NB: high pressure inflations
with the stent balloon are not always desirable, as the balloon ends
may overhang the stent itself and cause trauma to adjacent, normal,
segments of the target vessel.
Final result
• The final angiographic result should be assessed in at least two orthogonal
views, with the angioplasty guide wire removed from the coronary artery
to prevent anatomical distortion and artefactual appearances.
• Angiographic success is generally accepted as a final diameter stenosis of
less than 20% of the vessel lumen.
(a)
(b)
(c)
(d)
Fig. 8.13 Coronary stenting. Following lesion preparation (a), a stent catheter is

passed across the lesion and correctly positioned (b). The stent balloon is inflated,
deploying the stent (c) and reconstituting the vessel lumen as well as providing
scaffolding against recoil (d)
Intravascular ultrasound
How does it work?
• IVUS generates an anatomical picture of the lumen and vessel wall by
processing information from reflected ultrasound waves.
• High-frequency (40 MHz) ultrasound waves are produced from the
IVUS catheter by passing electricity through a piezo-electric crystal;
processed reflected ultrasound waves are transformed into an image.
• Imaging depends on a structure’s density (acoustic impedance):
• Low density (blood, vessel media) appears black.
• High density (vessel intima, adventitia) appears white/grey.
• Very high density (calcified tissue, stent struts) appears bright white,
sometimes with a black area (acoustic shadow) behind.
• Spatial resolution of IVUS: 80–100 μm axially/200–250 μm laterally.
Equipment and patient preparation
• The IVUS catheter has a short monorail segment and is passed into
the coronary artery over a guide wire, in a similar fashion to a balloon
catheter.
• Intracoronary GTN should be administered before and after imaging to
reduce vessel spasm.
• Imaging is performed by activating a mechanized automatic pullback
mechanism (rate 25 mm/second) and recorded onto a hard disk for
later review/retrieval.
• Computer-assisted measurements allow assessment of vessel and
lumen area, lesion length, and vessel calibre (reference diameter).
Indications
• Anatomical assessment of lesions of ambiguous severity: mean luminal
area less than 4 mm2 signifies likely ischaemia-producing stenosis in
native epicardial vessels (except LMS). See Fig. 8.14.
• Assessment of ambiguous anatomy: aneurysms, filling defects,
bifurcation lesions, heavily calcified vessels, hazy lesions.
• Accurate assessment of in-stent restenosis (Fig. 8.15).
• Measurement of vessel dimensions (true calibre, lesion length).
• Use in complex PCI (e.g. LMS, bifurcation lesions, in-stent restenosis).
Imaging artefacts
• Blood ‘speckle’: artefact from ultrasound reflected off slow-moving
blood in lumen. Flushing catheter may help.
• Guide wire artefact: acoustic shadow cast by metallic guide wire.
• Motion artefacts: include non-uniform rotation distortion (NURD)
due to transducer rotation, and axial catheter movement within the
coronary during the cardiac cycle.
Complications
• Vessel spasm (% p.152): occurs in less than 3% cases; usually
responsive to intracoronary GTN.
• Major complications: very uncommon (<0.3%)—include dissection,
thrombus formation in vessel, catheter entrapment by stent strut.
Intravascular ultrasound 211
Fig. 8.14 IVUS images: normal vessel (left) and vessel with atherosclerotic plaque
(right). Note eccentric intimal hyperplasia in diseased vessel
Fig. 8.15 IVUS-guided PCI for in-stent restenosis in the LAD: the angiogram

appears not to show severe luminal renarrowing. IVUS images before (left) and after
(right) further balloon angioplasty and repeat stenting. Note stent struts (indicated by
arrows); metal is high density and appears white due to high reflectivity
Utility in practice
• IVUS imaging provides additional information over angiography alone
and has been shown to improve outcomes when PCI is IVUS guided.
• Use may be limited by time, financial constraints, and operator training.
• Recommended use:
• Anatomical assessment of ambiguous anatomy.
• PCI for in-stent restenosis.
• PCI for LMS lesions.
Developments in anatomical imaging

Refinement of IVUS technology has led to ‘virtual histology’, where dif-
ferent tissue densities are assigned colours to aid interpretation.
Optical coherence tomography uses near infra-red instead of ultra-
sound; this improves spatial resolution, but requires a blood-free envir-
onment (i.e. saline-filled vessel) to adequately image the vessel.
Elastography and palpography rely on vessel elasticity and mechan-
ical properties detected by sound and touch respectively.
Pressure wire
The rationale behind pressure wire
The application of pressure wire assessment in interventional cardiology
has deeply changed the clinical definition of ‘significant coronary stenosis’
and revolutionized the indication for percutaneous revascularization over
the last decade.
The main application of pressure wire-derived indices is for the definition
of the ischaemic burden associated with angiographically intermediate cor-
onary stenosis.
In ideal conditions, the ischaemic potential of a lesion should be defined
by the reduction of flow caused by the stenosis itself. Directly measuring
coronary flow is difficult and logistically complex in the CathLab. For this
reason, intracoronary pressure assessment has been proposed as a sur-
rogate measure of intracoronary flow. This assumption (pressure ~ flow)
is possible only when coronary microvascular resistances are low/trivial.
Two main indices can be measured (and have been largely validated in
clinical trials) with current generation of pressure wire:
• Fractional flow reserve (FFR).
• Instantaneous wave-free ratio (iFR).
Both the two indices express the ratio between distal coronary pressure
detected by the pressure wire (Pd) and the aortic pressure detected by
the guiding catheter (Pa). The main difference is how, in measuring in each
index, the condition of absence of significant coronary microvascular resist-
ance is achieved:
FFR adopts maximal vasodilation (thus minimal resistance) achieved by
infusion (intracoronary or IV) of a vasodilator (usually adenosine). For such
reason, FFR is known as a hyperaemic index. FFR is the maximum coronary
blood flow in the presence of a stenotic lesion expressed as a proportion
of the maximum blood flow in the absence of any obstructive lesion. The
FFR gives information about the physiological importance of a stenosis, re-
moving observer bias and angiographic uncertainty.
iFR adopts wave intensity analysis (analysis of energies developed by
aorta and microvasculature during cardiac cycle) to identify a free-wave
phase of the cardiac cycle where resistance is null. This free-wave window
happens in diastole. Because there is no need to induce hyperaemia, iFR is
an example of a resting index.
Other resting and hyperaemic indices are coming on the scene (resting
Pd/Pa, contrast FFR, coronary flow reserve, resting full-cycle ratio, etc.) but
at the current stage only FFR and iFR have been largely tested and validated
for routine application in clinical practice.
Indications
• Physiological assessment of intermediate/ambiguous lesions; a derived
FFR of less than 0.75 indicates the lesion is flow-limiting (Fig. 8.16).
• Assessment of the relative contribution of serial stenoses in a single
vessel.
• Assessment of the relative lesion importance in multivessel disease.
Pressure wire 213
Fig. 8.16 Assessment of diffusely diseased intermediate vessel. Angiogram and

pressure wire pullback along diseased vessel. Arrows indicate pressure changes at
specific points. FFR shown at right of screen (0.63). Images courtesy of RADI Medical
Systems
Complications
• Adenosine may cause flushing/chest constriction and is contraindicated
in patients with asthma or those taking dipyridamole.
• The wire itself may rarely cause coronary dissection (% p.300).
Caution
Avoid FFR in STEMI (culprit vessel). Limited validation in:
• CTO (collateral donor artery).
• Aortic stenosis.
• Hypertrophic cardiomyopathy.
• Diabetes.
• Chronic kidney failure.
FFR or IFR?
Notably, FFR is an older index compared to iFR, meaning the amount
of evidence in favour of FFR application is much larger than for iFR.
However, recently, the DEFINE-FLAIR and iFR-SWEADHEART random-
ized trials have showed the non-inferiority of iFR in comparison to FFR.
Being a resting index, iFR could offer the following benefits compared
to FFR:
• Less time-consuming.
• Cheaper (adenosine free).
• Better tolerated by patient (adenosine can induce chest pain,
bronchospasm, bradycardia, and AV block).
Equipment for pressure wire study

• The pressure wire consists of a 0.014-inch wire and at 3 cm from the
tip of the wire (at the connection between the radiolucent and the
radiopaque segments) there is a pressure sensor.
• The pressure wire console system needs to receive an aortic
pressure tracing source from the CathLab equipment. In case of iFR
measurement, an ECG source is also required.
• Before use, the pressure wire needs to be appropriately flushed (to

eliminate any air) and zeroed.
• The pressure wire is then advanced towards the tip of the guiding
catheter. At this stage, the pressure wire console system will display
two waveforms, one from the guiding catheter (Pa) and one from the
pressure wire (Pd).
• Before proceeding, the two pressure waveforms must be equalized, in
order to be overimposed, assuring that the FFR/iFR value at the guiding
catheter is 1.0 (Pd = Pa l Pd/Pa = 1).
• After equalization the operator can advance the pressure wire, ensuring
that the pressure sensor is beyond the stenosis under investigation.
FFR measurement
• Vasodilator (adenosine) infusion is started. Venous infusion offers a
more stable hyperaemia compared to intracoronary adenosine, but it
requires 60–90 seconds before hyperaemia status is reached and can be
associated with a slightly higher rate of side effects.
• During adenosine infusion the Pd/Pa ratio will start to drop to a
minimum and steady value which corresponds to FFR (hyperaemic Pd/
Pa).
• The FFR is derived as the ratio of distal to proximal pressure during
maximal hyperaemia induced by adenosine (IV infusion or intracoronary
bolus).
• For vessels with multiple lesions, the wire may be withdrawn slowly
along the coronary and the importance of each assessed individually.
• It is good practice to retrieve the wire back into the guiding catheter to
check for pressure drifts (identified by Pd/Pa at the guiding catheter ≠
1) or assessment of jump in FFR in case of tandem lesions.
• At this point, adenosine can be stopped.
iFR measurement
• Once the pressure wire is in place, it is important to check for
satisfactory pressure and ECG tracings.
• Without need of vasodilator infusion, the console will identify the free
wave period of diastole (using an ECG signal) and will produce an
iFR value.
• Also, for iFR it is good practice to retrieve the wire back into the guiding
catheter to check for pressure drifts or assessment of jump in iFR in
case of tandem lesions.
FFR and iFR interpretation

FFR and iFR measurements may guide both PCI and deferral of PCI; de-
ferral of PCI when FFR is not reduced results in favourable outcomes.
• FFR ≤0.80 indication for revascularization.
• FFR >0.80 defer revascularization.
• iFR ≤0.89 indication for revascularization.
• iFR >0.89 defer revascularization.
Pressure wire 215
Optical coherence tomography
IVUS and optical coherence tomography (OCT) are the two main tech-
niques 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 scat-
tering of light produced by human tissues. This obstacle in OCT is repre-
sented 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 ac-
quisition 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
IVUS OCT
Catheter size (F) 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? 217
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.
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.
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 (<60 kg), with a history of active bleeding or stroke/
transient ischaemic attack.
• The TRILOGY ACS trial has failed to show the superiority of prasugrel
in ACS patients treated medically.
• Because it is indicated in patients referred for PCI, ideally prasugrel
should be considered for patients with known coronary anatomy or not
suitable for cardiac surgery.
• Because of its safety profile, prasugrel finds relatively small application as
a first-line antiplatelet agent in combination with aspirin. Its adoption is
usually considered in patients with stent thrombosis or recurrent stent
thrombosis when secondary prevention with other antiplatelet agents
has failed.
• Dosage: loading dose 60 mg. Maintenance dose 10 mg once a day.
Ticagrelor
• Ticagrelor belongs to the class of antiplatelet agents acting on the
P2Y12 receptor for ADP. However, compared to thienopyridine, it does
not interfere with the binding of ADP to the receptor. Conversely, it
reversibly binds the receptor in a different site than ADP, and it acts by
hampering the receptor’s ADP-induced activation.
• It presents more favourable pharmacokinetics and pharmacodynamics
compared to clopidogrel, offering a more potent and rapid onset of
action with no inter-individual variability in response.
• The PLATO study has confirmed the superiority of ticagrelor (combined
to aspirin) compared to clopidogrel in ACS patients in terms of
reduction of ischaemic events, without a significant increase of bleeding
events. Notably this translated into a mortality benefit in favour of
ticagrelor over clopidogrel.
• Possible side effects include (non-severe) dyspnoea in up to 15% of
patients within the first week of treatment, and bradycardia. It has
been hypothesized that dyspnoea is due to increased concentration of
adenosine in the circulation secondary to ticagrelor-mediated reduced
clearance of adenosine.
• Dosage: loading dose, 180 mg; maintenance dose, 90 mg twice a day.
New challenges with antiplatelet therapy
Over the last two decades, there has been a paradigm shift in the way
antiplatelet therapy is conceived. The introduction of new, safer, and more
potent antiplatelet agents (ticagrelor and prasugrel) combined with new-
generation DESs (with higher safety profile and lower rate of stent throm-
bosis) has led to different kinds of challenges:
• Balancing the risk of ischaemic events and bleeding complications.
• Switching from one antiplatelet agent to the other (Table 8.7).
• Best duration for double antiplatelet therapy.
• Best antiplatelet regimen in patients requiring oral anticoagulation
(e.g. AF).
• Interruption of antiplatelet therapy in patients going for surgery.
Table 8.7 Switching from one antiplatelet agent to another
Stable coronary disease Acute coronary syndrome

To C To T To P To C To T To P
From C 90 mg T 10 mg P Reload Reload 60
24 h after 24 h after 180 mg T mg P
last C last C
From T Reload Reload Reload Reload 60
600 mg C 60 mg P 600 mg C mg P 24 h
24 h after 24 h after 24 h after after last T
last T last T last T
From P 75 mg C 90 mg T Reload Reload
24 h after 24 h after 600 mg C 180 mg T
last P last P 24 h after 24 h after
last P last P
C, clopidogrel; P, prasugrel; T, ticagrelor.
Duration of dual antiplatelet therapy and

medical management
See Table 8.8 and Table 8.9.
Dual antiplatelet regimen in patients undergoing PCI
on oral anticoagulation
See Table 8.10.
Recent data suggest that oral anticoagulation with apixaban and
clopidogrel may be superior to additional use of aspirin in patients with
recent ACS or PCI.
Table 8.8 Duration of therapy
PCI with DES/BMS/DEB CABG

Stable CAD ACS Stable CAD ACS
Low High Low High No indication Low High
risk of risk of risk of risk of for DAPT risk of risk of
bleeding bleeding bleeding bleeding bleeding bleeding
A+C A+C A+T or A+C or A+T or A+C or
A+C or A+T A+C or A+T
A+P A+P
6 months 3 months 12 months 6 months 12 months 6 months
No
<1 month
A, aspirin; ACS, acute coronary syndrome; BMS, bare-metal stent; C, clopidogrel; CABG,
coronary artery bypass surgery; CAD, coronary artery disease; DAPT, dual antiplatelet therapy;
DEB, drug eluting balloon; DES, drug-eluting stent; P, prasugrel; PCI, percutaneous coronary
intervention; T, ticagrelor.
Table 8.9 Medical management
Stable CAD ACS

Low risk of High risk of Low risk of High risk of
bleeding bleeding bleeding bleeding
No indication for DAPT A+T or A+C or A+C
A+P
12 months >1 month
A, aspirin; ACS, acute coronary syndrome; C, clopidogrel; CAD, coronary artery disease;
DAPT, dual antiplatelet therapy; T, ticagrelor; P, prasugrel.
Table 8.10 Dual antiplatelet regimen
Ischaemic risk > Bleeding risk > ischaemic risk

bleeding 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 O O O
month
A, aspirin; C, clopidogrel; O, oral anticoagulation.
Table 8.11 Interruption of therapy for surgery
Stop ___ days before Restart on day___ after

surgery surgery
Prasugrel 7 1–4
SURGERY
Clopidogrel 5 1–4
Ticagrelor 3 1–4
Aspirin Do not stop —
(case-by-case decision)
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.
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
(<1 hour) half-life.
• Bleeding complications are common; management may require platelet
infusions (especially for abciximab).
• Studies with orally active GPIs have been disappointing.
Bivalirudin
• Recent data suggest bivalirudin has equivalent anticoagulant efficacy in
terms of ischaemic endpoint reduction when compared with heparin
and GPIs in both elective and acute PCI, with reduced bleeding
complications.
• Mode of action: direct thrombin inhibitor; preventing thrombus
stabilization and platelet activation.
• Dosage: weight-adjusted IV bolus and infusion for duration of
procedure.
• Bivalirudin is usually used as anticoagulant monotherapy but may be
combined with GPIs.
Specific techniques in complex PCI 225
Specific techniques in complex PCI

