John Chambers, Sandeep S. Hothi, Camelia Demetrescu

Echocardiography
This book sets echocardiography within a routine clinical context. It aims

to synthesise guidelines into a pragmatic clinical approach to real patients,
providing a step-by-step guide to performing, reporting, and interpreting a study.
We wrote it imagining we were the calm voice of a senior echocardiographer
teaching a junior colleague. This edition has been extensively revised with
an expansion of sections on acute, intensive care and emergency medicine.
COVID-19 has necessitated limiting exposure of both patient and operator to
infection and caused a huge increase in waiting lists. This has sharpened the
debate over matching the level of scan to the clinical question and also highlights
the importance of collaboration between clinicians and echocardiographers.
Key Features
● Expanded first chapter on levels of echocardiography
● New sections on COVID-19, cardio-oncology, multivalve disease, and
specialist valve clinics
● Incorporation of new international guidelines, grading criteria, and normal
data
● Guide to how cardiac CT and magnetic resonance can complement
echocardiography
● Reformatted text and extra diagrams and tables to improve understanding
Echocardiography
A Practical Guide for Reporting
and Interpretation
Fourth Edition
Camelia Demetrescu BSc, MSc, HSSE

Consultant Clinical Scientist in Cardiology
Guy’s and St Thomas’ Hospitals, London
Sandeep S Hothi MA, PhD, FRCP, FACC, FBSE, FESC

Consultant Cardiologist
Royal Wolverhampton NHS Trust
Honorary Senior Clinical Lecturer
University of Birmingham
John Chambers MD, FESC, FACC

Emeritus Professor of Clinical Cardiology
Guy’s and St Thomas’ Hospitals, London
Fourth edition published 2024
by CRC Press
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CRC Press is an imprint of Taylor & Francis Group, LLC
© 2024 Camelia Demetrescu, Sandeep S Hothi and John Chambers
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ISBN: 978-1-032-15160-1 (hbk)

ISBN: 978-1-032-15158-8 (pbk)
ISBN: 978-1-003-24278-9 (ebk)
DOI: 10.1201/9781003242789
Typeset in Universe
by Apex CoVantage, LLC
Contents
Prefaceix
Acknowledgementsxi
Authorsxiii
Disclaimerxv
Icons and QR Codes xvi
List of Abbreviations xvii
1 Defining the Study 1

Deciding the Level of Echocardiogram Required 1
The Basic Scan 3
The Focused Study 4
The Minimum Standard Study 5
The Comprehensive Study 7
Organisation of a Report 8
Escalation for Urgent Clinical Advice 10
Understanding the Report for Non-Echocardiographers 10
2 Left Ventricular Dimensions

and Function 15
LV Linear Cavity Dimensions 15
LV Wall Thickness 16
LV Volumes 18
LV Systolic Function 20
LV Diastolic Function 23
LVEF >50%: Diastolic Heart Failure (HFpEF)? 25
3 Acute Coronary Syndrome 29
4 The Right Ventricle 35
5 Pulmonary Pressure and Pulmonary

Hypertension43
Estimating PA Systolic Pressure 43
Assessing the Probability of Pulmonary Hypertension 45 v
Contents
6 The Atria and Atrial Septum 53

Left Atrium 53
Right Atrium 54
Atrial Septum 54
7 Cardiomyopathies 61
The Dilated LV 61
The Hypertrophied LV 65
Restrictive Cardiomyopathy 72
Non-Compaction74
Arrhythmogenic Right Ventricle Cardiomyopathy/Dysplasia
(ARVC/ARVD)75
Cardio-Oncology: Evaluation of Patients on Chemotherapy 77
8 Aortic Valve Disease 81

Aortic Stenosis 81
Aortic Regurgitation 90
Acute Aortic Regurgitation 96
9 Mitral Valve Disease 101

Mitral Stenosis 101
Mitral Regurgitation 106
Specialist Pre- and Post-Operative Assessment 116
10 Right-Sided Valve Disease 121

Tricuspid Regurgitation 121
Tricuspid Stenosis 125
Pulmonary Stenosis and Regurgitation 126
11 Mixed Valve Disease 133

Mixed Moderate Aortic Valve Disease 133
Mixed Moderate Mitral Valve Disease 133
Mixed Mitral and Aortic Valve Disease 134
12 Prosthetic Heart Valves 135

Core Information 135
Is there Dysfunction of the Prosthetic Valve? 140
13 Endocarditis 149
vi
Contents
14 The Heart Valve Clinic 155
15 The Aorta and Dissection 161