While the general approach to PCI is similar regardless of lesion type/
classification (% p.190), certain lesion subsets do pose particular problems
which will be discussed further in this section.
What makes PCI complex?
In general, PCI is complex when:
• Chance of success is reduced and/or a suboptimal result is likely.
• Risk of complication is high.
• Niche treatment modalities or specialized techniques are required.
• Prospects for long-term event-free survival are low.
Complexity of PCI may be influenced by lesion and patient factors:
Lesion characteristics
• Unusual or variant anatomy, including coronary anomalies (% p.160).
• ACC/AHA type C (% p.190) or SCAI type III/IV (% p.190) lesions.
• Vessel calcification.
• Presence of thrombus.
• Bifurcation lesions.
Patient characteristics
• Mode of presentation (acute vs elective).
• Unstable haemodynamic status/shock.
• LV impairment.
• Renal failure.
• Vascular access difficulty/peripheral vascular disease.
• Other significant co-morbidity.
PCI in acute myocardial infarction

Rationale
When a patient presents with acute MI, the immediate aim is to restore
antegrade flow in the infarct-related coronary artery (IRA) and hence re-
duce the amount of time that downstream myocardium remains ischaemic.
• Reduction of ischaemic time translates into less myocardial necrosis and
therefore less permanent cardiac damage and LV dysfunction.
• A patent IRA, regardless of mode of reperfusion, translates into a
halving of mortality risk.
Background
• The majority of MIs associated with STEMI on the ECG are caused by
occlusion of a coronary artery by thrombus following plaque rupture.
• Therapies designed to break up thrombus (thrombolytic/fibrinolytic
agents) have been shown to be highly effective in reducing MACE and
enhancing survival. However, such benefits are greatest in the early
stages of STEMI and decline rapidly with the passage of time.
• By 12 hours post MI, the potential bleeding-associated risks of
thrombolysis outweigh any positive gains.
• Early studies confirmed the utility of PCI to open the IRA, and
subsequent trials in the stent era have confirmed PCI as the default
strategy.
STEMI
Treatment of STEMI represents one of the main emergencies and more
prognostically impacting procedures performed in the CathLab. Even
though the incidence is decreasing in Western countries, STEMI is still
associated with a 10% 1-year mortality and an even larger burden of co-
morbidity mainly driven by development of heart failure over time.
Pre-hospital care
Prompt diagnosis of STEMI by the medical or paramedic team is paramount
to start reperfusion therapy as soon as possible in agreement with the
golden rule that ‘time is muscle’. In order to minimize delays, every area/
region should have in place a network of hub and spoke hospitals with an
integrated, efficient, and prioritized ambulance service.
Network requisites
• Shared protocols.
• Pre-hospital triage of the STEMI patient to an appropriate institution,
bypassing hospitals without a PCI service or bypassing the Emergency
Department when referring patients straight to the CathLab.
• If the diagnosis is unclear and the patient is referred to a non-PCI
centre, the ambulance should wait until the diagnosis of STEMI has been
confirmed or ruled out.
PCI in acute myocardial infarction 227
Diagnosis of STEMI is typically based on

• Symptoms: typical chest pain l shortness of breath, nausea, fatigue,
palpitation, syncope.
• ECG changes: ST elevation in two contiguous leads or new-onset left
bundle branch block.
Initial care should include
• O2 therapy if O2 saturation is less than 90%.
• Pain relief with opioids or benzodiazepine.
• Antiplatelet therapy (aspirin and clopidogrel/ticagrelor loading dose).
Reperfusion therapy
• Reperfusion therapy should be offered for all patients with chest pain
lasting less than 12 hours.
• Mechanical, catheter-based reperfusion by primary PCI (% p.228) is
considered the perfusion strategy of choice.
• An alternative strategy is to consider fibrinolysis, particularly if the delay
from STEMI diagnosis (not from first medical contact) to PCI is expected
to be longer than 120 minutes. Fibrinolysis should be administered
within 10 minutes from STEMI diagnosis.
• After fibrinolysis, the patient should then be referred to a PCI centre,
where salvage PCI (% p.230) should be provided if reperfusion criteria
post fibrinolysis are not met: that is, ST resolution less than 50% at
90 minutes after thrombolysis, electric/haemodynamic instability, and
persisting chest pain.
• Fibrinolysis may result in normalization of ECG changes but restoration
of flow in the IRA occurs in only approximately half of all patients.
• In patients who have received fibrinolytic agents, or other
anticoagulant/antiplatelet strategies designed to improve IRA flow, a
pharmaco-invasive strategy (% p.230) may be considered.
Primary PCI
Background
• Referral to the CathLab for primary PCI should be considered if the
time from STEMI diagnosis (not from first medical contact) to PCI is less
than 120 minutes.
• Primary PCI strategy should be considered for STEMI patients
with chest pain for longer than 12 hours, in case of ongoing pain,
haemodynamic/electric instability.
• No benefit in reperfusion therapy in stable STEMI patients with chest
pain onset of great than 48 hours (OAT trial).
• See Fig. 8.18.
Technical aspects of primary PCI
• Secondary (inter-hospital) transfers:
• Avoid if at all possible (time delays to reperfusion).
• Patients should be delivered direct to the PCI centre (and preferably
direct to the CathLab) to reduce delays further.
• Consent:
• May be problematic if the patient is moribund or has received opiate
analgesia.
• Appropriate action should be taken in the patient’s best interests
and/or consent obtained by proxy.
• Anticoagulant/antiplatelet therapy:
• Should be administered as per local protocol as early as is practical.
Fundamentals of primary PCI
• Radial access is the default vascular approach. The largest trials
(MATRIX, RIFLE, and RIVAL) have showed that primary PCI is the
setting where radial access can truly offer a prognostic benefit.
• New-generation DESs have shown a significant clinical benefit in STEMI
over BMSs (mainly in terms of repeated revascularization) and they are
the new standard (EXAMINATION, NORSTENT, and COMFORTABLE
AMI trials).
• Unfractionated heparin should be the standard anticoagulant intra-and
post-procedurally (MATRIX and HEAT-PPCI trials). Bivalirudin can be
considered as an alternative.
• Routine thrombus aspiration is not recommended (% p.252). Thrombus
aspiration should be reserved for STEMI patients with evidence of a
large thrombotic burden (TASTE and TOTAL trials).
Immediate stenting versus deferred stenting
The PAMI study has largely showed that stenting in the primary PCI set-
ting is not associated with a mortality benefit, but only with a lower rate
of reinfarction or need of urgent revascularization. However, a ‘deferring
stenting’ approach has been suggested over the years. The rationale behind
this is that stenting and post-dilation are procedural steps at high risk of
inducing distal embolization of atherothrombotic debris.
Primary PCI 229
Fig. 8.18 Primary PCI. Top left panel shows proximal occlusion of LAD; top right
panel shows appearances after balloon pre-dilation—note presence of intracoronary
thrombus indicated by arrows. Bottom panel shows final result after stent
deployment
The deferring stenting strategy would then consist of restoring flow in

the culprit vessel with pre-dilation and thrombus aspiration and proceeding
to stenting at a later stage (variable from hours to days later according to
studies). In this way, stenting would be performed when part or most of
the thrombotic material might have been dissolved by antiplatelet and anti-
coagulant therapies. Theoretical benefits of deferred stenting include:
• Reduced risk of distal embolization/no reflow.
• Improved stent sizing assessment (because of reduced thrombotic
burden) with lower risk of stent undersizing/malapposition.
• The DANAMI-DEFER trial has failed to show an improvement in
outcome in STEMI patients randomized to deferred stenting 48
hours post primary PCI. The study reported a higher rate of urgent
revascularization of the target vessel.
• In light of these results, current guidelines do not recommend a
deferring stenting strategy in STEMI patients.
Facilitated PCI versus a

pharmaco-invasive strategy
• The term ‘facilitated PCI’ refers to primary PCI with upfront
administration of fibrinolysis and/or GPIs, in order to allow early
reperfusion while transferring patients for PCI. This approach implies
that PCI is performed in every case as urgent/emergent irrespective of
fibrinolysis success or failure.
• This strategy was initially meant to buy some time and thus extend the
time-window for mechanical revascularization in patients expected to
have a relative delayed access to primary PCI.
• Two randomized trials (ASSENT-4 and FINESSE) have, however,
disproved the benefit of facilitated PCI. ASSENT-4 was actually
prematurely stopped because of the observed increased risk of adverse
events in the facilitated arm, including death, heart failure, intracranial
haemorrhages, and even ischaemic events.
• While the ‘facilitated PCI’ strategy has not showed benefit, the
‘pharmaco-invasive’ strategy is instead recommended by guidelines.
• This approach differs from ‘facilitated PCI’ since it implies that the
patient is transferred to a PCI centre after fibrinolysis, but a coronary
angiogram is performed as rescue (if fibrinolysis failed) or in a non-
urgent regimen.
• The recommended time-gap between successful fibrinolysis and
coronary angiogram is 2–24 hours.
• The ‘pharmaco-invasive’ strategy has been proved to be superior to
fibrinolysis alone in the CARESS-AMI and TRANSFER AMI studies and
non-inferior to primary PCI in patients presenting within 3 hours from
symptoms onset and with a time-delay to PCI of greater than 1 hour.
Cardiac arrest in STEMI

• Mechanical revascularization with primary PCI should be the strategy of
choice in STEMI patients surviving out-of-hospital cardiac arrest.
• Current guidelines recommend referral to the CathLab for emergent
coronary angiogram l primary PCI in all patients (also unresponsive
survivors) with evidence of:
• ST elevation post recovery of spontaneous circulation (ROSC).
• Chest pain before arrest.
• Previous history of coronary disease.
• It is reasonable to delay coronary angiography in patients without ST
elevation on the ECG who have survived cardiac arrest (and in whom
MI is suspected) until the patient has recovered.
Further reading
Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary angiography after cardiac arrest
without ST-segment elevation. N Engl J Med 2019; 380: 1397–407.
Primary PCI in cardiogenic shock 231
Primary PCI in cardiogenic shock

Multivessel PCI versus culprit only
The idea of achieving full revascularization in patients presenting with STEMI
complicated by cardiogenic shock has historically been based on the theor-
etical benefit of improving function and perfusion. In 2017, the CULPRIT
SHOCK trial showed for the first time a lower 30-day risk of all-cause mor-
tality and severe renal failure in the culprit-only PCI group compared with
immediate multivessel PCI. The guidelines now recommend culprit vessel-
only revascularization in patients with MI complicated by cardiogenic shock.
To unload the left ventricle versus to not unload
the left ventricle
The intra-aortic balloon pump (IABP) (% p.268) is the main ventricular assist
device available in the vast majority of CathLabs. More recently, percutan-
eous mechanical circulatory support devices have become available. After
the results of the CRISP-AMI and IABP SHOCK trials, the routine use of an
IABP in patients with MI complicated by cardiogenic shock is not routinely
recommended. The amount of data to support a benefit from mechanical
circulatory support devices is still scarce and no significant improvement in
30-day survival has been noted when compared to IABP. Currently no rec-
ommendation is given for their routine application in cardiogenic shock and
adoption should be assessed on a case-by-case basis taking into account the
patient’s age, co-morbidities, neurological function, and the prospects for
long-term survival and predicted quality of life.
Primary PCI in multivessel

disease: culprit-only versus
non-culprit PCI
The role and the best timing of PCI to bystander disease of the non-culprit
vessels in STEMI patients have been largely debated. This matter is rele-
vant when you consider that nearly half of STEMI patients present with
multivessel disease. Over the last few years, four randomized trials have
specifically addressed the role of multivessel PCI in STEMI. Even though
they differ in their design, all four trials came to the main conclusion that
complete revascularization in STEMI offers prognostic benefit, even though
such benefit is based on a lower risk of revascularizations (rather than on
improved survival or lower risk on non-infarct related artery MI).
Differences in design across the studies were mainly about the definition
of bystander disease:
• PRAMI study: angiography based (stenosis >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 233
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 235
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 pa-
tient 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: ra-
tionale 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.
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 237
‘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
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 <90°.
• In both approaches the main branch is stented first. After rewiring, the
side branch is stented, landed the proximal edge of stent right a the
osmium of the side branch (T-stenting) or slightly protruding into the
proximal main branch (TAP).
Postdilation of the proximal main branch (proximal optimization technique
(POT)) and final kissing balloon inflation is strongly recommended.
Crush stenting
• The crush technique and its variants mandate a two-stent strategy and
may be employed when there is severe compromise of a reasonably
sized side branch which is likely to be compromised further by main
vessel intervention.
• Both stents are positioned as if to perform a ‘kissing’ inflation; the side-
branch stent is deployed and the side-branch wire withdrawn.
• The main vessel stent is then deployed, crushing the tail of the side-
branch stent against the vessel wall.
• The side branch is then rewired and a ‘kissing’ inflation performed
(Fig. 8.21, part 4).
• Variants: reverse crush, ‘mini-crush’ (Fig. 8.21, part 3).
V-stenting
• Two non-overlapping stents are deployed simultaneously in the distal
portion of the main vessel and the proximal portion of the side-branch,
respectively (Fig. 8.21, part 8).
• Variant: shotgun/‘kissing’ stents—where stents overlap (Fig. 8.21,
part 10).
Bifurcation PCI techniques 239
Double Kissing Crush technique (DK Crush)

• The side branch is stented first, with the stent protruding into the
proximal main branch. A balloon is kept in the proximal main branch and
used to crush the proximal part of the stent deployed in the side branch.
• After rewiring the side branch a first kissing balloon inflation is performed
followed by deployment of the second stent in the main vessel.
After proximal optimisation technique, the side branch is rewired and a
second final kissing inflation is performed
Culotte stenting
• The main vessel is stented initially, with subsequent rewiring of the side
branch and stent deployment from the main vessel into the proximal
side branch.
• After re-crossing into the main vessel, a final kissing inflation is mandatory,
given the potential risks of under-deployment, as there is a double thickness
of stent in the proximal portion of the main vessel (Fig. 8.21, part 7).
Drug-eluting stents in bifurcation lesions

• Due to the amount of metal deployed in many complex bifurcation
techniques, it is unsurprising that restenosis rates are high.
• DESs (% p.202) may reduce restenosis in such situations, but may
increase the risk of stent thrombosis by more than 5% when more
than one DES is deployed.
• Recent data suggest that manipulation of the side branch following
DES deployment is unnecessary (in terms of outcomes) unless it
occludes during the procedure.
Fig. 8.21 Methods of treating bifurcation lesions. The numbering refers to the order
in which the stents are deployed. All these methods have been tried, but recent data
suggest that the ‘provisional stent’ technique produces the best results. Adapted
from Louvard Y, Lefèvre T, Morice M-C. Percutaneous coronary intervention for
bifurcation coronary disease. Heart 2004;90:713–722, with permission from the BMJ
Publishing Group Ltd
Left main stem PCI

Background
• Significant obstructive lesions affecting the LMS have traditionally been
an indication for CABG.
• Increasingly, LMS lesions are considered potential targets for PCI, due to
their large vessel calibre, lack of tortuosity, and short lesion length (and
thus lower risk of restenosis after PCI, see Fig. 8.22).
• Registry data for BMSs have demonstrated low procedural complication
rates with good medium-term vessel patency (up to 3 years).
• Recent DES data suggest improved MACE-free survival, but clinical
follow-up is currently limited.
Technical aspects of LMS PCI
• IVUS (% p.210) should be used before PCI to measure vessel reference
diameter and assess lesion length, and after PCI to ensure adequate
stent deployment/expansion.
• IABP (% p.268) should be used electively in patients with impaired LV
function; patients with normal LV function will generally tolerate LMS
balloon inflations well.
• Emerging data suggest that restenosis may occur if the LMS is not
routinely stented back to the ostium.
• Terminal LMS bifurcation lesions may be treated with any of the
dedicated bifurcation stenting techniques (% p.238).
• LMS in-stent restenosis is potentially disastrous; operators may
therefore electively repeat coronary angiography 3–6 months after PCI.
Indications for LMS PCI
• Urgent/emergency situations:
• For dissection/complications involving the LMS during PCI (Fig. 8.23).
• Primary PCI for STEMI.
• Elective situations—utility of LMS PCI remains controversial:
• ‘Protected’ LMS lesions (when patent grafts to LAD/Cx are present).
• Patients who refuse CABG.
• Patients unsuitable for CABG due to co-morbidity or high risk.
• Patients with suitable anatomy after appropriate informed discussion
and consent.
• Clinical trials to determine the optimum treatment strategy.
Complications
• Stent malapposition: the coronary reference diameter may be
underestimated visually, leading to stent undersizing, resulting in
restenosis or stent thrombosis. IVUS guidance eliminates such issues.
• Compromise of major branches: depending on stent strategy used,
the LAD or Cx ostium may be compromised. Additional stents may
improve angiographic outcome, but result in additional restenotic and/
or thrombotic risk.
• Haemodynamic compromise: short inflations and the use of
prophylactic IABP are advisable.
Left main stem PCI 241
IABP
Fig. 8.22 Elective PCI for LMS lesion. Top panel demonstrates undermined
atherosclerotic ulcer followed by severe lesion in body of LMS (indicated by arrows).
Bottom panel demonstrates result after IVUS-guided PCI with stenting. IABP used
electively; outline seen at left of images (arrows). Note improved antegrade flow in
LCA branches after PCI
Fig. 8.23 Emergency PCI for iatrogenic LMS dissection. Left panel shows linear LMS
dissection as a result of deep guiding catheter intubation during proximal LAD PCI;
right panel shows result after stent deployment back to ostium of LMS. IABP support
not used
Chronic total occlusion PCI