The Aorta 161
Dissection and Acute Aortic Syndromes 166
16 Adult Congenital Heart Disease 171

Simple Defects 171
Sequential Segmental Approach to Assessment
of Congenital Heart Disease 181
Post-Procedure Studies 184
17 Pericardial Disease 189

Pericardial Effusion 189
Pericardial Constriction 194
Acute Pericarditis 196
18 Masses 201
Mass Attached to a Valve 201
Left or Right Atrial Mass 202
Left or Right Ventricular Mass 205
Pericardial Mass 208
Extrinsic Mass 208
Mass in the Great Vessels 210
19 Echocardiography in Acute
and Critical Care Medicine 213
The Critically Ill Patient 213
The Acutely Ill Patient 213
Further Indications for Echocardiography
on Critical Care Units 216
Echocardiography in COVID-19 218
20 General Clinical Requests 221
Appendices229
Index245
vii
Preface
This book sets echocardiography within a routine clinical context. It aims

to synthesise guidelines into a pragmatic clinical approach to real patients,
providing a step-by-step guide to performing, reporting, and interpreting
a study. We wrote it imagining we were the calm voice of a senior
echocardiographer teaching a junior. We also designed lists and tables as aides-
memoires for the experienced echocardiographer or interpreting physician.
How We Handled Guidelines and Data

We took account of all up-to-date guidance from the ESC and ACC/AHA
and also any other national or international body of authority that offered
complementary or corroborative data or advice. Where guidelines disagreed
or deviated from usual clinical practice, we conducted informal polls of
internationally respected colleagues and reported the range of actual clinical
practice marked by a logo to note the need for discussion within an individual
department. If there were more recent normal ranges based on better
collected data from larger populations than quoted in international guidelines,
we used these. For example, we used the NORRE data for aortic diameters.
Expansion of Echocardiography
Since the third edition, echocardiography has expanded further into acute,
intensive care, and emergency medicine. COVID-19 has necessitated limiting
exposure of both patient and operator to infection and also caused a huge
increase in waiting lists. This has sharpened the debate over the balance
between abbreviated scans and comprehensive studies and highlighted the
importance of collaboration between clinicians and echocardiographers. It
is clear that the nature of the cardiac scan should be tailored to the clinical
question, and this has led to the development of a range from basic, through
focused, to standard and comprehensive echocardiograms. We discuss this in
an expanded first chapter.
ix
Preface
New Sections
We also include new sections on COVID-19, cardio-oncology, multivalve
disease, and specialist valve clinics. We incorporated new international
guidelines, grading criteria, and normal data. Since the third edition, there has
been further development of cardiac CT and magnetic resonance, and we
explain where these techniques are complementary to echocardiography and
should be incorporated in a multimodality approach to normal clinical practice.
General Changes
The text has been reformatted to be more easily accessible, and numerous
diagrams have been added or updated. Images and clips have been placed in a
web-based archive.
This book will be relevant to all echocardiographers, including cardiac
physiologists, clinical scientists, cardiologists, and clinicians in acute, critical
care, general, and emergency medicine. It will also be useful to hospital and
community physicians needing to interpret reports.
x
Acknowledgements
We should like to thank the people who took part in our online straw polls:
Brian Campbell, Laura Dobson, Madalina Garbi, Jane Graham, Antoinette
Kenny, Navroz Masani, Jim Newton, Petros Nihoyannopoulos, Keith Pearce,
Bushra Rana, Dominik Schlosshan, Roxy Senior, Benoy Shah, and Rick Steeds.
We are also grateful to colleagues who read through chapters and offered
helpful advice: Claire Colebourne, Jane Draper, Yaso Emmanuel, Madalina
Garbi, Jane Graham, Jeffrey Khoo, Simon MacDonald, Peter Saville, and David
Sprigings. Any remaining mistakes are ours and not theirs. We should also like
to thank Phillip Bentley, graphic designer, for updating the diagrams.
xi
Authors
Camelia Demetrescu, BSc, MSc, HSSE, is Consultant Clinical

Scientist in Cardiology, with specialist interest in echocardiography, at Guy’s
and St Thomas’ Hospital. She has extensive NHS clinical, teaching, research,
managerial, and leadership work experience across multiple London NHS tertiary
trusts. She has a specialist interest in the management of patients with heart valve
disease and interventional cardiology, inherited cardiomyopathies, heart transplant
and assist devices, and most recently, in the research and development of AI
technology. She is an active member of the European Association of Cardiovascular
Imaging, the British Society of Echocardiography, British Heart Valve Society,
Academy for Healthcare Science, and the National School of Healthcare Science.
Sandeep S Hothi, MA, PhD, FACC, FBSE, FESC, FRCP, is