Background
• CTOs are defined as complete occlusion of a coronary artery for longer
than 3 months and remain one of the ‘final frontiers’ of interventional
cardiology.
• The anatomy and chronicity of the lesion affect the chances of successful
PCI: success is commoner in relatively recent occlusions, of short length,
remote from adjacent side branches. The presence of a tapered ‘run-in’
to the occlusion increases the chances of success further.
Technical aspects of CTO PCI
• Good guiding catheter support (% p.192) is essential.
• Use of specially designed stiff, heavyweight angioplasty guide wires
(% p.193) prevent deflection of the wire tip from its intended path and
aid penetration of the cap of the CTO. Such wires are often coated with
a hydrophilic polymer. Vessel perforation is not uncommon with such
wires, and may lead to cardiac tamponade (% p.308).
• Use of OTW balloons (% p.196) may add further support to prevent
wire tip deflection.
• If the lesion is crossed with the wire but antegrade flow remains absent,
injection of dye through an OTW balloon or multifunctional probing
catheter may confirm whether the wire is intra-or extraluminal.
• In some circumstances, simultaneous injection of the contralateral
coronary artery may allow retrograde filling to visualize the target vessel
beyond the occluded segment (Figs. 8.24–8.26).
Complications
• Extraluminal passage of the guide wire: hints that this has occurred
include abnormal course or motion of the wire during the cardiac cycle
and multiple ventricular extrasystoles.
• Vessel perforation: diagnosed by accumulation of dye in the pericardial
space or dye exit from the vessel in pulsatile fashion. Cardiac tamponade
is not uncommon (% p.284). Rapid pericardiocentesis, fluid resuscitation,
and prolonged inflation of a balloon at the site of perforation will
stabilize the patient. Reversal of heparin with protamine and subsequent
deployment of a covered stent (% p.284) may be necessary.
• Restenosis/reocclusion: even if PCI is technically successful, rates of
restenosis and reocclusion remain high, although DESs (% p.202) have
been demonstrated to reduce restenosis.
Novel/evolving approaches in CTO PCI

• Retrograde approach: CTOs may be crossed retrogradely from the
contralateral coronary artery (e.g. proximal RCA CTO crossed from
LAD via septal collaterals).
• Ultrasonic and laser guide wires: deployment of ultrasound or laser
energy through specially designed guide wires may aid passage through
long chronically occluded segments.
• Blunt dissection: novel catheter-based devices allow guided blunt
dissection of occluded segments to aid wire and equipment passage.
Chronic total occlusion PCI 243
Fig. 8.24 PCI to RCA CTO 1. Proximal RCA occlusion with minimal antegrade flow
Fig. 8.25 PCI to RCA CTO 2. Distal RCA beyond occlusion (white arrows)
visualized by retrograde filling from contralateral injection of LCA to confirm PCI
guide wire remains intraluminal
Fig. 8.26 PCI to RCA CTO 3. Final result after stent deployment

Vein graft PCI
Background
• Saphenous vein grafts (SVGs) used in CABG are prone to premature
failure, with around 50–60% being occluded at 10 years after surgery
and many of the remainder being significantly diseased (% p.166).
• Due to their size and nature, SVGs pose particular challenges for PCI.
• An alternative approach is to consider PCI to native vessels, either those
that are effectively CTOs, or protected LMS lesions with a patent LIMA
graft, or those that may be accessed via patent graft conduits.
Technical aspects of SVG PCI
• Generally, JR4 or coronary bypass guiding catheters are used for
SVG PCI.
• Depending on the exact anatomy and location of the SVG ostium
(which will vary considerably from patient to patient), El Gamal,
Amplatz, or multipurpose catheters may also be useful.
• SVG lesions tend to be more friable than native coronary lesions and
have a higher thrombus burden. Prevention of distal embolization of
thrombus is therefore important.
• Randomized trials have demonstrated incontrovertible benefit from the
use of distal protection devices, and such devices should be considered
mandatory in SVG PCI (Fig. 8.27).
• Although the presence of thrombus predisposes to no-reflow and
procedural complications, routine use of GPI (% p.224) in SVG PCI has
not been demonstrated to confer benefit.
Complications
• Complication rates are high: reports suggest in-hospital mortality rates
in excess of 5% and periprocedural MI rates of 2–5%. Nevertheless, PCI
carries less risk than redo CABG in most circumstances.
• No-reflow phenomenon (% p.246).
• Distal embolization of thrombus: may be prevented by mechanical distal
protection devices (% p.244), although thrombectomy devices do not
appear to have a protective effect.
• Restenosis: despite the generally larger stent diameters used (commonly
at least 3.5 mm and usually 4.0 mm or greater), restenosis is still a major
problem. Recent studies have demonstrated lower restenosis and target
vessel revascularization rates with DESs (% p.202).
Distal protection devices

Distal protection devices protect the distal coronary circulation from em-
bolization of thrombotic/atherosclerotic material, and have been shown
to reduce no-reflow and periprocedural adverse events during SVG PCI.
• Distal occlusion balloon: a guide wire-mounted balloon is inflated distal
to the lesion, and the static column of blood above aspirated after PCI.
• Filter devices: a variety of filter devices are available, consisting of a
mesh or metal basket positioned beyond the target lesion, designed to
catch embolized debris. The device is then retrieved through a sheath
after successful PCI.
Vein graft PCI 245
Fig. 8.27 Vein graft PCI using distal protection filter device. Top panel demonstrates
severe lesion in 8-year-old SVG to RCA extending from ostium into proximal vessel.
Middle panel shows balloon pre-dilation of lesion after deployment of filter device
(loop of filter basket shown by arrow); inset images show deployed filter wire device
and particulate debris retrieved from basket after PCI. Bottom panel shows final
result after stenting
The ‘no-reflow’ phenomenon
Although successful PCI may result in a patent target vessel, patency
does not necessarily correlate with normal perfusion of downstream
myocardium.
‘No-reflow’ occurs when there is inadequate myocardial perfusion in the
absence of mechanical obstruction of the epicardial vessel, that is, blood
can pass the site of the target lesion but cannot reach the myocardium. This
occurs due to:
• Microvascular dysfunction due to ischaemia/reperfusion injury.
• Distal embolization of thrombus/atheromatous debris.
No reflow may occur after pre-dilation, but is more common after stent
deployment or post-dilation. It is associated with increased short-and long-
term post-PCI mortality.
Diagnosis and presentation
• Angiographic evidence of sluggish/absent antegrade flow in the target
vessel after PCI (TIMI 0 or 1 flow).
• Lack of evidence of myocardial ‘blush’ in the territory of the target
vessel (downstream myocardium should show blushing due to contrast
efflux following injection into an unobstructed vessel).
• Chest pain and ST-segment elevation, sometimes associated with
hypotension in the context of the previously mentioned angiographic
findings.
Prevention
• Consider the possibility of no reflow in bulky/thrombus-filled lesions,
especially in SVGs or ectatic native vessels, and during primary PCI.
• Consider thrombectomy devices where thrombus is present.
• Deployment of distal protection devices in SVG lesions and lesions with
visible thrombus.
• Pretreatment with GPIs may reduce thromboembolization.
• Pretreatment with vasodilators may reduce vasospasm that contributes
to microvascular dysfunction.
Management
• Once established, no reflow is difficult to treat; prevention is the key in
potentially vulnerable target lesions.
• Administration of drugs used for prevention (% p.246) may be useful.
• Avoid repeated injections of contrast into the affected vessel—this will
worsen ischaemia; flow will often improve with time and application of
vasodilators.
• Consider insertion of an IABP (% p.268) to maximize coronary
perfusion pressure if hypotension persists.
The ‘no-reflow’ phenomenon 247
Vasodilators in ‘no reflow’

For prevention, agents may be injected directly into the coronary artery
via the guiding catheter; where no reflow is established, antegrade flow is
absent, and such agents should be administered through an OTW balloon
or multifunctional probing catheter, as close to the distal vascular bed as
possible. Useful agents include:
• Verapamil 100–500-microgram slow intracoronary injection—may be
given repeatedly (NB: beware of heart block).
• Adenosine 30–50-microgram intracoronary injection—may be given
repeatedly (avoid in asthmatics/patients taking dipyridamole).
• Sodium nitroprusside 50–100-microgram intracoronary injection—
may be given repeatedly.
• GTN and other nitrates have not been shown to be useful in no
reflow.
Rotational atherectomy
Background
• The concept of atherectomy (removal of atheroma) refers to an old
technique (directional atherectomy) developed to reduce the volume of
stenotic coronary lesions prior to angioplasty and/or stenting.
• Rotational atherectomy (‘rotablation’) was developed three decades
ago as an evolution of directional coronary atherectomy. Compared to
directional atherectomy, rotational atherectomy has survived the test
of time. However, over the years the rational for performing rotational
atherectomy has changed.
• Rotational atherectomy is today used specifically for the treatment of
highly calcified, undilatable coronary lesions.
• Intravascular imaging studies have confirmed that rotational atherectomy
acts more by cracking calcium and modifying atherosclerotic plaque
texture and composition rather than by debulking the lesion as thought
in the past (Fig. 8.28 and Fig. 8.29).
Equipment
The Rotablator™ Rotational Atherectomy System (Boston Scientific,
Marlborough, MA, USA) consists of:
• OTW, high-speed rotating diamond-coated burr available in different
sizes (from 1.25 to 2.5 mm).
• 0.009-inch wire (RotaWire™).
• Advancer (RotaLink™) drive shaft.
• Motor console that converts compressed gas into rotational energy.
• Compressed helium gas tank.
• Pedal for rotaburr activation.
• Continuous flushing solution with mix of vasodilator agents (to allow
rotaburr tip cooling and prevent vasospasm).
The recently introduced RotaPro™ (Boston Scientific, Marlborough, MA,
USA) is an iteration of the previous version, making rotation atherectomy
easier to perform by a single operator, offering a user-friendly interface and
easy-to-use controls all integrated on the advancer.
Contraindications
• Severe tortuous anatomy (increased risk of coronary perforation and
rotaburr entrapment).
• Presence of coronary dissection.
Complications
• Coronary perforation (% p.308).
• No reflow (secondary to vessel overheating and distal embolization of
pulverized calcified debris (5–10 μm)) (% p.246).
• Severe bradycardia—heart block (% p.291).
Technical aspects of rotational atherectomy
• Once indication for rotational atherectomy has been agreed due to:
• Clear evidence of calcium on angiogram.
• Calcified arch greater than 180° on intravascular imaging.
Rotator burr
Fig. 8.28 Rotational atherectomy of calcified proximal circumflex lesion. Lesion

indicated by arrow (left panel) before intervention; passage of burr across lesion
(inset); and final result after deployment of stent in proximal vessel
Fig. 8.29 Rotational atherectomy burr. The diamond-studded Rotablator™ burr is

pictured threaded on its guiding wire. Different sizes of burr are used depending on
vessel calibre; generally, the burr should not exceed 0.6 × vessel reference diameter.
Photograph courtesy of Boston Scientific
• Failed balloon pre-dilation/failed lesion crossing with balloon

(undilatable/uncrossable) lesion.
• The RotaWire™ is delivered distal to the lesion. Direct wiring with the
RotaWire™ is theoretically possible but practically challenging because
of the properties of the wire. A microcatheter can be used to cross the
lesion and to exchange the workhorse wire with the RotaWire™.
• Inability to cross the lesion with a microcatheter poses a main limitation
for rotational atherectomy. In this case, alternative strategies, such as
laser ablation, might become necessary.
• The rotaburr size is typically selected according to a burr-size:artery
ratio of 0.5–0.6.
• Before starting rotational atherectomy it is important to check the
patient’s heart rate and baseline ECG to establish the likelihood of
severe bradycardia or complete heart block occurring. In this case, it is
good practice to pre-treat the patient with atropine. Some operators
consider a prophylactic implant of a temporary wire, especially when

treating a large right coronary artery.
• After checking connections with the console and checking levels of
compressed helium gas in the tank, it is important to test for burr
revolution speed. The ideal speed range is between 135,000 rpm and
180,000 rpm.
• Once rotational atherectomy is started, the rotaburr is advanced
repeatedly across the target lesion in a ‘pecking’ motion. It is important
to avoid a significant drop in revolution speed while advancing the
rotaburr through the stenosis.
• It is advisable to avoid decelerations greater than 5000 rpm or to wedge
the burr within the lesion in order to prevent lodging/entrapment of
the rotaburr. In this regard, it must be remembered that the rotaburr
has ablating elements (diamonds) on the anterior segment and not on
the posterior end.
Alternative techniques to rotational atherectomy
Over the past years, two novel technologies have been developed for treat-
ment of significant calcified coronary lesions. While results of efficacy from
randomized clinical trials are still awaited, these new techniques have pro-
gressively extended their presence in the CathLab.
Orbital atherectomy
This consists of an eccentrically mounted diamond-coated 1.25 mm crown,
connected to a drive shaft and to a controller powered by a pneumatic
console (CSI Diamond 360® Coronary Orbital Atherectomy System). The
crown presents diamond chips on both the front and back allowing ablation
during both antegrade and retrograde motion of the crown, making the
entrapment of the crown theoretically impossible.
The crown is advanced over a dedicated 0.014-inch wire (ViperWire®).
The operator can move the crown forward and backward and regulate the
speed of crown orbit (80,000–120,000 rpm). The procedure is performed
during continuous intracoronary infusion of a dedicated lubricant solution
(ViperSlide®).
The mode of action of orbital atherectomy consists of fast elliptical ro-
tation of the crown with a progressive increase of the orbit diameter as
rotation speed increases. The centrifugal force generated ‘sands away’ the
calcified component of the plaque. By increasing its orbit as rotational speed
increases, it is possible to ablate calcium using the 1.25 mm crown in vessels
up to 3.5 mm diameter, without needing to upsize the crown.
Lithoplasty balloon
This system consists of pulsatile mechanical energy delivered at a fre-
quency of 1 Hz via miniaturized emitters placed along the length of a semi-
compliant rapid-exchange balloon (Shockwave Coronary Rx Lithoplasty®
System, Shockwave Medical, Fremont, CA, USA). This energy vibrates cal-
cified components (both superficial and deeper within the coronary plaque),
cracking and fracturing the calcium. The main limitation for lithoplasty is an
inability of the balloon to cross tight lesions; however, because of its ease of
use, it is the most promising technique with the potential to be the ‘default’
approach in the management of calcified and undilatable lesions.
Aspiration catheters
Thrombus aspiration has for a long time been one of the main techniques
to deal with thrombus-containing lesions, especially in patients with STEMI.
The advocated benefits of acting on thrombus burden by thrombectomy
include:
• Preventing the risk of distal embolization.
• Improving visualization of the atherosclerotic lesion.
• Improving the evaluation of vessel size.
• Favouring direct stenting.
• Reducing the risk of stent malapposition secondary to disappearance
of the thrombus initially located between the stent struts and the
vessel wall.
The routine application of thrombus aspiration has not, however, been
proved to be associated with better clinical outcomes in two large ran-
domized clinical trials (TASTE and TOTAL). For this reason, thrombec-
tomy is not routinely recommended. Targeted and selected application of
thrombus aspiration in cases with evidence of large thrombotic burden is,
however, still advised and adopted by the vast majority of operators.
Two main kinds of thrombus aspiration devices are available: manual and
mechanical. In manual aspiration devices, thrombus is aspirated by a suction
force exerted manually by the operator. In mechanical aspiration devices,
the aspirating force is generated by technique/tool-specific mechanisms
that vary according to device. However, because of a slow learning curve,
mechanical aspiration is rarely performed in the CathLab.
Manual thrombus aspiration devices consist of 6 F compatible dual-lumen
catheters with a smaller lumen for the mono-rail rapid exchange system and
a larger lumen connected to a Luer-lock syringe. By creating a vacuum in
the Luer-lock syringe, a suction/aspirating force is generated which is re-
sponsible for thrombus removal while crossing the lesion with the aspiration
catheter. For an effective and safe thrombus aspiration it is necessary that:
• Aspiration is performed while crossing the thrombotic lesion.
• Multiple forward and backward passages are performed with the
aspiration catheter.
• Good guiding catheter engagement and ongoing aspiration is applied
while retrieving the aspiration catheter (to reduce the risk of stroke).
• Guiding catheter and line are properly cleared from possible thrombotic
debris, allowing backspilling of blood before injecting contrast.
253
Chapter 9
Additional procedures
Pericardiocentesis 254
Temporary pacemaker 256
Endomyocardial biopsy 258
Cardioversion/defibrillation 260
Mechanical cardiopulmonary resuscitation 262
Intra-aortic balloon pump 268
Impella® 274
Extracorporeal membrane oxygenation 276
254 Chapter 9 Additional procedures
Pericardiocentesis
Emergency drainage of the pericardial space is usually performed for the
management of cardiac tamponade. When known or suspected tam-
ponade has created a cardiac arrest situation, the procedure can and should
be performed as an immediate and potentially life-saving measure. In other,
less critical, cases, echocardiography should be performed first. This inves-
tigation allows confirmation of the diagnosis and provides important infor-
mation about the wisdom of and approach to pericardial aspiration.
Following PCI, just a small amount of blood can result in tamponade
of a cardiac chamber, making percutaneous drainage technically difficult.
Occasionally, an apical approach may be required. Obtain expert advice if
time and circumstance permit.
Imaging during the procedure is recommended with radiographic
screening and pressure monitoring and/or echocardiography.
• Position the patient at 45° if possible to encourage pooling of the
effusion at the inferior surface of the heart.
• Prepare the skin and drape the patient in a sterile fashion.
• Infiltrate local anaesthetic along the drainage track (passing just under
the costal margin, following a line towards the tip of the left scapula).
• Conscious sedation may be required (e.g. midazolam).
• The skin incision point lies just below the xiphisternum (Fig. 9.1). Use
a scalpel blade to make a small incision to reduce skin friction for the
passage of the drainage catheter.
• Advance the needle, with syringe attached, maintaining negative
pressure, and observe for the aspiration of fluid.
• If echocardiography is used, agitated saline may be used to confirm the
presence of the needle in the pericardial space.
• Remove the syringe when fluid is obtained and advance the guide wire
through the needle so that it loops in the cardiac shadow on X-ray
screening or is visible in the pericardial space with echocardiography.
• Remove the needle, leaving the guide wire in place.
• Advance a dilator over the wire. Several passes may be required.
• Advance the catheter over the wire and into the pericardial space.
• Fluid can now be aspirated with a syringe.
• Symptoms and haemodynamic compromise in tamponade will improve
with removal of modest volumes of fluid (e.g. 20–50 mL).
• Samples are sent for biochemical, immunological, and microbiological
analyses if necessary.
• The drainage bag can then be connected, secured with sutures at the
skin entry point, and dressed with transparent occlusive dressings.
• The catheter is usually left in situ for several hours to gauge the rate of
drainage.
• Perform echocardiography immediately following pericardiocentesis and
then serially to examine for re-accumulation.
Pericardiocentesis 255
Key items of equipment