Consultant Cardiologist and Clinician-Scientist with expertise in advanced
cardiac imaging. He studied at the University of Cambridge for undergraduate
and postgraduate medical and scientific degrees: 1st Class BA (Hons) degree,
clinical medical and surgical degrees (MB BChir) and a research degree (PhD)
in cardiac cellular and whole heart physiology. He is a Consultant Cardiologist
at New Cross Hospital, Wolverhampton, and Honorary Senior Clinical Lecturer
at the University of Birmingham. He is accredited (SCMR, EACVI CMR, BSE,
SCCT) in Echocardiography (transthoracic, transoesophageal, stress echo),
Cardiac MRI and Cardiac CT. He holds societal roles with the British Society of
Echocardiography as elected Trustee and Council Member, lead examiner for
TOE accreditation, and Accreditation committee member.
John Chambers, MD, FRCP, FESC, is Emeritus Professor of Clinical

Cardiology at Guy’s and St Thomas’ Hospital and KCL and was previously Head of
Adult Echocardiography there. He helped in the foundation of the British Society
of Echocardiography and was President from 2003 to 2005, responsible for
establishing minimum standards for performing and reporting echocardiograms.
He also helped set up individual transthoracic, transoesophageal, and departmental
accreditation and a training system for basic echocardiography. He ran the London
Echo Course for ten years and remains a faculty member of many national
teaching courses. He has helped write a number of international documents on
the imaging assessment of valve disease, including prosthetic valves. He was
a founder-member and the first president of the British Heart Valve Society and
helped set standards for specialist valve clinics and heart valve centres. He has
written ten books on echocardiography, heart valve disease, and general medicine.
He was awarded the British Cardiovascular Society 2023 Mackenzie medal for his
career-long work in echocardiography and heart valve disease. xiii
Disclaimer
The information in this book is based on a synthesis of data and guidelines

available at the time of printing. The reader should be aware that clinical
interpretation may change, and the writers cannot be held responsible for
clinical events associated with the use of this book.
xv
Icons and QR Codes
A number of new icons and QR codes have been used in this edition of the
book to increase its usefulness to practitioners.
Throughout the book, the CHECKLIST icon is used to signal checklist boxes
summarising the main information on topics discussed.
The ALERT icon flags up points to be particularly aware of or mistakes to

avoid.
The THINK icon marks a point of controversy or where consensus has not
been reached.
A point requiring discussion in an individual patient with integration into the

clinical context is indicated by the DISCUSSION icon.
xvi
Abbreviations
AF atrial fibrillation LV left ventricle/ventricular

Ao aorta LVDD LV end-diastolic diameter
ARVC/D arrhythmogenic LVEDV LV end-diastolic volume
right ventricular LVEDVi LV end-diastolic volume
cardiomyopathy/dysplasia indexed to BSA
AR aortic regurgitation LVESV LV end-systolic volume
AS aortic stenosis LVESVi LV end-systolic volume
ASD atrial septal defect indexed to BSA
AVSD atrioventricular septal defect LVEDP LV end-diastolic pressure
BSA body surface area LVOT LV outflow tract
CABG coronary artery bypass graft LVSD LV end-systolic diameter
CMR cardiovascular magnetic MOA mitral orifice area
resonance MR mitral regurgitation
CSA cross-sectional area MS mitral stenosis
CT computerised tomography PA pulmonary artery
CW continuous wave
PCI percutaneous coronary
DCM dilated cardiomyopathy intervention
dP/dt rate of developing pressure PDA persistent ductus arteriosus
ECG electrocardiogram PEEP positive end-expiratory
ECMO extracorporeal membranous pressure
oxygenation PET positron emission
EF ejection fraction tomography
EOA effective orifice area PFO patent fossa ovalis
EROA effective regurgitant orifice PH pulmonary hypertension
area PISA proximal isovelocity surface
FDG fluorodeoxyglucose area
HCM hypertrophic cardiomyopathy PR pulmonary regurgitation
IVC inferior vena cava PS pulmonary stenosis
IVS interventricular septum RA right atrium/atrial
LA left atrium/left atrial RF regurgitant fraction
LAA left atrial appendage RV right ventricle/ventricular
LBBB left bundle branch block RVOT right ventricular outflow
LMS left main stem tract
xvii
Abbreviations
RVEDV RV end-diastolic volume TS tricuspid stenosis

RVESV RV end-systolic volume TTE transthoracic
RWT relative wall thickness echocardiogram/
STJ sinotubular junction echocardiography
SV stroke volume Vmax peak velocity
SVC superior vena cava VSD ventricular septal defect
TAPSE tricuspid annulus peak VTI velocity time integral
systolic excursion (VTIaortic measured on
continuous wave Doppler
TAVI transcatheter aortic valve
through the aortic valve,
implantation
VTImitral measured on
TDI tissue Doppler imaging continuous wave Doppler
TOE transoesophageal across the mitral valve,
echocardiogram/ and VTIsubaortic measured
echocardiography on pulsed Doppler in the
TR tricuspid regurgitation LV outflow tract)
xviii
Defining the Study
1
Deciding the Level of Echocardiogram
Required
● Cardiac ultrasound has now expanded in:
● Setting—from the echocardiography laboratory to include cardiac and
general wards; GP surgery and community echo clinics; the interventional
laboratory, theatre, and intensive therapy unit; the emergency room and
emergency settings, e.g. the road side or battlefield.
● Application—from cardiology to acute, emergency, and intensive care
medicine; to exclude significant structural disease in the community or
the outpatient clinic.
● Hardware—from high-end system through mid-range portable machines
to handheld devices.
● Training—from the use of cardiac ultrasound as an aid to resuscitation
(by first responders) to basic studies (by the accredited physician
in charge of the case or by accredited and highly experienced
echocardiographers), to focused echocardiograms e.g. for community
screening projects (often by nurses), to standard echocardiograms
(by accredited echocardiographers), and to comprehensive studies
(accredited and highly experienced echocardiographers).
● Cardiac ultrasound (e.g. FATE or FEEL protocols), usually including chest
and abdominal imaging, is separate from echocardiography and part of
emergency management.
● There are four levels of transthoracic echocardiography (TTE) (Table 1.1).
● Deciding the level of scan requires collaboration between clinician and
echocardiographer (Figure 1.1) via:
● A system of formal triage, including cases which do not need an
echocardiogram at all (e.g. repeat studies with no clinical change).
● Discussion about individual cases (e.g. in valve or heart failure specialist
clinics).
● The decision on the level of scan will be based on:
● The likelihood of disease. A basic TTE is sufficient to confirm the
clinical impression of normality in low-risk cases, for example, flow
murmurs or perceived palpitation in a young person1, 2. By comparison,
1
DOI: 10.1201/9781003242789-1
Defining the Study
Table 1.1 Aims of the four levels of echocardiogram (TTE) (Figure 1.1)
Basic scan—can be performed with a handheld device with colour by an

accredited* and highly experienced echocardiographer.**
● To detect pathology requiring immediate correction in the emergency
setting (often performed by the physician in charge of the case).
● To determine what further investigations are indicated.
● To exclude the need for a minimum standard study in a patient at low
clinical risk of disease.
Focused study—typically performed using a mid-range machine by an
accredited echocardiographer* or operator specifically trained for a community
screening project.
● To identify specific abnormalities in screening projects, for example, LV
systolic and diastolic dysfunction, heart valve disease3, 4.
● To detect change, for example, after an intervention in ITU, a new
pericardial effusion after a cardiac intervention, an improvement in LV
function after heart failure therapy, or in LV function on serial cardio-
oncology scans.
● To detect significant change requiring a comprehensive study in patients
with previous minimum standard studies, for example, moderate valve
disease in a specialist valve clinic.
Minimum standard study—performed with at least a mid-range machine by an
accredited echocardiographer,* if necessary, under supervision.
● This is the set of views and measurements (Tables 1.2 and 1.3) without
which a study cannot be relied on to exclude significant pathology.
Comprehensive study—performed using a high-end machine by an accredited*
and highly experienced echocardiographer.**
● This is a minimum standard study with additional disease-specific
measurements (Table 1.4) as described in the chapters in this book.
* Accredited by a recognised national board or system, for example, the British Society of
Echocardiography, European Association of Cardiovascular Imaging, American Society of
Echocardiography, Australian BSc.
** Highly experienced echocardiographers are expected to notice mild abnormalities requiring
a more extended study more readily than junior echocardiographers do.
a comprehensive study is more appropriate for a patient with a family

history of cardiomyopathy.
● The results of previous studies. Confirming the stability of a previously
noted abnormality does not usually need a comprehensive TTE.
● The clinical question. This might range from detecting signs of subtle
disease (needing a comprehensive study) to whether the LV ejection
fraction has changed (suitable for a focused study).
● Team working means that studies can be extended if unexpected pathology
is detected.
2
The Basic Scan
Figure 1.1 Choosing the level of echocardiogram.
The Basic Scan