A number of manufacturers now supply pericardial drainage packs that
incorporate the necessary equipment. Check carefully before starting the
procedure that you have all the necessary components:
• Long needle (15 cm) of at least 18-gauge calibre. A short bevel is an
advantage to avoid potential cardiac laceration.
• ‘J’-tip guide wire (0.035-inch diameter).
• Dilator (5–7 F).
• Pigtail or other drainage catheter with multiple distal side holes.
• Large-calibre syringe for aspiration.
• Drainage bag and connecting tubing.
Fig. 9.1 Pericardiocentesis and landmarks for the needle

Temporary pacemaker
Consider external pacing as a temporizing measure if immediate support
is required.
Transvenous temporary pacemaker insertion
• Obtain venous access (usually femoral vein) with a sheath of larger
diameter than the temporary wire to be used (% p.59).
• Under X-ray screening, advance the pacing wire into the right atrium.
The wire has a J-shaped distal contour which allows the tip to be
directed by rotation of the proximal end of the wire.
• Direct the wire towards the apex of the right ventricle (this lies just
medial to the apex of the cardiac silhouette on AP screening).
• If the wire does not move directly over the tricuspid valve it may be
necessary to form a loop of wire in the atrium, usually achieved with the
tip on the right lateral atrial border. Rotation and advancement of the
wire may then result in prolapse through the tricuspid valve.
• As the wire enters the ventricle some ectopic activity is usual and helps
confirm a ventricular position.
• The wire can inadvertently enter the coronary sinus. Its orifice lies
above the tricuspid valve. A wire in the coronary sinus appears more
cranial on AP screening and on a lateral view moves posterior (rather
than the desired anterior direction of a RV lead).
• Manipulate the wire so that the tip curves downwards to the apex of
the ventricle. In its final position the line of the wire should resemble the
heel of a sock in the right atrium (Fig. 9.2), with the toe in the apex of
the right ventricle.
• Connect the lead to the pacing box and test the threshold for capture.
Pace at a rate above the intrinsic cardiac rate while slowly turning down
the box output (start at 3 V). The ECG monitor is observed to identify
the output at which capture is lost. Increase again slowly to recapture.
Fig. 9.2 Right ventricular pacing wire

Temporary pacemaker 257
This is the pacing threshold. A threshold of 1 V or lower is desirable.

Output is set to at least three times the pacing threshold.
• Suture the lead and sheath to the skin and apply transparent occlusive
dressings.
• Secure the external portion of the lead with tape or other fixatives.
Fixing a loop on the skin should mean that inadvertent tugs on the wire
will tighten the loop rather than pulling out the wire.
External (transcutaneous) temporary pacing
With gel pads at the apex and right parasternal position, set rate to 70 beats
per minute in demand mode. Turn up output until electrical capture and
confirm output with pulse. Uncomfortable skeletal muscle contraction will
occur and may result in ECG artefact. Sedation is usually required.
Configuring the pacemaker settings
• Set to ‘demand’ at the required rate of, for example, 70 beats per
minute (Fig. 9.3).
• The pacemaker will, on a beat-to-beat basis, pace when it does not
detect ventricular activity above that rate.
• The red pace light will illuminate on each occasion.
• When the spontaneous ventricular rate is above the pacemaker rate,
the box will inhibit and the red sense light will illuminate.
• An output set to at least three times pacemaker threshold will ensure
that each impulse ‘captures’ the ventricle.
• The sensitivity should be adjusted to ensure that each intrinsic beat
is detected but that skeletal muscle interference does not lead to
pacemaker inhibition (the lower the setting, the more sensitive the
pacemaker).
• Ensure that the pacemaker is set to demand. Asynchronous pacing risks
inducing ventricular arrhythmias.
Fig. 9.3 Temporary pacemaker box

Endomyocardial biopsy
Endomyocardial biopsy is performed in the monitoring of cardiac allograft
rejection, in the diagnosis of myocarditis and acute heart failure, restrictive
cardiomyopathies, and cardiac masses. Biopsy is usually taken from the right
ventricle (due to the risk of systemic embolization when performed on the
left). See Fig. 9.4.
Complications
• Cardiac perforation.
• Cardiac tamponade.
• Emboli (tissue/air/thrombus).
• Arrhythmias (atrial and ventricular).
Procedure
• A suitable sheath is inserted into the right internal jugular vein.
• A 7–9 F stiff bioptome is advanced into the right atrium.
• The procedure is performed under intracardiac echocardiography or
fluoroscopic guidance (60° LAO or 30° RAO).
• Contact with the RV myocardium is confirmed by resistance to
advancement and presences of ventricular ectopics.
• Biopsy is performed by withdrawing the bioptome forceps slightly,
opening, advancing, closing, and then withdrawing them again.
• Slight resistance is expected.
• Each biopsy should be examined for quantity and carefully flushed into a
suitable specimen pot.
• Four or five samples should be taken.
• The patient should be observed for signs of cardiac tamponade for
several hours after the procedure.
Endomyocardial biopsy 259
Fig. 9.4 Endomyocardial biopsy of a tissue mass at the junction of the right atrium
(RA) and right ventricle (RV) imaged using intracardiac echocardiography. The
bioptome forceps tip can be seen embedded within the tissue
Cardioversion/defibrillation
• During cardiac catheterization procedures, cardioversion of atrial
arrhythmias, SVT, and VT is usually performed under sedation with IV
benzodiazepines or under general anaesthesia.
• Place gel electrode contact pads over the sternum and at the apex of
the heart.
• Ensure the defibrillator electrodes are connected firmly to the machine,
connect the ECG leads of the defibrillator to the patient, and select a
lead with the tallest QRS complex.
• Ensure the defibrillator is set to ‘sync’ so that the defibrillation shock is
timed to coincide with the R wave. A dot should appear on the R wave
of the ECG (and not the T wave). Use different leads if synchronization
is not optimal.
• Typical starting energies for the cardioversion of stable arrhythmias are
200 J monophasic and 150 J biphasic.
• Firm pressure on the defibrillator electrodes (8–12 kg) significantly
improves the cardioversion success rate by reducing thoracic
impedance.
• Defibrillation for VF should be performed as quickly as possible using
unsynchronized high initial energies (200–360 J monophasic, 150–200 J
biphasic).
• If defibrillation is repeatedly unsuccessful, check the device settings and
consider a different defibrillator.
• Internal cardioversion (% p.261) using a balloon flotation catheter
can be considered for arrhythmias that are resistant to external
cardioversion (Fig. 9.5).
Cardioversion/defibrillation 261
Fig. 9.5 Balloon flotation, internal cardioversion catheter. There are two shocking
coils; one located in the left pulmonary artery, the other in the right atrium. A pace-
sense electrode is in the middle of the picture, positioned within the right ventricle
Mechanical cardiopulmonary
resuscitation
High-quality chest compression as part of cardiopulmonary resuscitation
(CPR) is a key element in the cardiac arrest chain of survival. Both American
and European guidelines highlight that chest compression should be de-
livered with a depth of at least 5 cm at a rate of 100 repetitions per minute
allowing chest recoil and re-expansion after each compression.
However, meeting these standards is very difficult and they are rarely
met when chest compression is performed by a human rescuer, especially
in case of prolonged cardiac arrest scenarios.
Mechanical CPR devices have been introduced to address specifically this
limitation. According to the modality through which chest compression is
delivered, the mechanical CPR devices can be categorized as:
• Piston based (Lucas®, Physio-Control Inc./Jolife AB, Lund, Sweden)
(Fig. 9.6a).
• Load-distributing band based (AutoPulse®, Zoll Medical, Chelmsford,
MA, USA) (Fig. 9.6b).
A piston-based device consists of a plunger (either compressed gas or
electric powered) compressing over the sternum at a predefined rate.
Some devices (like the Lucas®) also present a suction cup at the end of the
piston to facilitate chest decompression after each compression.
The load-distributing band-based devices consist of a backboard on
which the patient is positioned and a pneumatically or electrically powered
constricting band passing around the patient’s armpits and compressing the
sternum.
These devices are utilized always more frequently by ambulance crews,
Emergency Department staff, and more recently also by the CathLab team.
Current American and European guidelines, however, do not recommend
the routine use of mechanical CPR devices in cardiac arrest due to limited
supportive outcome data.
Possible explanations for the lack of benefit in applying mechanical CPR
devices are:
• Possible mechanical damage to internal organ.
• Higher rate of sternum (Lucas®) and rib (AutoPulse®) fracture.
• Interruption of chest compressions during device positioning.
• Shifting device position during use to vulnerable places on the chest or
abdomen.
Mechanical circulatory support devices
The rationale behind the application of mechanical circulatory support
(MCS) devices in the CathLab is to intervene as soon as possible to stop
the ‘failing heart downward spiral’ (Fig. 9.7).
MCS aims to
• Normalize cardiac output.
• Normalize mean arterial pressure.
• Decrease PCWP.
• Optimize O2 saturation.
(a)
(b)
Fig. 9.6 (a) Piston-based mechanical CPR device. (b) Load-distributing band-based

CPR device
Myocardial infarction
Systemic
inflammation
Myocardial dysfunction
Systolic Diastolic
↓ Cardiac output ↑ End-diastolic

and stroke volume pressure
Hypotension Pulmonary congestion
↓ Coronary Perfusion Hypoxia
Worsening myocardial ischaemia
Worsening myocardial dysfunction
Death
Fig. 9.7 Failing heart downward spiral
• Improve coronary blood flow.

• Reduce myocardial workload and myocardial O2 demand.
• Act as a bridge to definite ventricular support device/heart transplant.
Even though these devices are progressively and increasingly entering in
everyday clinical practice, it must be said that no trial has showed a convin-
cing net benefit on survival.
Indications
MCS has three main current indications:
• Protected PCI in complex high-risk indicated patients (CHIP).
• Cardiogenic shock.
• Salvage potential in MI.
The coexistence of the following features defines a CHIP case to: Complex
and high risk coronary intervention (CHIP):
Complex coronary anatomy
• PCI on unprotected LMS disease.
• PCI on multivessel disease (Syntax Score >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 ac-
cording to the severity and acuteness of shock. See Fig. 9.8.
severe
ECMO
Heart failure
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
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.
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.
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
• 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.
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
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
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
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 avail-
able 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 ® 275
LV IMPELLA®
Cardiac output: 2.5 L/min
Access site size: 12 F


Cardiac output: 4 L/min

IMPELLA® RP Access site size: 23 F
Fig. 9.18 The LV Impella® and Impella® RP systems

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).
277
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
278 Chapter 0 Complications
Risks of complications
Cardiac catheterization is an invasive study that involves real risks to the pa-
tient. 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 car-
diac 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 279
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; occasion-
ally in patients with normal coronary arteries), massive air embolism (%
p.306), intractable ventricular arrhythmias (% p.288), and pericardial tam-
ponade (% 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 com-
plication 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 con-
tacted and what has been said.
Handling staff (including yourself )

A death in the cardiac CathLab often involves a prolonged attempt at car-
diac resuscitation and a large number of staff. It is physically and psycho-
logically 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.
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 measure-
ment of cardiac enzymes (particularly creatine kinase-MB isoenzyme and
cardiac troponins) following PCI, small enzymatic events are being recog-
nized 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.
• 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 281
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.
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, hyperten-
sion, 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 syr-
inges 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 sys-
temic anticoagulation in high-risk cases and monitor the coagulation time
(% p.218).
• 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 283
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).
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).
• 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 285
Protamine sulphate
This is used to reverse the effects of heparin. In high doses it has an anti-
coagulant 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 min-
utes of heparin). Heparin is rapidly excreted (half-life around 60–90 min-
utes) 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.
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 pro-
found 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.
• 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 elec-
trical activity (% p.289) with chest compressions and ventilation.
Vasovagal reaction 287
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 reac-
tions are also seen at the time of arterial puncture or during compression
haemostasis.
Patients often complain of feeling non-specifically unwell, fatigued, nause-
ated, and sweaty. The heart rate will usually start to slow before the blood
pressure drops. The patient may become pale, syncopal, apnoeic, and ap-
pear 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).
Arrhythmia
Transient benign arrhythmias are frequently seen during cardiac catheter-
ization, particular supraventricular and ventricular ectopics and sinus brady-
cardia. 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 289
• 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

• 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 <150 bpm, breathless, and/or mild
hypotension) then:
• Give heparin (5000–10,000 IU IV) then regular weight-adjusted
subcutaneous low-molecular-weight heparin if AF persists.
• If the patient has good haemodynamics, no pulmonary oedema,
and no known structural heart disease (no previous ischaemic heart
disease or valve disease and a normal transthoracic echocardiogram),
give flecainide 2 mg/kg (max. 150 mg) IV over 30 minutes. Plan for
electrical cardioversion 2–3 hours later if drug treatment fails.
• Consider pharmacological cardioversion with amiodarone 300 mg IV
over 1 hour (though efficacy is poor).
Supraventricular tachycardia
See Fig. 10.6.
• Usually occurs as a result of catheter manipulation in the right atrium
and right ventricle in a patient with a predisposition to tachycardia (e.g.
an accessory pathway).
• Atrial and ventricular ectopics trigger (usually) a narrow complex
tachycardia.
• The SVT may be broad complex if there is bundle branch block or rate-
related aberrancy (right or left bundle branch block morphology will be
present).
• Vagal manoeuvres—carotid sinus massage, Valsalva manoeuvre, ocular
pressure, ice application.
• Adenosine IV bolus 6–18 mg backed up by a saline flush.
• If SVT reinitiates immediately after adenosine administration, consider
verapamil 5–10 mg IV slow injection. Avoid if known impaired LV
function or significant hypotension as it may cause a further fall in blood
pressure.
• Alternative drug treatments in the emergency setting include flecainide,
esmolol, or sotalol IV after expert consultation.
• DC cardioversion (200–360 J) if pharmacological treatment fails to
terminate SVT.
Fig. 10.6 Atrioventricular nodal re-entrant tachycardia. A rapid, regular tachycardia.

Usually narrow complex (unless bundle branch aberrancy occurs). Retrograde P
waves occur during the QRS complex and are difficult to see, although typically
appear as a ‘pseudo-R wave’ in lead V1 (arrows)
Arrhythmia 291
• First episodes do not usually require prophylactic drug therapy.

• Maintenance drug therapy or referral for radiofrequency ablation
depends upon frequency, duration, and severity of symptoms.
Bradycardia and heart block
See Fig. 10.7.
• Transient bradycardia or junctional rhythms are common during
coronary angiography injection. These typically recover quickly
spontaneously or following administration of atropine 0.5–1 mg IV.
• Bradycardia may be a sign of a vasovagal reaction (% p.287) and can
precede hypotensive collapse.
• More advanced degrees of heart block (% p. 292) usually occur in
the setting of known conduction delay in patients undergoing cardiac
catheterization with either direct mechanical damage to the (usually
right) bundle branch or due to myocardial ischaemia (typically the right
coronary artery).
• Conduction recovery is usually seen within minutes unless there is
ongoing ischaemia.
• First-degree and Mobitz type I second-degree (Wenckebach) block do
not normally require urgent intervention. Mobitz type II and complete
AV block may require urgent temporary transvenous pacing (% p.256).
• Atropine (1 mg IV) may improve AV node conduction.
• IV isoprenaline (bolus 25–50, infusion 5–10 micrograms/min) or other
sympathomimetic drugs rarely improve conduction but can increase
sinus node automaticity.
Fig. 10.7 Junctional bradycardia. If the sinus node pacemaker fails, the AV junction
is the next in line in the pacemaker hierarchy. P waves originate from the AV node
area and are therefore negative in leads II, III, and aVF. They occur just before, during,
or after the QRS (arrows), depending upon which point in the AV junction they
originate. There is a QRS complex, usually narrow, for every P wave
Classification
See Figs. 10.8–10.11.
First-degree AV block
Fig. 10.8 The PR interval is greater than 200 ms (one large square). There is a QRS
after every P wave
Second-degree AV block Mobitz type I (Wenckebach)
Fig. 10.9 The PR interval lengthens after each successive P wave until finally one P
wave is not conducted
Second-degree AV block Mobitz type II
Fig. 10.10 P waves fail to conduct to the ventricle in a fixed ratio without preceding
lengthening or variation in the PR interval
Third-degree/complete AV  block
Fig. 10.11 All P waves fail to conduct to the ventricle, resulting in a slow,

dissociated ventricular escape rhythm. QRS complexes may be narrow or wide
depending upon the site of the escape rhythm origin
Arrhythmia 293
Vascular complications
Haemorrhage
• Bleeding from the site of arterial puncture usually presents with a
progressively enlarging swelling and haematoma formation.
• This can be extremely painful and can occasionally precipitate
cardiovascular collapse due to a vagal reaction (% p.287).
• Groin, thigh, and abdominal discoloration may develop with time.
• Compression of the femoral nerve and leg weakness has been reported.
• Blood loss can be quite extensive so check the blood count and send
blood for group and save.
• Patients who have received anticoagulants, thrombolysis, or
glycoprotein IIb/IIIa receptor antagonists are at higher risk.
Management of haematoma is with firm manual pressure and the use of
mechanical compression devices (% p.66). Check distal pulses and listen
for bruits (?arteriovenous fistula % p.294). Large haematomas should be
carefully examined to exclude a pseudoaneurysm (% p.294). Arrange ultra-
sonography if uncertain.
Retroperitoneal haematoma
• Retroperitoneal bleeding can occur with a high femoral puncture (above
the inguinal ligament) and can be incessant and fatal.
• Patients may present with progressive hypotension or cardiovascular
collapse.
• Flank bruising can occasionally be seen.
• CT of the abdomen will confirm the diagnosis.
• Manual compression is unlikely to help.
• Management is with fluid and blood replacement, reversal of
anticoagulation, and occasionally with surgical repair of the artery.
Pseudoaneurysm
A pseudoaneurysm (or false aneurysm) is a contained leakage of blood
from the artery into a chamber contained by the surrounding tissues (Fig.
10.12). There is flow in to and out of the chamber to the artery via a
channel (or neck). The presentation is as for a local haematoma. The diag-
nosis is confirmed with Duplex ultrasonography.
The management of a pseudoaneurysm is either with ultrasound-guided
compression or by direct injection of thrombin (Box 10.1). Surgical repair
and endovascular stent closure can be considered if these measures fail.
Arteriovenous fistula
Arteriovenous fistulae typically occur if needle puncture of both the ar-
tery and vein have occurred, with haemorrhage from one vessel tracking
across to the other. This may also occur if a needle and sheath pass through
one vessel into the other. They are associated with punctures below the
common femoral artery (% p.54). Management is usually surgical.
Vascular complications 295
Fig. 10.12 Ultrasonography of a femoral artery pseudoaneurysm
Box 10.1 Thrombin injection

• 5000 IU of bovine thrombin should be mixed in a small syringe with
0.9% saline to a volume of 5 mL (1000 units/mL).
• Under ultrasound guidance, the pseudoaneurysm is punctured using a
23-gauge (blue) needle.
• Use local anaesthesia if the site is extremely tender.
• Injecting a small amount of thrombin may help locate the needle tip.
• The usual dose required is 500–1000 units (0.5–1 mL).
• With slow injection of thrombin, blood within the cavity will be seen
to ‘smoke’ and clot. This can occur very rapidly.
• The clotted pseudoaneurysm then gets reabsorbed over time (5–6
weeks).
• Leakage of thrombin into the circulation is rare.
Infection
Infection at the vascular puncture site is uncommon and usually results from
Staphylococcus aureus infections. Patients can present with pain, erythema,
discharge from the wound, and fever. Management is with antibiotics (ac-
cording to cultures) and (rarely) with abscess drainage.
Limb ischaemia
Development of acute limb ischaemia is an access-related complication that
can be encountered in the CathLab. It can involve the lower limb during
transfemoral procedures and the upper limb (usually the forearm) during
transradial procedures. The modality by which acute limb ischaemia is es-
tablished differs between the upper and the lower limb.
Lower limb acute ischaemia
Lower limb ischaemia is typically associated with the use of femoral closure
devices, adopted to achieve quicker and controlled haemostasis, especially
when large-size femoral sheaths are used. Such devices usually act in two
main ways:
• Internal suture-based devices (e.g. ProGlide™, Abbott Vascular, Santa
Clara, CA, USA) can lead to limb ischaemia as consequence of an
overtightened knot, especially when multiple devices are used to close
up larger holes.
• Sealing plug-based devices (e.g. Angio-Seal™, Terumo, Somerset, NJ,
USA) can lead to ischaemia by generating a new stenosis, typically in
case of the presence of pre-existing vessel atherosclerosis or in case of
small size femoral arteries.
Prevention
• Correct site puncture is crucial to prevent lower limb ischaemia.
Fluoroscopy-guided or ultrasound-guided puncture can help to identify
a location of the common femoral artery with relatively good size and
free from atheroma.
• Performing a femoral artery angiogram before removing the sheath can
be helpful in further confirming the site of puncture, calibre, and disease
extension (if any) of the femoral artery.
• In case of puncture below the bifurcation (e.g. puncture of superficial
or profunda femoral artery) or in case of a small-calibre femoral artery,
haemostasis by manual or mechanical compression should be preferred.
The lower limb should be regularly checked by the nursing team for signs
of ischaemia:
• Pale/cyanotic appearance.
• Cold limb.
• Loss/weakness of peripheral pulses.
• Pain.
• Motility/sensory deficit.
Management
Prompt diagnosis is pivotal as well as early involvement of the vascular
surgical team. Doppler ultrasound scan l CT to be arranged to confirm
diagnosis.
Limb ischaemia 297
Upper limb acute ischaemia

Transient occlusion of the radial artery after a coronary procedure can have
an incidence up to 7–8%. Such an event is, most of the time, silent and not
associated with symptoms, since the ulnar artery can supply the function of
the occluded radial artery.
Acute upper limb ischaemia is therefore a rare event and usually associ-
ated with the occurrence of large and uncontrolled forearm haematoma/
bleeding with the development of compartment syndrome. This is a very
rare condition with an incidence between 0.004% and 0.13%. This can be
related to:
• Inadequate or poor haemostasis/compression.
• Undetected/undiagnosed perforation of a radial artery side branch
(usually guide wire induced).
• Radial artery laceration during sheath insertion or removal in the setting
of severe radial artery vasospasm.
• Extravasation of IV drugs or saline from a misplaced IV cannula.
Possible risk factors include female sex, small patient size, impaired renal
function, and large sheath size.
• Rare cases of forearm compartment syndrome without haematoma
are described. Sheath/catheter-induced forearm muscle ischaemia
and consequent oedema and swelling has been hypothesized as an
underlying causative mechanism.
• Acute arm ischaemia can also be related to lost equipment (e.g.
entrapped wire; Fig. 10.13) requiring, of course, immediate surgical
intervention.
Fig. 10.13 A rare case of a guide wire wrapping in the radial artery requiring
surgical intervention
Prevention
Initial conservative management with mechanical compression of the
forearm (typically using a pressure cuff inflated up to 15 mmHg below the
systolic pressure value) can help to prevent evolution into compartment
syndrome when forearm haematoma is noted.
• Pain relief.
• Optimal control of blood pressure.
• Heparin reversal.
Management
Early diagnosis is pivotal. Clinical suspicion should be raised in the presence
of a swollen forearm with evidence of:
• Pain (usually worsened by passive stretching).
• Pallor.
• Pulselessness.
• Paralysis.
• Paraesthesia.
The vascular surgical team should be early involved if diagnosis is confirmed
or there is a high suspicion of compartment syndrome.
Limb ischaemia 299
Coronary dissection
Coronary dissection is a pathological separation of the layers of the cor-
onary vessel wall, usually separating the intima from the media. During cor-
onary angiography, it usually occurs due to injection of contrast; during PCI,
it is often the result of wire manipulation (% p.194) or balloon inflation
(% p.196).
Avoiding dissection
• The risk of coronary dissection during routine coronary angiography
is low.
• Do not advance a guide wire or catheter against resistance.
• Use gentle test injections of contrast to check positioning.
• The ostium of the LIMA is more prone to dissection and care should be
taken with catheter manipulation here.
• The risk of dissection can be reduced by taking care to ensure a normal
pressure trace before contrast injection.
• Do not inject with a damped or ventricularized trace (indicating that the
catheter tip is against the vessel wall or plaque).
• When the catheter is engaged into the ostium of the coronary artery,
care should be taken to avoid moving it, particularly advancing it up
against a plaque.
Coronary dissection is usually recognized instantly on coronary angiography
as a linear opacity within or outside of the vessel (Fig. 10.14). Patients are
usually asymptomatic unless the dissection is large enough to compromise
coronary flow. In some instances, coronary dissection results in sharp chest
pain and can develop vagal symptoms.
Classification
Coronary dissections are classified according to the US National Heart,
Lung and Blood Institute (NHLBI) classification into:
• Type A: minor radiolucent area within the coronary lumen during
contrast injection or persistence of contrast after dye has cleared.
• Type B: double-lumen appearance with bright line separating the two
lumens during contrast injection with persistence of contrast after dye
has cleared.
• Type C: contrast outside the coronary lumen, with persistence of
contrast after dye has been cleared away.
• Type D: ‘barber shop pole dissection’ with spiral lumen filling defect
during contrast injection with persistent contrast staining of the
false lumen.
• Type E: new luminal persistent filling defect during contrast injection.
• Type F: dissection associated with occlusion of the coronary artery, with
no distal antegrade flow.
Coronary dissection 301
Fig. 10.14 Dissection of the left circumflex coronary artery (Cx) complicating an

angioplasty procedure. There is a linear opacity in the vessel wall extending back into
the left main coronary artery
Management
• Do not perform any further injections of contrast.
• If coronary flow has been affected:
• Treat for coronary ischaemia with high-flow O2 and analgesia.
• Intracoronary nitrates may help associated spasm.
• Arrange urgent transfer for PCI with stent insertion or CABG.
• Small asymptomatic dissections usually settle conservatively. Consider
referring the patient to an interventional centre for repeat imaging after
a few months.
Left main stem dissection

Iatrogenic LMS dissection is particularly important because of the very large
amount of myocardium that can be suddenly jeopardized, with a high risk
of rapid haemodynamic deterioration. It is a rare complication with an in-
cidence of 0.02%.
LMS dissection can be induced by:
• Guiding catheter manipulation (especially 7 F/8 F).
• Contrast injection with guiding catheter pointing towards the roof of
the LMS.
• Wiring (more likely when using polymeric-covered and hydrophilic-
coated wires).
• Balloon dilation.
• Stent deployment (stent proximal/distal edge dissection).
Management
Even though a conservative approach could be considered in low-degree
dissections and in haemodynamically stable patients with no impairment
of antegrade flow, the unpredictable evolution of LMS dissection typically
requires intervention.
The involvement of the LMS bifurcation is a crucial element in defining the
modality of intervention:
• The more extensive the dissection (involving the bifurcation), the more
cardiac surgery becomes the reference treatment. However, if the
patient is haemodynamically unstable, it is likely that timing and logistics
for surgery are not feasible and the PCI option must be promptly
offered.
• Femoral access needs to be prepared and ready to allow for circulatory
support (IABP/Impella® % p.274).
See Table 10.1.
Left main stem dissection intervention
The challenges in PCI for LMS dissection include:
• Ensuring positioning of the guide wire in the true lumen, with double
complexity if LMS bifurcation involved, requiring both wires (LAD and
left Cx) to be in the true lumen.
Table 10.1 Left main stem dissection
Bifurcation spared Bifurcation involved

Patient stable Patient unstable Patient stable Patient unstable
PCI PCI Cardiac surgery Discuss cardiac
surgery
Conservative PCI two-stent
approach techniques PCI two-stent
techniques
Left main stem dissection 303
• IVUS can help in confirming wire position (better than OCT, since it
prevents the need for contrast injection, which may expand the false
lumen).
• Need for two-stent technique if bifurcation involved.
• In extreme cases, the simultaneous kissing stent (SKS) technique can
represent a prompt fixing to rescue a rapidly deteriorating situation.
Downsides of SKS include the need for a large-size guiding catheter and
building of a long neo-carina in the centre of the lumen of the LMS.
Iatrogenic type A aortic dissection

IA is a rare but potentially life-threatening complication of coronary inter-
vention with an incidence of 0.01%. Causes can be categorized as:
• Stent related: after stent implantation, an intimal flap can be lifted up
in the coronary artery at the proximal edge, with the possibility of
proximal propagation toward the aorta.
• Guiding catheter related: during manipulation, the guiding catheter can
tear the intima layer of the aortic wall (usually in proximity of the right
or left coronary ostia) with a false lumen filled by blood pushed at high
pressure during each systole, with a consequent risk of propagation.
See Fig. 10.15.
Management
• Compared to spontaneous type A aortic dissection, iatrogenic
dissection tends to have a more benign prognosis. The aortic wall is
indeed not intrinsically diseased (compared with other aortopathies
associated with dissection), so there is a higher degree of resistance
to the propagation of the dissection. This means that the iatrogenic
dissection tends to contain itself and eventually seals.
• A conservative approach for this reason can be considered in the first
instance.
• CT should be performed after the procedure and repeated after
24 hours to assess the extension and evolution (either healing or
propagation) of the dissection.
• When it appears clear that the dissection has started at the level of one
of the coronary ostia, stenting the ostium can eventually seal the entry
point of the dissection and facilitate its healing.
• Surgical repair should be considered in case of:
• Dissection propagation towards neck vessels with occurrence of
neurological symptoms.
• Development/worsening of pericardial effusion (sign of retrograde
propagation of the dissection towards the aortic root).
• Development of severe aortic regurgitation.
• Haemodynamic instability (possible association with tamponade,
aortic regurgitation, but also rupture of the ascending aorta).
Iatrogenic type A aortic dissection 305
Fig. 10.15 Example of right coronary artery dissection with vessel occlusion