● This is effectively an extension of the clinical examination and has these
features4–6:
● Basic views, usually: (1) parasternal long- and (2) short-axis (scanning
from papillary muscles to aorta); (3) apical 4- then tilting to 5-chamber; (4)
subcostal (Figure 1.2).
● Systematic assessment of key cardiac structures: (1) LV size and
function; (2) RV size and function and IVC; (3) valves; (4) presence of
pericardial fluid.
● Includes colour Doppler to detect significant valve disease.
● The result is classified as:

● Major abnormality requiring immediate action, for example, pericardial
tamponade, RV dilatation (as a surrogate for massive pulmonary embolism)7.
● Normal.
● Requiring higher-level TTE (which can often be done immediately if

equipment and operator appropriate), for example, more than trivial
abnormalities, or basic scan apparently normal but patient unwell.
3
Defining the Study
Figure 1.2 A template showing views for the basic echocardiogram.
● A suggested aide-memoire is given in Figure 1.2, but individual laboratories

may add extra views or measurements as routine, for example, apical
2-chamber view or measurement of LV septal thickness or TR Vmax if tricuspid
regurgitation is detected or LA diameter in an electrophysiology request.
The Focused Study

● This always starts with a basic scan, to which specific ‘add-ons’ are
determined by a clinical or research protocol or as directed by the clinician in
charge of the case8.
● Examples of ‘add-ons’ are:
● TR Vmax if more than mild TR shown9.
● RV tissue Doppler S′ velocity, TAPSE, and TR Vmax in sickle cell disease, in

SLE, or in pulmonary embolism before and after thrombolysis.
● Aortic dimensions and aortic regurgitation in a patient in an aortopathy clinic.
4
The Minimum Standard Study
● LV measurements to estimate LV mass in hypertension10.

● LV systolic function alone9 or IVC reactivity11 in follow-up heart failure clinics.
The Minimum Standard Study

● A minimum dataset of views and measurements is required to:
● Confirm normal cardiac structure and function (Tables 1.2 and 1.3).
● Reduce the risk of missing significant abnormalities.
● Minimise inter- and intra-observer variability and enable accurate

comparison of serial TTE.
● Provide a structure for departmental quality audit.
● Clinically important measurements should be included in the text of the report.

● Confining all measurements to a computer-generated section
encourages their proliferation. Clinically important measurements may
not be noticed especially if the requestor is a non-echocardiographer.
● Each department should decide how many measurements to make and
which should be brought into the text.
● Some protocols suggested by professional societies for a minimum standard
study include measurements more properly classified as comprehensive.
● Each department needs to discuss how to manage measurements in atrial
fibrillation.
● Most aim to obtain measurements on cycles with instantaneous heart
rates close to 60–70 bpm.
● Once critical disease has been excluded by a basic TTE, it may be
appropriate to bring the patient back once rate-controlled to continue
the minimum standard study.
Table 1.2 Minimum standard adult transthoracic echocardiogram (TTE)

protocol12–15
View Essential imaging modalities**

P/S long axis 2D, colour Doppler
2D, colour Doppler
P/S RV inflow
CW of TV if TR found
P/S RV outflow 2D, colour Doppler
2D, zoom, colour Doppler
PW in RV outflow
P/S short axis at AV CW of PV and main PA
CW of PR
5
(Continued)
Defining the Study
Table 1.2 Minimum standard adult transthoracic echocardiogram (TTE)