extending proximally towards the aorta (false lumen with stain of contrast in
the aorta)
Air embolism
Coronary air embolism occurs in approximately 0.4% of coronary angiog-
raphy procedures. It has been shown to be training dependent and probably
occurs more frequently during PCI. The size of air embolism ranges from
small microbubbles that are caught up in the injection mechanism to a full
syringe of air inadvertently injected.
• The diagnosis is occasionally only made during post-procedure film
review in an asymptomatic patient (Fig. 10.16).
• Vessel occlusion depends on the size of the air bubble; small distal
vessels are predominantly affected.
• Small vessel occlusion is usually associated with symptoms of chest
discomfort, pallor, and nausea.
• Main coronary artery occlusion can occur resulting in STEMI,
cardiogenic shock, and ventricular arrhythmias.
Management
The management principles described here are based on limited case re-
ports and case series and some of the interventions themselves carry a risk
of complication. Seek expert help if required.
• Administer high flow, 100% O2 to accelerate embolus reabsorption.
• In asymptomatic patients no further treatment is usually required.
• Opiate analgesia should be given for ischaemic pain.
• Aspirate on the catheter to try and dislodge the air bubble.
• Intracoronary nitrates (% p.152) may relieve any associated spasm.
• Mechanical disruption using an angioplasty guide wire and the use of
dedicated aspiration catheters have been tried with some success.
• If the vessel remains occluded then treat the patient as for MI (% p.280).
• Consider intra-aortic balloon pumping (% p.268) in cardiogenic shock.
• Emergency coronary artery bypass surgery may be required.
Air embolism 307
Fig. 10.16 Right coronary angiography showing a large air bubble in transit. The
distal vessel subsequently occluded
Coronary perforation
This is not reported during routine diagnostic cardiac catheterization
studies but complicates 0.3% of PCI procedures. Perforation is more com-
monly seen in complex cases (CTOs, ostial lesions, tortuous vessels) and
during PCI that include debulking procedures (atherectomy). Half of cases
are guide wire related.
• The diagnosis is usually immediately visible on angiography with leakage
of contrast out of the vessel (Fig. 10.17).
• Some cases, however, present insidiously with progressive hypotension
and cardiac tamponade back on the ward.
• Bleeding into the pericardium can rapidly result in cardiac tamponade
(% p.284) with cardiovascular collapse. Immediate pericardiocentesis
(% p.254) should be performed.
Management
• If perforation is recognized during PCI then the culprit vessel should be
immediately occluded using a balloon to prevent further bleeding.
• Prolonged balloon inflation may be required. Perfusion balloons are
available to reduce downstream ischaemia.
• If patients are anticoagulated then consider reversing heparinization
with protamine (% p.285) and giving platelets if the glycoprotein IIb/IIIa
antagonist ReoPro® has been given.
• Covered stents have been used to seal the site of perforation.
• Coil embolization can be successful in small vessel leaks (Fig. 10.18).
Coronary perforation 309
Fig. 10.17 Perforation of the left anterior descending (LAD) coronary artery just
distal to a large stent. There is free flow of contrast into the pericardial space. Cx,
circumflex coronary artery
Fig. 10.18 Coil embolization (left) of a diagonal (diag) branch of the left anterior
descending (LAD) coronary artery. There is a distal perforation with blood leaking
into the pericardium. A series of small highly thrombogenic coils are inserted
through a catheter into the diagonal branch. Repeat coronary angiography (right) the
following day reveals successful occlusion of the vessel
Renal failure
Renal failure complicating cardiac catheterization is usually a result of con-
trast nephropathy but can be a result of cholesterol embolization (% p.314)
or administration of other nephrotoxic medication (e.g. aminoglycosides).
Transient renal dysfunction complicates up to 15% of cases during coronary
intervention. About 7 in 1000 will develop acute kidney injury requiring
renal support.
Renal failure 311
Contrast nephropathy
Contrast nephropathy is more common in patients with pre-existing renal
dysfunction and in patients with diabetes mellitus. It is also more likely in
patients with:
• Increasing age.
• Hypertension.
• Hypovolaemia.
• Congestive cardiac failure.
• Peripheral vascular disease.
• High contrast volumes used.
Avoiding contrast nephropathy
Identify patients at risk and:
• Hydrate with 0.45–0.9% saline at 1 mL/kg/hour for 12 hours before
and for 12 hours after the procedure.
• Withhold nephrotoxic medication if possible.
• Use small amounts of contrast for angiography.
• Consider biplane imaging (% p.98) to reduce contrast load.
• Consider a non-ionic, hypo-or iso-osmolar contrast medium (% p.79).
• Consider four, 12-hourly doses of N-acetylcysteine 600 mg starting the
day before the procedure in patients with severe renal dysfunction.
• An alternative (or adjunct) is an infusion of sodium bicarbonate, starting
1 hour before the procedure.
Usually asymptomatic. Contrast nephropathy is defined as a rise in serum
creatinine of 44 µmol/L (0.5 mg/dL) or by more than 25% of the base-
line level at 24–48 hours post procedure. Creatinine peaks 4–5 days after
contrast exposure so relying on blood tests at 48 hours may miss some
episodes of contrast nephropathy.
Management
Renal function usually gradually returns to baseline over a week. Less than
1% of patients develop irreversible dialysis-dependent renal failure.
Importance of contrast-induced nephropathy

• Significance of minor rises in creatinine has yet to be proven.
• Dialysis-requiring acute kidney injury after angiography carries a high
mortality (35% at 1 year).
• Increases of creatinine of 25% or more confer excess mortality risk
even in the absence of acute kidney injury, as well as a significantly
increased risk of sepsis and bleeding.
• However, measures to combat nephropathy have yet to be shown to
ameliorate these risks.
Contrast nephropathy 313
Further reading
Recio-Mayoral A, Chaparro M, Prado B, et al. The reno-protective effect of hydration with so-
dium bicarbonate plus N-acetylcysteine in patients undergoing emergency percutaneous coronary
intervention. J Am Coll Cardiol 2007; 49: 1283–88.
Schweiger MJ, Chambers CE, Davidson CJ, et al. Prevention of contrast-induced nephropathy: re-
commendations for the high risk patient undergoing cardiovascular procedures. Catheter
Cardiovasc Interv 2007; 69: 135–40.
Cholesterol embolization
Distal showers of cholesterol crystals from disrupted atherosclerotic plaque
result in systemic complications in the brain, eyes, kidneys, and extremities.
It typically occurs during manipulation of catheters in the aorta of patients
with widespread atheroma. It is more common in patients with aortic an-
eurysm and in those with cerebrovascular disease. Cholesterol emboliza-
tion may be underdiagnosed in routine practice. Prospective series suggest
the incidence may be as high as 1.4% during routine diagnostic coronary
angiography.
Avoiding cholesterol embolization
As the mechanism of embolization is usually mechanical, disruption of ath-
erosclerotic plaques can be minimized by careful catheter manipulation
within the aorta and the use of guide wires to exchange catheters. Use soft-
tip catheters and avoid high-pressure injections against vessel walls.
• Cutaneous symptoms and signs—livedo reticularis, blue toe syndrome,
and digital gangrene.
• Visual disturbance and neurological deficits.
• Renal impairment (persisting after 2 weeks).
• Eosinophil count often rises acutely.
• Tissue biopsy will demonstrate cholesterol crystals in occluded
arterioles.
Management
• Management is supportive.
• Careful hydration and control of blood pressure.
• Surgery is rarely required for distal ischaemia.
• Enlist expert renal advice for severe renal dysfunction.
• The use of anticoagulants, statins, and steroids is controversial.
• The prognosis of patients with multisystem cholesterol embolization is
poor (up to 90% die within 3 months).
315
Chapter 
Post procedure
Nursing care 316
The patient 317
Results 318
Communication 319
Discharge plans 320
Discharge summary 321
316 Chapter  Post procedure
Nursing care
Most catheterization units will have a dedicated ward or day-case unit for
patients to be admitted to, and recover in, after the procedure. These are
usually staffed by specialist nurses who are trained to care for patients at the
time of a cardiac catheterization study. They will have some responsibility
for checking the patient in, recording medication, checking observations,
and discussing the procedure. Importantly, they are immediately available
when the patient returns after the procedure to observe for complications
(% p.35) and can help with arterial and venous line removal if required
(% p.55).
The patient 317
The patient
• Once the patient has returned to the ward it is important that nursing
staff are handed over information about:
• The procedure performed (and by whom).
• Any difficulties or complications that may have arisen.
• Medication, anticoagulation, or sedation used.
• Access sites, closure devices, lines in situ, and timing(s) of their
removal.
• The patient should have their pulse and blood pressure measurements
checked and documented immediately on arrival on the ward.
• A quick neurological assessment should take place to exclude any
neurological event that may have occurred during transfer.
• Arterial and venous access sites should be examined for bleeding or
bruising and if sheaths are still in place, a plan made for line removal
(% p.55).
• Regular observations should include pulse, blood pressure, and oxygen
saturations, particularly if the patient has received sedation (% p.23).
• An ECG should be recorded in patients who have had complex PCI to
help diagnose procedural myocardial infarction (% p.280).
• In patients with known or suspected renal dysfunction, a record of urine
output should be made and blood tests may be requested to assess any
change in renal function.
Becoming ambulant
• Following cardiac catheterization, most patients need to rest and be
observed for a short period of time.
• With radial access in particular (% p.50), percutaneous vascular
closure devices (% p.68) and with smaller femoral sheaths (% p.68),
the time before becoming ambulant can be short (1 hour).
• A plan should be established for when the patient is able to sit up and
become ambulant and when they are allowed to eat and drink.
• This advice will vary according to local institutional practice and the
choice of access sites, size of punctures, and venous/arterial access.
• As a guide, patients with a 6 F femoral arterial puncture are
encouraged to lie flat for an hour after line removal and only mobilize
2½ hours following line removal.
Results
After a cardiac catheterization study, it is important to review all of the data
regarding the case. These include the clinical indication for the test, the diag-
nostic information obtained from the case, and any additional information
obtained during the patient’s admission. These review sessions are excellent
educational and training opportunities and all members of the team should
be invited to participate.
• For diagnostic angiography and PCI, each stored loop of images should
be examined and complications (such as dissection or embolism)
excluded.
• Quantification of vessel stenosis should be reassessed (% p.209).
• Haemodynamic data should be examined and results noted.
• Blood results should be made available for comment, particularly renal
function and cholesterol and glucose levels.
• In patients who have undergone complex PCI, the ECG and a cardiac
troponin level may need to be checked to exclude significant myocardial
injury (% p.280).
Communication 319
Communication
Once the coronary anatomy and results of the study have been examined,
it is important to communicate the findings to the patient and their relatives.
• Remember that some patients may have had sedation. Telling someone
their results while they are still sedated with midazolam is unhelpful.
• Find somewhere quiet and away from other patients to discuss
sensitive findings. For example, breaking the news that bypass surgery is
necessary in a ward full of other patients is inappropriate.
• Check that patients are comfortable with other family members or
friends being there for the consultation. If not, then ask them to leave.
• Talk through the procedure and ask the patient how they found the
experience—it may help you adjust your practice for future cases.
• Discuss the results and explain medical terms in a way that is
non-technical.
• Drawing diagrams of coronary anatomy improves patient understanding
and it also allows them to review the findings later and show family
when they get home.
• Give the patient time to ask questions.
• Offer information sheets or point them towards websites for more
information.
• If they are being referred for further treatment (e.g. CABG), try and
indicate a likely timeframe within which it may happen.
• Review all medications with the patient—there may be drugs that can
be stopped. Tell them why they may be starting new tablets and how
long they should be continued for. This is particularly important for
drugs like clopidogrel (% p.218).
• Finally, document your consultation in the medical notes.
Discharge plans
Before admission to hospital, a plan should have been made for the ex-
pected duration of hospital stay. Most diagnostic procedures can now be
performed as a day case, but some more complex cases are electively ad-
mitted for overnight observation.
• Check that the patient is fully ambulant and that arterial and venous
access sites are satisfactory.
• Patients should be advised to have someone at home with them on the
evening of discharge in case of difficulties.
• The patient should be instructed when they are allowed to drive (usually
at least 24 hours after arterial puncture) and when they should return
to work.
• Patients with renal dysfunction or patients restarting anticoagulation
therapy should have instructions on when to have blood tests repeated.
• Give the patient a telephone number they can call for advice when they
go home (e.g. coronary care unit).
Discharge summary 321
Discharge summary
Unfortunately, this is often poorly completed and occasionally given just
brief thought. Without a full discharge summary, however, the referring
doctor and general practitioner may have little idea about the heroic pro-
cedure that the patient has undergone. Clear communication is vital for
effective, safe patient management.
• When the patient leaves the department, they should be issued a
discharge note indicating what procedure(s) they have had and any
important points of communication (e.g. drug changes).
• If there are important points that need communication (e.g. blood tests
for renal function that need arranging) then call the necessary personnel
and let them know.
• The discharge note should be followed up as quickly as possible (ideally
on the day of discharge) with a formal and comprehensive typed
discharge summary indicating as a minimum:
• A diagnosis.
• Date of and summary of procedure.
• A subsequent management plan.
• Full list of medications including any changes.
• Follow-up arrangements.
323
Index
Notes Abbreviations used in the index can be found in the symbols and abbreviations table
vs. indicates a comparison Tables, figures and boxes are indicated by t, f and b following the
page number
A anaphylaxis, contrast
agents, 286b
aorta
ascending see ascending
abciximab, 224 angiography aorta enlargement
abdominal aortic bypass graft coarctation of the
aneurysm, 47 angiography, 168 aorta, 47
abdominal X-ray, radiation coronary angiography see iatrogenic type A aortic
risk, 16t coronary angiography dissection, 304, 305f
Absorb® BVS 1.0 (Abbot diagnostic angiography vs. aortic pressure wave, 89
Vascular), 204 PCI, 188 aortic regurgitation, 111
Academic Research Council, femoral artery access, 55 aortic stenosis, 108,
206, 207t iliofemoral 109f, 109t
ACC see American College angiography, 110b aortic valve
of Cardiology (ACC)/ invasive angiography, 8 area calculation, 95, 108
American Heart left ventricular angiog- crossing in aortic stenosis,
Association (AHA) raphy, 127f, 127 108b, 109f
access route, TAVI, 110 pulmonary angiography, left heart catheterization,
accredited training, 116f, 119f, 119 87b, 87f
cardiologists, 29 quantitative coronary see also transcatheter
acquisition (cine) angiography, 156 aortic valve
fluoroscopy, 12 radial artery access, 50, 52f intervention (TAVI)
activated clotting time angioplasty balloons, 196 aortic waveforms, 74
(ACT), 55 angioplasty guide wires, 194 aortography, 166b, 167f
acute ST myocardial infarc- characteristics, 194 cardiac catheterization,
tion, coronary angiog- construction, 194 104f, 104, 105f
raphy indications, 6 preparation and place- apprenticeships, 28
adenosine ment, 195b, 195f, 195 AP (anteroposterior)
fractional flow reserve selection, 194 view, left heart
measurements, 214 Angio-Seal® (St Jude catheterization, 86
supraventricular Medical), 68, 69f, 296 AR-MOD (modified
tachycardia, 290 angle of projection, cor- Amplatz) catheters,
AHA see American College onary angiography, 158 83f, 132
of Cardiology (ACC)/ anteroposterior (AP) arrhythmias, 288f, 288
American Heart view, left heart arterial closure devices,
Association (AHA) catheterization, 86 68, 69f
air embolism, 306, 307f anticoagulation therapy, arterial vascular access, 46
ALARA (as low as reason- 64, 224 coronary artery bypass
ably achievable), radi- arterial vascular access, 47 grafts, 46
ation safety, 15 cardiac femoral artery see femoral
Allen test, 52b catheterization, 64 artery access
ambulant post patient protection, 20 radial artery see radial
procedure, 317 antiplatelet therapy, artery access
American College of 218, 219f arteriovenous fistula, 294
Cardiology (ACC)/ dual therapy, 222t ascending aorta
American Heart duration of therapy, 221t enlargement, 131f
Association (AHA) interruption of aortography, 104f
coronary angiography therapy, 222t ASD (atrial septal defect),
indications, 6 new challenges, 220 120f, 120
lesion classification, patient protection, 20 as low as reasonably achiev-
190, 191t switching between, 220t able (ALARA), radiation
amiodarone, 288 antiproliferative agents, safety, 15
Amplatz left catheters, 83f drug-eluting stents, 202 aspiration catheters, 252
324 INDEX
aspirin, 218 flush infusion, 76 cardiac catheterization,

interruption of guide wires, 76 82f, 82, 83f, 84f
therapy, 222t manifolds, 76 coronary angiography,
ASSENT trial, 230 pressure injector, 76 132, 134
atherectomy cardiac computed French catheters, 82f
orbital atherectomy, 250 tomography guide catheters see guide
rotational atherectomy contraindications, 9 catheters
see rotational indications for, 8 IABP, 269f
atherectomy invasive angiography vs., 8 intra-aortic balloon
atrial fibrillation, 289f, 289 transcatheter aortic valve pump, 269f
atrial septal defect (ASD), intervention, 9 Judkins left catheters,
120f, 120 cardiac magnetic resonance 82f, 132
AutoPulse® (Zoll Medical), imaging, 8 Judkins right
262, 263f cardiac output catheters, 82f
calculation, 94 knotting in right heart
cardiac physiologists, 38 catheterization, 91b
B damping, 40 left coronary artery, 132
background radiation, 14 electrocardiography, 39 left coronary bypass
barium enema, 16t pressure tracings, 39 (LCB) catheters, 168
bifurcation percutaneous recording/ left coronary extra-
coronary intervention, documentation, 40 support catheter, 192f
236f, 236, 238, 239f roles, 38 modified Amplatz (AR
biological effects, cardiac tamponade, MOD) catheters,
radiation, 14 284f, 284 83f, 132
bioresorbable scaffolds cardiac waveforms, 74 multipurpose
(BRS), 204 cardiogenic stock, primary catheters, 84f
bivalirudin, 224 PCI, 231 Pigtail left catheters, 83f
bradycardia, 291f, 291 cardiologists, 26 Pigtail right catheters, 83f
Brockenbrough sign, certification, 30 radial catheters, 8
125b, 125f intra-procedural care, 26 right coronary bypass
bypass graft logbooks, 29 (RCB) catheters, 168
angiography, 168 post-procedural care, 27 Sones catheters, 83f
bypass graft catheters, 84f pre-procedural care, 26 TIG catheter, 136
role, 26 ventriculography, 97
training, 27 Williams (3DRC)
C Cardiology Audit and catheter, 132
CABG see coronary artery Registration Data Williams (3DRC)
bypass grafts (CABG) Standards (CARDS), 29 catheters, 83f
CAD (coronary artery cardiomyopathies, catheter-tip spasm, 152,
disease), 158 124f, 124 153f, 159
calibre/size, guide cardiomyopathy certification,
catheters, 193 hypertrophic cardiomy- cardiologists, 30
cardiac arrest, STEMI, 230 opathy, 124f, 124 CHD (coronary heart
cardiac catheterization, 72 restrictive disease), 6
anticoagulation cardiomyopathy, 124 chest X-ray, patient radi-
therapy, 64 Takotsubo cardiomyop- ation risk, 16t
aortography, 104f, athy, 127f, 127 CHIP (complex high-risk
104, 105f cardiopulmonary resuscita- indicated patients),
calculations, 94 tion (CPR), 262 264, 265
definition, 2 mechanical see mechan- cholesterol
history of, 3 ical cardiopulmonary embolization, 314
indications for, 4 resuscitation chronic total occlusion
left heart, 72, 86f, 86, 87f cardioversion, 260, 261f percutaneous coronary
right heart see right heart CARESS-AMI trial, 230 intervention (CTO
catheterization catheter laboratory PCI), 242, 243f
ventriculography see preparation, 22 cine (acquisition)
ventriculography catheters fluoroscopy, 12
cardiac catheterization Amplatz left circulating nurses, 32
equipment, 76 catheters, 83f circumflex coronary
catheters, 82f, 82, 83f, 84f aspiration catheters, 252 artery, 131f
contrast media see bypass graft catheters, 84f anomalous origin, 160
contrast media CABG, 168 grafts, 171f, 171
INDEX 325
normal anatomy, 158 physiological response, 80 saphenous vein grafts