protocol (Continued)
View Essential imaging modalities**

P/S short axis at MV 2D, colour Doppler*
P/S short axis at pap muscles 2D, colour Doppler*
P/S short axis at apex 2D, colour Doppler*
2D, colour Doppler
PW of MV
Apical 4 chamber
Doppler tissue MV and TV annulus
2D, colour Doppler of TV
RV/RA modified Apical 4 chamber M-mode TAPSE ± tissue Doppler
2D, colour Doppler
Apical 5 chamber PW of LVOT
CW of AV
Apical 2 chamber 2D, colour Doppler
Apical long axis 2D, colour Doppler
2D, zoom on IVC and IAS, colour
Subcostal long axis Doppler (IAS; hep vein)
IVC reactivity by eye
Subcostal short axis 2D, colour Doppler
Subcostal abdominal aorta 2D, colour Doppler
Suprasternal notch–aortic arch 2D, colour Doppler
* To exclude a VSD.
** Extra views are suggested by some guidelines12–15, e.g. CW of valves even if imaging and
colour normal, LV strain.
Table 1.3 Minimum measurements for standard adult TTE protocol
Left ventricle
Diameters 2D: LVDD; LVSD; IVSd; PWd
2D volumes or 3D (when available)—BSA indexed*: LVEDVi and LVESVi
EF (using 2D or 3D volumes); VTIsubaortic
Mitral E/A and E/E’ ratio using E’ at septum ± lateral ± averaged according to
local protocols
Left atrium
2D Volume (biplane method) or 3D—BSA indexed
Right ventricle
RV basal diameter; TAPSE and/or S’ on tissue Doppler
TR Vmax; acceleration time of PW in RV outflow tract
6 Inferior vena cava (inspiratory change): RA pressure assessment
The Comprehensive Study
Right atrium
2D area—2D Volume or 3D (when available)—BSA indexed
Aorta
2D diameter at sinuses, sinotubular junction, and ascending aorta indexed to
height if at extremes of height
Aortic valve
CW Vmax
* If BMI > 30 Kg/m2, do not index to BSA, which underestimates the degree of cardiac remodelling.
The Comprehensive Study

● This is a minimum standard study plus extra views and measurements
depending on the clinical question or known pathology (Table 1.4).
Table 1.4 Views and measurements or descriptions as add-ons to the

minimum standard according to the indication for the study
Measurements/
Indication Views
observation
Possible LV ● Zoom LVOT and MV in ● RWT and LV mass
dysfunction HCM BSA indexed (g/m2)
(indication ● Zoom LV apex ● 2D/3D dyssynchrony
heart failure, +/– colour Doppler in parameters
cardiomyopathy) cardiomyopathy or ● 3D volume and
myocardial infarction ejection fraction
● Modified LV views in ● GLS
suspected post-infarct ● LVOT obstruction at
VSD rest/Valsalva in HCM
● Contrast study for
endocardial border
delineation/thrombus
Possible RV ● RV-specific views ● RV 2D P/S long- and
dysfunction (page 35) short-axis diameters
● Zoom RV apex ● RV fractional area
● M-mode of annulus in change
zoomed 4-chamber view ● RV EF on 3D
Aortic stenosis ● Zoom in LVOT ● LVOT diameter
● CW at apex and RICS ● Vmax, mean ∆P, EOA
● CW to exclude
coarctation
● Evidence of PHT
(Continued) 7
Defining the Study
Table 1.4 Views and measurements or descriptions as add-ons to the

minimum standard according to the indication for the study (Continued)
Measurements/
Indication Views
observation
Aortic regurgitation ● Zoom aortic root and ● Colour jet width
ascending aorta ● AR pressure half-time
● AR CW ● Flow reversal in
● Colour M-mode descending aorta
suprasternal (PW and colour)
Mitral regurgitation ● Zoom MV in all views ● Detailed valve
● PW in pulmonary vein morphology and
mechanism of MR
● MV annulus size
● Tenting height/area
● PISA/vena contracta
● Evidence of PHT
Mitral stenosis ● Zoom MV in all views ● MV orifice
planimetered area
● Vmax, pressure 1/2
time (and estimated
area), mean gradient
● Evidence of PHT
Pericardial ● PW at MV (slow sweep ● Look for septal
constriction speed) bounce
● PW in hepatic veins ● Resp variability in
● MV annulus tissue transmitral PW
Doppler ● Septal and lateral
tissue Doppler E’
Organisation of a Report
1. The minimum standard report16 should include:
● Basic data:
● Patient name, date of birth, and hospital number.
● Echocardiographer ID (initials/name).
● Information regarding echocardiographic machine, type of image

storage media, and location is recommended to facilitate review.
● Minimum patient observations:
● Age and sex and body dimensions (height, weight, body surface area).
● A good-quality ECG trace for heart rate and rhythm.

8
Organisation of a Report
● Indication. A TTE should not usually be performed without a written

request (except in life-threatening emergencies). The request should
include:
● The indication (ideally including previous medical history).
● Clinical questions to be answered.
● Referrer details (name, title, address, email).
● Minimum measurements (see Table 1.3). Clinically important

measurements need to be given in the text of the report, and it is not
sufficient to have these in a list of machine-generated numbers.
● The main text should include:
● A description of image quality (poor, adequate, good).
● A description of the morphological and functional findings of all

parts of the heart and great vessels.
● If it was not possible to image a region, this should be stated.
● Preliminary interpretation can be included where it aids

understanding, for example, ‘rheumatic mitral valve’. The grade
of stenosis or regurgitation can also be stated as long as the
observations used are included.
● No consensus exists about reporting minor abnormalities (e.g. mild
mitral annulus calcification), normal variants (e.g. Chiari network),
or normal findings (e.g. trivial mitral regurgitation). We suggest
describing these in the text but omitting them from the conclusion.
● The summary:
● Must answer the clinical question posed by the referrer.
● Must emphasise abnormal findings in descending order of clinical

importance.
● Should identify the abnormality (e.g. mitral regurgitation), its
cause (e.g. mitral prolapse), and the secondary effects (e.g. LV
dilatation and hyperactivity).
● Should compare with previous findings if available.
● Should avoid abbreviations and be understood by non-specialist

healthcare professionals.
● Should not usually include clinical advice. This requires the
echocardiographic findings to be integrated with the broader clinical
assessment, which is not available to the echocardiographer. However,
it may be reasonable to offer implicit management advice in the
report, for example: 1) ‘Valve suitable for balloon valvotomy based on
echocardiographic assessment.’; 2) ‘Valve suitable for repair based on
echocardiographic assessment.’; 3) ‘Severe mitral regurgitation with LV
dilatation at thresholds suitable for surgery.’
9
Defining the Study
Escalation for Urgent Clinical Advice

● Each laboratory should have a system of identifying critical findings
(Table 1.5) and communicating them to the referrer or a cardiologist.
● Documentation of communication of the critical findings must be recorded
in the report and/or in the patient’s medical record.
Table 1.5 Examples of critical findings requiring urgent clinical advice
Critically unwell patient, regardless of echocardiographic findings

Pericardial effusion: large or with evidence of tamponade
Aortic dissection or grossly dilated ascending aorta or abscess
Previously undiagnosed severely impaired LV systolic function
Serious complications of an acute coronary syndrome:
● Ventricular septal rupture
● Papillary muscle rupture
● False aneurysm
RV dilatation or hypokinesis in a patient with suspected pulmonary embolism
New severe valve disease
New cardiac mass or thrombus
Understanding the Report for

Non-Echocardiographers
1. Some findings are almost never of clinical importance:
● Mild tricuspid and pulmonary regurgitation, which are both normal
findings. Isolated moderate tricuspid regurgitation is also within normal
limits if the RV is not dilated and the left heart is normal.
● Mild mitral regurgitation with a normal valve appearance and normal LV
size and function.
● ‘Sigmoid septum’ (or ‘septal bulge’), which is common in the elderly
and may cause a murmur.
● Trivial pericardial fluid especially localised around the right atrium (in
the absence of chest pain, suggesting pericarditis).
● An incidental patent foramen ovale in the absence of a relevant clinical
history (TIA or stroke, peripheral embolism, diving).
10
Understanding the Report for Non-Echocardiographers
2. What do class 1, 2, and 3 diastolic dysfunction mean?

● Echocardiographers are now encouraged to describe the pattern of LV
filling using a system of classification. ‘Slow filling’, which is common and
arguably normal in the elderly, has become ‘class 1 diastolic dysfunction’.
● Class 2 and 3 dysfunctions suggest high LV filling pressures, but these
classes are easily confused with diastolic heart failure, which is a
clinical diagnosis that cannot be made on TTE alone.
● If the patient is well, it is likely that LV diastolic dysfunction is an
incidental observation of no clinical significance.
3. How do I interpret a probability of pulmonary hypertension?
● If the request was to detect pulmonary hypertension (e.g. in the
context of SLE), then the recommendation is to report a low,
intermediate, or high probability of pulmonary hypertension (see
Chapter 5). TTE cannot estimate PA pressure reliably enough to make a
management-changing diagnosis. Further investigation potentially with
a right heart catheter is then needed.
● If the patient has valve disease:
● In mitral stenosis, a PA systolic pressure >50 mmHg at rest is an
indication for balloon valvotomy even in the absence of symptoms.
● In severe aortic stenosis (AS), a PA systolic pressure >60 mmHg
indicates a high risk of dying, unless surgery or a TAVI is performed.
● A rise in TR Vmax is a secondary sign of deterioration in any type of
valve disease.
● If the request was for any other reason and no other cardiac
abnormalities are reported, seek a cardiac opinion.
4. In specific diseases, there are echocardiographic findings that might
trigger changes in management (Table 1.6).
Table 1.6 Alerts in the echo report by pathology
Asymptomatic severe valve disease. Check that LV size and