side branches of, 158 reaction to, 286 see saphenous vein
circumflex vessel (Cx), side effects, 79 grafts (SVGs)
saphenous vein underuse of, 159 coronary artery disease
grafts, 169f ventriculography, 98 (CAD), 158
class 1 indications, coronary viscosity, 79 coronary artery imaging,
angiography, 6 contrast nephropathy, 312 138, 139t, 140f, 141f,
clopidogrel, 218, 222t conus branch of right cor- 142f, 143f, 144f, 145f,
closed-cell stent onary artery, 136b 146f, 147f, 148f, 149f,
design, 199f core curriculum, cardiolo- 150f, 151f
coarctation of the aorta, gist training, 28 Oxford University
47, 105f, 105 coronary anatomy, 130 Hospitals imaging
coated guide wires, 194 unusual types, 160, 161f sequence, 139
collagen plug closure de- coronary angiography, 129 coronary artery spasm,
vices, 68, 69f catheter choice, 132 myocardial infarction
collateral filling, CABG, catheter with non-obstructed
177f, 177 manipulation, 134 coronary arteries, 126
COMFORTABLE AMI common pitfalls, 159 coronary dissection,
trials, 228 coronary artery 300, 301f
common femoral imaging, 138 coronary heart disease
artery, 54f definition, 2 (CHD), 6
communication post indications, 6 coronary perforation, 307f,
procedure, 319 interpretation, 158 308, 309f
COMPARE ACUTE left internal mammary coronary spasm,
study, 232 artery, 179f nitrates, 152
competitive filling, CABG, limitations of, 154 Cournaud, André, 3
176f, 176 nitrates, 152 CPR (cardiopulmonary
complete revascularization, normal vessel resuscitation), 262
multivessel PCI, 234 anatomy, 158 CRISP-AMI trial, 231
complex high-risk indi- orientation and crush stenting, bifurcation
cated patients (CHIP), nomenclature, 158 PCI, 238, 239f
264, 265 patient radiation risk, 16t CSI Diamond 360®
complex percutaneous cor- stenoses quantification, Coronary Orbital
onary intervention, 225 154, 155f Atherectomy
compliance, angioplasty valve assessment, 6 System, 250
balloons, 196 coronary arteries CTO-PCI (chronic total
complications of cardiac anomalous origin, 160 occlusion percutaneous
surgery, 278 imaging see coronary coronary intervention),
CompressARTM (Advanced artery imaging 242, 243f
Vascular Dynamics), 66 single, 162 culotte stenting, bifurcation
compression devices, 66f, coronary artery by- PCI, 238, 239f
66, 67f pass grafts (CABG), culprit-only percutaneous
computed 165, 167f coronary intervention,
tomography (CT) arterial grafts, 178 non-culprit PCI vs., 232
cardiac see cardiac com- arterial vascular CULPRIT SHOCK
puted tomography access, 46 trial, 231
patient radiation risk, 16t catheter choice, 168 cutting balloon angioplasty,
consent, PCI, 208 collateral filling, 197f, 197
constrictive pericarditis, 177f, 177 CvLPRIT study, 232
122f, 122 competitive filling,
construction, angioplasty 176f, 176
guide wires, 194 gastroepiploic artery, D
contrast media, 78f, 78 181f, 181 damping
characteristics, 79 graft location, 168, 169f cardiac physiologists, 40
coronary artery left internal mammary coronary angiography,
imaging, 138 artery, 178, 179f 134b, 135f
dose-dependent patency rates, 166, 166t DANAMI-DEFER trial, 229
reactions, 79 PCI vs., 234 DANAMI PRIMULTI
idiosyncratic reactions, 79 procedure, 168 study, 232
ionic vs. non-ionic radial artery, 181 death, 279
agents, 79 right internal mammary documentation, 279
osmolarity, 79 artery, 180f, 180 reporting, 279
326 INDEX
deferred stenting, imme- extracorporeal life support ventriculography,

diate stenting vs., 228 (ECLS), 276 100, 101f
defibrillation, 260 extracorporeal mem- glyceryl trinitrate
DES (drug-eluting stents), brane oxygenation (GTN), 152
202, 238 (ECMO), 276 intravascular
diabetes mellitus, 21 ultrasound, 210
diagnostic angiography, PCI radial artery access, 50
vs., 188 F glycoprotein IIb/IIIa
diatrizoate (Hypaque® facilitated percutaneous antagonists, 224
50), 78f coronary intervention, Gorlin formula, 95
diazepam, 23b pharmaco-invasive Grüntzig, Andreas, 3,
direct oral anticoagulants strategy vs., 230 184, 185f
(DOACs), 65 faints (vasovagal GTN see glyceryl
discharge plans, 320 reaction), 287 trinitrate (GTN)
discharge summary, 321 fellowships, 28 guide catheters
distal protection devices, femoral artery access, 54 iatrogenic type A aortic
vein graft PCI, 244b anatomy, 54f, 54, 55f dissection, 304
documentation angiography, 55 PCI, 192f, 192, 193t
cardiac physiologists, 40 complications, 56 guide wires
death, 279 line removal, 55 angioplasty see angio-
DOSCs (direct oral monitoring by nurses, 36 plasty guide wires
anticoagulants), 65 procedural approach, 54 cardiac catheterization, 76
dose-dependent reactions, femoral compression de-
contrast media, 79 vices, 66f, 66
dosimetric quantities, radi- femoral vein, 54f H
ation safety, 14 access, 59 haematoma
Dotter, Charles, 184 FemoStop® (RADI Medical forearm haematoma, 52
drug-eluting stents (DES), Systems), 66f, 66 local haematoma, 52
202, 238 FFR see fractional flow retroperitoneal
dual antiplatelet reserve (FFR) haematoma, 294
therapy, 222t Fick method, 94 haemorrhage, 294
FINESSE trial, 230 heart block, 291f,
first-degree AV block, 291, 292f
E 291f, 291 HEAT-PCI trial, 228
echocardiography fistulae, coronary heparin, 224
stress echocardiography, 8 arteries, 162 atrial fibrillation, 289, 290
transoesophageal flat-panel detectors, 11 protamine sulphate as
echocardiography, floppy guide wires, 194 antagonist, 285b
120f, 120 fluoroscopy, 12 radial artery access, 50
transthoracic echocardi- flush infusion, cardiac saline flush infusion, 76
ography, 123f catheterization, 76 Hexabrix® (ioxaglate), 78f
ventriculography vs., 96b forearm haematoma, radial high approach, internal
ejection fraction (EF) artery access, 52 jugular vein access, 61
calculation,  100–1 formal learning, cardiologist high-risk plaque, OCT, 217
elasticity, guide wires, 194 training, 28 history, patient
electrocardiography Forssmann, Werner, 3 protection, 20
(ECG), 39 fractional flow Hypaque® 50
end-diastolic volume (EDV) reserve (FFR) (diatrizoate), 78f
calculation,  100–1 interpretation, 214b hypertrophic cardiomyop-
endomyocardial biopsy, intravenous wave-free athy, 124f, 124
258, 259f ratio (iFR) vs., 213 hypotension, 283
end systolic volume (ESV) measurements, 214
calculation,  100–1 pressure wire, 212
epinephrine, 286b FREEDOM study, 234 I
European Association French catheters, 82f IABP see intra-aortic bal-
of Percutaneous loon pump (IABP)
Cardiovascular iatrogenic type A aortic
Interventions G dissection, 304, 305f
(EAPCI),  27–8 gastroepiploic artery, idiosyncratic reactions,
EXAMINATION trial, 228 CABG, 181f, 181 contrast media, 79
external (transcutaneous) global left ventricular iFR see intravenous wave-
temporary pacing, 257 function, left free ratio (iFR)
INDEX 327
iliofemoral angiography, inverse square law, 15 left ventriculography, 98,

TAVI, 110b investigations, patient 99f, 100f
image intensifiers, 11 protection, 20 right coronary artery
image planes, coronary ar- iobitridol (Xenetix®), 78f imaging, 148f, 148
tery imaging, 138, 139t, iodixanol (VisiplaqueTM), 78f left atrial pressure wave, 89
140f, 141f, 142f, 143f, iohexol (OmnipaqueTM), 78f left circumflex (Cx) cor-
144f, 145f, 146f, 147f, Ionising Radiation (Medical onary artery, 130
148f, 149f, 150f, 151f Exposure) Regulations anomalous anatomy, 161f
immediate stenting, de- 2017, 15b left coronary artery (LCA)
ferred stenting vs., 228 iopamidol (Isovue®), 78f anatomy, 130
Impella®, 274, 275f iopromide (Ultravist®), 78f angiography, 140f, 140,
Impella® RP-system, 275f iotrolan (Isovist®), 78f 141f, 142f, 143f, 144f,
inadequate projec- ioversol (Optiray®), 78f 145f, 146f, 147f
tions, coronary ioxaglate (Hexabrix®), 78f aortography, 104f
angiography, 159 IRA (infarct-related cor- catheter choice, 132
incorrect projections, coronary artery), 226 Oxford University
onary angiography, 159 ISDN (isosorbide Hospitals imaging
infarct-related coronary dinitrate), 152 sequence, 139
artery (IRA), 226 isosorbide dinitrate saphenous vein
infections, 295 (ISDN), 152 grafts, 169f
inferior vena cava, right Isovist® (iotrolan), 78f left coronary bypass (LCB)
heart catheterization, Isovue® (iopamidol), 78f catheters, 168
91f, 91 IVUS see intravascular left coronary extra-support
inflammation, PCI ultrasound (IVUS) catheter, 192f
restenosis, 200 left heart catheterization,
inguinal canal, 54f 72, 86f, 86, 87f
inguinal ligament, 54f J left heart pressures and
internal jugular vein access, Judkins left (JL) catheters, waveforms, 88f, 88
60f, 60 82f, 132 left internal mammary
internal suture-based Judkins, Melvin, 184 artery (LIMA), 46
devices, 296 Judkins right catheters, 82f access to, 178
intra-aortic balloon pump CABG, 178, 179f
(IABP), 268 cannulation
augmented diastolic K difficulties, 180
flow, 269f kissing inflations, 237f, 237 coronary
catheter, 269f Kussmaul’s sign, 122 angiography, 179f
indications/ LAD anastomosis, 179f
contraindications, 269b left lateral (90º/0º) view,
insertion tips, 270, 271f L left coronary artery
sizing, 268 late-lumen loss (LLL), 203 imaging, 145f, 145
timing, 270, 272f, 273f LCA see left coronary left main stem (LMS) cor-
transport, 270 artery (LCA) onary artery, 130, 134
intracoronary stents, LCB (left coronary bypass) dissection, 302, 302t
198, 199f catheters, 168 PCI, 240, 241f
intra-procedural care, lead equivalent (LE), 15 left subclavian artery
cardiologists, 26, 28 left anterior descending access, 178
intravascular ultrasound (LAD) coronary artery, left ventricular angiography,
(IVUS), 210, 211f 130, 131f 127f, 127
left main stem PCI, 240 branches of, 158 left ventricular end-diastolic
optical coherence tom- grafts, 170f, 170 pressure (LVEDP),
ography vs., 216, left internal mam- 80, 89b
216t, 217 mary artery mitral stenosis, 112f, 112
intravenous wave-free anastomosis, 179f left ventricular filling
ratio (iFR) saphenous vein pressure, 89b
fractional flow reserve grafts, 169f left ventricular pressure
vs., 213 left anterior oblique (LAO) (LVP), 114f
interpretation, 214b projection left ventricular thrombus,
measurement, 214 caudal (50º/-30º) projec- 101, 102f
pressure wire, 212 tion, 144f, 144 left ventriculography, 96
invasive angiography, cranial (50º/20º) pro- difficulties with, 98
cardiac computed jection, 143f, 143, global left ventricular
tomography vs., 8 150f, 150 function, 100, 101f
328 INDEX
left ventriculography, mechanical circulatory National Institutes

(Contd.) support (MCS) devices, of Health (NIH)
left ventricular thrombus, 262, 264f catheters, 84f
101, 102f mechanical injector neointima formation, PCI
regional wall motion, 101 pumps, 76 restenosis, 200
ventricular septal defect, Medirad® injector, 76 NHLBI (National Heart,
121f, 121 metoprolol, 288 Lung and Blood
views, 98, 99f, 100f MI (myocardial Institute), 300
lesion severity, stenoses infarction), 280 NIH (National Institutes of
quantification, 154, 155f mid approach, internal Health) catheters, 84f
lidocaine jugular vein access, 61 nitrates
femoral artery access, 54 midazolam, 23b coronary
femoral vein acces, 59 MINOCA (myocardial angiography, 152
subclavian vein access, 62 infarction with non- intraoperative administra-
LIMA see left internal mam- obstructed coronary tion, 152, 153f
mary artery (LIMA) arteries), 126 no-flow phenomenon,
limb ischaemia, 296 mitral regurgitation, 114f, PCI, 246
lower limb acute 114, 115f non-culprit percutaneous
ischaemia, 296 mitral stenosis, 112f, coronary intervention,
upper limb acute is- 112, 113t culprit-only PCI vs., 232
chaemia, 297f, 297 mitral valve area NORSTENT trial, 228
line removal calculation, 95 nurses, 32
femoral artery access, 55 mixed venous saturation patient checks, 33
radial artery access, 50 calculation, 95 post-procedural care, 35
lithoplasty balloon, 250 Mobitz type I AV block, sedation, 35
LLL (late-lumen loss), 203 292f, 292 sign out, 34
load-distributing band Mobitz type II AV block, training, 33
based cardiopulmonary 292f, 292 nursing care,
resuscitation, 262, 263f modified Amplatz (AR post-procedure,  316
local haematoma, 52 MOD) catheters,
83f, 132
logbooks, cardiologists, 29
long-term patency, saphe- modular intracoronary O
nous vein grafts, 173 stents, 198, 199f OmnipaqueTM (iohexol), 78f
lower limb acute monorail angioplasty open-cell/modular stent
ischaemia, 296 balloons, 196f design, 199f
Lucas® (Physio-Control ‘over-the-wire’ angio- optical coherence tomog-
Inc), 262, 263f plasty balloons vs., 196 raphy (OCT), 216
lumbar spine X-ray, 16t multipurpose catheters, 84f indications, 217
LVEDP see left ventricular multivessel percutaneous intravascular ultrasound
end-diastolic pressure coronary intervention, vs., 216, 216t, 217
(LVEDP) 231, 234 Optiray® (ioversol), 78f
LV Impella®, 274, 275f technical aspects, 234 orbital atherectomy, 250
LVP (left ventricular myocardial bridging, cor- osmolarity, contrast
pressure), 114f onary arteries, 163 media, 79
myocardial infarction overdrive pacing,
(MI), 280 arrhythmias, 289
M see also ST-segment ‘over-the-wire’ (OTW)
Magmaris® (Biotronik), 204 elevation myocardial angioplasty balloons,
magnesium-based infarction (STEMI) monorail angioplasty
bioresorbable myocardial infarction balloons vs., 196
scaffolds, 204 with non-obstructed Oxford University
magnetic resonance imaging coronary arteries Hospitals imaging
(MRI), 8 (MINOCA), 126 sequence, 139
manifolds, cardiac myocarditis, 126
catheterization, 76
P
MATRIX trial, 228
mechanical cardiopul- N paclitaxel, 202
monary resuscitation, N-acetyl cysteine Palmaz, Julio, 184
262, 263f (NAC), 312 Palmaz–Schatz stent, 199f
choice of, 265f National Heart, Lung paradoxical embolus, 126
haemodynamic and Blood Institute patients
features, 266 (NHLBI), 300 check by nurses, 33
INDEX 329
post-procedure saphenous vein graft pressure injectors, 76, 77f

care, 317 failure treatment, 174 pressure tracings, cardiac
preparation, 22 stent positioning, physiologists, 39
protection of, 20 209f, 209 pressure waveforms,
radiation safety, 16, 16t stent thrombosis, 74, 75f
selection for PCI, 208 206, 207f pressure wire, 212, 213f
self-care,  36 vein graft, 244, 245f primary percutaneous
PCI see percutaneous cor- pericardial tamponade, coronary intervention,
onary intervention (PCI) 123f, 123 228, 229f
PCWP see pulmonary pericardiocentesis, cardiogenic stock, 231
capillary wedge 254, 255f left ventricle loading vs.
pressure (PCWP) equipment, 255b unloading, 231
Perclose ProGlide® (Abbott peripheral arterial vascular multi vessel disease, 232
Vascular), 68 access, 46 ProGlideTM, 296
percutaneous coronary personnel, preparation, 22 protamine sulphate, 285b
intervention (PCI), 183 PET (positron emission provisional T-stenting, bi-
angioplasty balloons, 196 tomography), 8 furcation PCI, 238, 239f
angioplasty guide wires pharmaco-invasive strategy, Prussian helmet sign,
see angioplasty facilitated PCI vs., 230 108b, 109f
guide wires pharmacological procoagu- pseudoaneurysm, 294, 295f
antithrombotic effects, lant patches, 68 pullback trace,
218, 219f Pigtail left catheters, 83f hypertrophic
bifurcation lesions, Pigtail right catheters, 83f cardiomyopathy, 124f
236f, 236 piston-based cardiopul- pulmonary angiography,
bifurcation techniques, monary resuscitation, 116f, 119f, 119
238, 239f 262, 263f pulmonary capillary wedge
bioresorbable plaque rupture, 126 pressure (PCWP), 93f
scaffolds, 204 PLATO study, 220 mitral regurgitation, 114f
CABG vs., 234 polymer-based mitral stenosis,
chronic total occlusion, bioresorbable 112f, 112
242, 243f scaffolds, 204 pulmonary embolism, 118
consent, 208 positron emission tomog- pulmonary oedema, 281
development, 184 raphy (PET), 8 pulmonary regurgitation,
diabetic patients, 235b posterioantral (PA) 116f, 116
diagnostic angiography projection pulmonary stenosis, 116
vs., 188 caudal (0º/-30º), pulmonary valve
drug-eluting stents, 202 142f, 142 disease, 116
guide catheters, 192f, cranial (0º/40º), 141f, pulmonary vascular resist-
192, 193t 141, 151f, 151 ance calculation, 95
history, 184, 185f left coronary artery impulse fluoroscopy, 12
indications for, 186 aging, 140f, 140 push, angioplasty guide
intracoronary stents, posterior descending cor- wires, 194
198, 199f onary artery, 131f
left main stem, 240, 241f posterior pulmonary
lesion classification, angiogram, 116f Q
190, 191t post-procedural care, 315 quantitative coronary
lesion imaging, 188 cardiologists, 27, 28 angiography, 156
multivessel see multivessel nurses, 35
percutaneous cor- post-procedural loss of
onary intervention radial pulse, 52 R
myocardial infarction, 226 PRAM study, 232 radial access, 48
no-flow prasugrel, 219 monitoring by nurses, 35
phenomenon, 246 interruption of radial artery, CABG, 181
non-culprit vs. culprit-only therapy, 222t radial artery access, 50
PCI, 232 pre-hospital care, anatomy, 50, 51f
patient selection, 208 STEMI, 226 angiography, 50, 52f
primary see primary per- pre-medication,  23b complications, 52
cutaneous coronary preparation of line removal, 50
intervention equipment, 22 procedural approach, 50
radiography, 188, 189t pre-procedural care, 26, 28 snuff box radial approach,
recommendations, 186 pressure gradients, aortic 53f, 53
restenosis, 200, 201f stenosis, 108, 109f radial artery spasm, 52
330 INDEX
radial catheters, coronary right coronary artery SCAI (Society for

angiography, 8 imaging, 149f, 149 Cardiovascular
radial compression devices, right atrial pressure wave Angiography and
66, 67f form, 93f Interventions),
radiation protection, 15 right coronary artery 190, 191t
radiation safety, 14 (RCA), 131f, 132 Schatz, Richard, 184
ALARA (as low anatomy, 130, 131f scrub nurses, 32
as reasonably angiography, 148f, 148, sealing plug-based de-
achievable), 15 149f, 150f, 151f vices, lower limb acute
biological effects, 14 aortography, 104f ischaemia, 296
dose excess, 18, 18t coronary second-degree AV block
dosimetric quantities, 14 angiography, 135 (Mobitz type I),
patient risk, 16, 16t grafts, 172f, 172 292f, 292
protection, 15 marginal branches, 158 second-degree AV block
radiographers, 42 normal anatomy, 158 (Mobitz type II),
radiographic contrast Oxford University 292f, 292
media, 78 Hospitals imaging sedation, nurses, 35
radiology sequence, 139 Seldinger technique, 44, 45f
chest X-ray, 16t saphenous vein femoral artery access, 54
lumbar spine X-ray, 16t grafts, 169f femoral vein access, 59
PCI, 188, 189t vein graft occlusion, 169f internal jugular vein ac-
radiology equipment, 10 right coronary bypass cess, 60f, 60
X-ray detectors, 11 (RCB) catheters, 168 selective engagement/
X-ray generators, 10, 11t right heart catheterization, injection, 159
radionuclide cardiac 72, 90, 91f SHOCK trial, 231, 240
studies, 16t difficulties, 90 Shockwave Coronary
RadiStop® (RADI Medical right heart pressures and Rx Lithoplasty®
Systems), 66–7, 67f waveforms, 92f, 92, 92t System, 250
RCA see right coronary right internal mammary shunt quantification, 97
artery (RCA) artery (RIMA), 46 side branch protection,
recording, cardiac CABG, 180f, 180 PCI of bifurcation
physiologists, 40 right ventriculography, lesions, 236
regional wall motion, left 96, 97f sign out, nurses, 34
ventriculography, 101 RIVAL trial, 228 simultaneous kissing stent
relatives, informing of pa- RotablatorTM Rotational (SKS), 303
tient death, 279 Atherectomy System simultaneous left and right
renal failure, 310 (Boston Scientific), 248 heart catheterization, 72
renal function, patient RotaLinkTM, 248 single coronary
protection, 21 rotational atherectomy, arteries, 162
reperfusion therapy, 227 248, 249f single-photon emission
reporting death, 279 alternative computed tomography
respiratory variation, right techniques, 250 (SPECT), 8
heart pressures and RotaWireTM, 248, 249 sirolimus, 202, 203f
waveforms, 93f, 93 routine administration, analogues, 202
restenosis, PCI, 200, 201f nitrates, 152 SKS (simultaneous kissing
restrictive stent), 303
cardiomyopathy, 124 snuff box radial artery
retroperitoneal S access, 53f, 53
haematoma, 294 saphenous vein, 54f Society for Cardiovascular
Richards, Dickinson, 3 saphenous vein grafts Angiography and
RIFLE trial, 228 (SVGs), 169f, 170, 244 Interventions (SCAI),
right anterior oblique circumflex coronary 190, 191t
(RAO) projection artery grafts, 171f, 171 Sones catheters, 83f
coronal (-30º/-20º) view, factors in failure, 173 Sones, Mason, 3
146f, 146 failure treatment, 174 SPECT (single-photon
cranial (-45º/20º) view, left anterior descending emission computed
147f, 147 coronary artery grafts, tomography), 8
left heart 170f, 170 stable angina, 6
catheterization, 86 long-term patency, 173 Staphylococcus aureus
left ventriculography, 98, right coronary artery infection, 295
99f, 100f grafts, 172f, 172 stenoses quantification
INDEX 331
alternative imaging
strategies, 156b
T U
coronary angiography, tachycardia ultrasound, intravenous
154, 155f supraventricular tachy- see intravascular
stents cardia, 290f, 290 ultrasound (IVUS)
closed-cell stent ventricular tachycardia, Ultravist® (iopromide), 78f
design, 199f 288f, 288 unexpected death, 279
crush stenting, 238, 239f Takotsubo cardiomyopathy, unstable coronary
culotte stenting, 127f, 127 syndromes, 6
238, 239f TASTE trial, 228, 252 upper limb acute ischaemia,
deferred vs. TAVI see transcatheter 297f, 297
immediate, 228 aortic valve
intervention (TAVI)
drug-eluting stents,
202, 238 temporary pacemakers, V
failure in OCT, 217 256f, 256 valve area, aortic
iatrogenic type A aortic settings configuration, stenosis, 108
dissection, 304 257f, 257 valve assessment, coronary
intracoronary stents, thermodilution method, angiography, 6
198, 199f cardiac output vascular access, 43
modular intracoronary calculation, 94 arterial routes see arterial
stents, 198, 199f third-degree/complete AV vascular access
Palmaz–Schatz block, 292f, 292 closure devices, 68, 69f
stent, 199f thrombin, 285b compression devices, 66f,
positioning in PCI, ticagrelor, 220 66, 67f
209f, 209 ticagrelor, interruption of Seldinger technique,
simultaneous kissing therapy, 222t 44, 45f
stent, 303 TIG catheter, 136 trends in, 48
suboptimal results, 217 time out, WHO venous access see
thrombosis, 206, 207f checklist, 34 venous access
tubular slotted tirofiban, 224 vascular clip devices, 68
intracoronary stents, torque, angioplasty guide vascular complications, 294
198, 199f wires, 194 vascular resistance
V-stenting, 238, 239f TOTAL trial, 228, 252 calculation, 94
stiff guide wires, 194 training vascular suture devices,
stress echocardiography, 8 cardiologists, 27 68, 69f
stroke, 281 nurses, 33 vasodilators, 247
structural myocardial transcatheter aortic valve vasovagal reaction
dysfunction, 127 intervention (TAVI), 110 (faints), 287
strut thickness, cardiac compute vein grafts
intracoronary tomography, 9 occlusion, 169f
stents, 199 transcutaneous (external) PCI, 244, 245f
ST-segment elevation temporary pacing, 257 veno-arterial (VA) extra-
myocardial infarction TRANSFER AMI trial, 230 corporeal membrane
(STEMI), 280f, 280 transoesophageal echocar- oxygenation, 276
cardiac arrest, 230 diography, 120f, 120 venous access, 58
PCI, 226 transthoracic femoral vein access, 59
subclavian vein access, echocardiography, 123f internal jugular vein,
62, 63f transvenous temporary 60f, 60
suboptimal stent results, pacemaker insertion, subclavian vein, 62, 63f
OCT, 217 256f, 256 ventricular fibrillation,
superficial femoral TR-band® (Terumo), 67 288f, 288
artery, 54f tricuspid regurgitation, 117 ventricular septal defect
support tricuspid stenosis, 117 (VSD), 121f, 121
angioplasty guide tricuspid valve ventricular tachycardia,
wires, 194 disease, 117 288f, 288
guide catheters, 193 TRILOGY ACS trial, 219 ventriculography, 96
supraventricular tachy- TRITON TIMI 38 echocardiography vs., 96b
cardia, 290f, 290 study, 219 left see left
SYNTAX study, 234 tubular slotted ventriculography
systemic vascular resistance intracoronary stents, procedure, 97
calculation, 94 198, 199f right, 96, 97f
332 INDEX
verapamil, 50 V-stenting, bifurcation PCI, Williams (3DRC) catheters,

vessel sizing, OCT, 217 238, 239f 83f, 132
vessel spasm, 210 workhorse guide
ViperSlide® lubricant, 250 wires, 194
viscosity, contrast W
media, 79 warfarin, 21
visibility, angioplasty guide continuation of, 64 X
wires, 194 stopping of, 64 Xenetix® (iobitridol), 78f
VisiplaqueTM (iodixanol), 78f WHO (World Health X-ray detectors, 11
VSD (ventricular septal Organization) X-ray generators, 10,
defect), 121f, 121 checklist, 33 11t

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

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OXFORD MEDICAL PUBLICATIONS

Giovanni Luigi De Maria

‘The only good is knowledge and the only evil is ignorance’

‘An investment in knowledge always pays the best interest’

Can the history and techniques of cardiac catheterization really be encom-

Professor Patrick W. Serruys, MD

This latest edition of Cardiac Catheterization and Coronary Intervention ex-

Symbols and abbreviations xiii

Symbols and abbreviations

INR international normalized ratio

SVG saphenous vein graft

• The small risks of the additional procedure are believed to be

It is extremely unusual for asymptomatic patients with no evidence of

Cardiac CT or invasive angiography?

Currently, these are the main indications for cardiac CT

• Clarifying coronary anatomy, distal landing zone, and proximal cap

Effect on number of Effect on photon

Ionising Radiation (Medical Exposure) Regulations 2017

The inverse square law

• Keep the image intensifier as close as possible to the patient.

Table 1.2 Risk estimates to the patient by examination

Examination Typical effective Equivalent Additional lifetime

Table 1.3 Recommended limits of radiation exposure for CathLab staff

Effective dose Skin and Eye

Warfarin is typically withheld for 3–​5 days prior to the procedure. Most

• To lead the management of cardiac arrest or complications, should they

The training programme should be assessed and evaluated according to:

• Complications and management:

• To take clear and thorough documentation of the procedure and to

Firstly, all members of the team should be present at the beginning of

• To record any unexpected issues that needs to be addressed.

• Managing bleeding and haematomas.

• Percutaneous puncture of the desired

• Passage of an atraumatic, curved-

• Removal of the needle leaving the

• Passage of an introducer sheath (with

• Removal of the guide wire, leaving the

Fig. 3.1 Seldinger technique

Which arterial access route to use?

• Most commonly, cardiac catheterization and selective coronary

• Despite convincing data, uptake of radial access is highly variable and

Snuff box radial approach

Fig. 3.6 Angiogram highlighting femoral artery anatomy. Contrast injected through

Angiography via the femoral route

How to obtain venous access

Internal jugular vein access

Carotid artery Internal jugular vein

Sternal head of Clavicular head of

Insert needle at 45°

Tips for cannulation of internal jugular/​subclavian veins

Direct oral anticoagulants (DOACs)

puncture site is compressed by further Velcro® straps attached to a

Fig. 3.10 Radial compression devices. The RadiStop® (top panel) consists of a

Fig. 3.11 Angio-​Seal™ closure device. A bioabsorbable anchor is deployed via an

Fig. 4.2 Pressure manifold

Fig. 4.3 Medrad® injector. Image courtesy of Bayer

Fig. 4.4 Summary characteristics of commonly used angiographic contrast agents

• It is good practice not to exceed 5–​7 mL/​kg of patient (depending

Prior cardiac catheterization

Fig. 4.5 French (F) catheter scale

Fig. 4.6 Judkins left and right catheters

Fig. 4.7 Pigtail and Amplatz left catheters

Fig. 4.8 Pigtail right and Williams catheters

Fig. 4.9 Modified Amplatz and Sones catheters

Giovanni Luigi De Maria

INR international normalized ratio

SVG saphenous vein graft

Ionising Radiation (Medical Exposure) Regulations 2017

The inverse square law

Table 1.3 Recommended limits of radiation exposure for CathLab staff

Effective dose Skin and Eye

Warfarin is typically withheld for 3–5 days prior to the procedure. Most

The training programme should be assessed and evaluated according to:

Tips for cannulation of internal jugular/subclavian veins

Fig. 3.11 Angio-Seal™ closure device. A bioabsorbable anchor is deployed via an

Fig. 4.3 Medrad® injector. Image courtesy of Bayer

Fig. 4.4 Summary characteristics of commonly used angiographic contrast agents

• It is good practice not to exceed 5–7 mL/kg of patient (depending

Fig. 4.5 French (F) catheter scale

Fig. 4.12 Crossing the aortic valve

The ‘difficult aortic valve’

Fig. 4.13 Directed guide wire across the aortic valve

• A soft-tipped J guide wire (% p.76) can be introduced into the

Fig. 4.16 Accessing the right heart from the inferior vena cava

Fig. 4.21 Schematic of RAO view

Fig. 4.22 Schematic of LAO view

Fig. 4.25 RAO projection left ventriculography showing end-diastole (left), systole

Fig. 4.26 Left ventriculogram revealing a well-circumscribed filling defect at the left

Fig. 4.29 Aortogram demonstrating significant enlargement of the ascending aorta

Fig. 5.11 Transthoracic echocardiography (apical four-chamber view)

Myocardial infarction with non-

LAO cranial (50°/20°)

Fig. 6.6 LAO cranial—useful for separating the LAD from diagonals

LAO caudal—‘spider view’ (400/−30°)

Fig. 6.7 LAO caudal—visualizes proximal vessels particularly LMS, proximal LAD,

Left lateral (90°/0°)

Fig. 6.8 Left lateral—mid LAD/left internal mammary artery (LIMA) anastomosis,

RAO caudal (−30°/−20°)

Fig. 6.9 RAO caudal—proximal Cx, LMS. AV Cx, atrioventricular circumflex

RAO cranial (−45°/20°)

Fig. 6.10 RAO cranial—main LAD

Fig. 6.11 LAO—proximal, mid, and distal RCA

Fig. 6.12 RAO—proximal and mid RCA

LAO cranial (50°/20°)

Fig. 6.13 LAO cranial—distal RCA/PDA

Fig. 6.14 PA cranial—distal RCA/PDA

Fig. 6.15 Response to GTN. Mid-RCA spasm seen in patient presenting with

Fig. 6.16 Coronary spasm—catheter tip spasm at the ostium of the RCA