function are normal
In severe mitral regurgitation, surgery may be indicated for a systolic diameter
>40 mm or LV ejection fraction approaching 60% (see Chapter 9).
In severe aortic regurgitation, surgery may be indicated for a systolic diameter
>50 mm, diastolic diameter >65 mm, or LV ejection fraction approaching 50%
(see Chapter 8).
Moderate disease may still be significant if the LV size and function are abnormal.
(Continued)
11
Defining the Study
Table 1.6 Alerts in the echo report by pathology (Continued)
In suspected heart failure:

Diastolic heart failure cannot usually be diagnosed on the TTE alone without
clinical features and BNP levels. Diastolic dysfunction does not necessarily
imply diastolic heart failure.
Heart rate and rhythm may interfere with the assessment of ventricular systolic
and diastolic function.
The LV ejection fraction depends on preload and afterload, both of which can
change quickly according to a patient’s clinical condition.
Estimations of LV ejection fraction are highly operator-dependent, and small
changes should not be over-interpreted.
Patient’s fitness for surgery:
The TTE evaluates only some aspects of the cardiovascular system. It cannot
detect myocardial ischaemia.
Is there a cardiac source for embolism?
TTE is the modality of choice to demonstrate intraventricular mass or
thrombus when images are satisfactory.
TTE does not image the left atrial appendage adequately. TOE may be required
if it changes clinical management.
When patent foramen ovale must be excluded as a source of cryptogenic
stroke in young patients, transthoracic bubble contrast study is recommended
(see pages 56, 57).
In suspected pericarditis or pericardial effusion:
Uncomplicated pericarditis has no pathognomonic features on TTE.
TTE can detect complications of pericarditis, such as a pericardial effusion.
Tamponade is a clinical diagnosis, though TTE is useful to assess
haemodynamic changes.
References
1. Draper J, Subbiah S, Bailey R & Chambers J. The murmur clinic. Validation of a
new model for detecting heart valve disease. Heart 2019;105(1):56–9.
2. Smith J, Subbiah S, Hayes A, Campbell B & Chambers J. Feasibility of an outpatient
point-of-care echocardiography service. J Am Soc Echo 2019;32(7):909–10.
3. Ploutz M, Ju JC, Scheel J, et al. Handheld echocardiographic screening for
rheumatic heart disease by non-experts. Heart 2016;102(1):35–9.
4. Hammadah M, Ponce C, Sorajja P, et al. Point-of-care ultrasound: Closing guideline
gaps in screening for valvular heart disease. Clin Cardiol 2020;43(12):1368–75.
12
Understanding the Report for Non-Echocardiographers
5. Spencer KT, Kimura BJ, Korcarz CE, et al. Focused cardiac ultrasound:
Recommendations from the American Society of Echocardiography J Am Soc
Echo 2013;26(6):567–81.
6. Cardim N, Dalen H, Voigt J-U, et al. The use of handheld devices: A position
statement of the European Association of Cardiovascular Imaging (2018 update).
Europ Heart J 2019;20(3):245–52.
7. Hall DP, Jordan H, Alam S & Gillies MA. The impact of focused echocardiography
using the focused intensive care echo protocol on the management of critically ill
patients, and comparison with full echocardiographic studies by BSE-accredited
sonographers. J Intensive Care Soc 2017;18(3):206–11.
8. Rice JA, Brewer J, Speaks T, et al. The POCUS consult: How point of care ultrasound
helps guide medical decision making. Int J Gen Med 2021;14:9789–806.
9. Dowling K, Colling A, Walters H, et al. Piloting structural focused TTE in outpatients
during the COVID-19 pandemic: Old habits die hard. Br J Cardiol 2021;28:148–52.
10. Senior R, Galasko G, Hickman M, et al. Community screening for left ventricular
hypertrophy in patients with hypertension using hand-held echocardiography. J Am
Soc Echo 2004;17(1):56–61.
11. Gundersen GH, Norekval TM, Haug HH, et al. Adding point of care ultrasound
to assess volume status in heart failure patients in a nurse-led outpatient clinic.
A randomised study. Heart 2016;102(1):29–34.
12. Harkness A, Ring L, Augustine D, Oxborough D, Robinson S, Sharma V &
Stout M. Normal reference intervals for cardiac dimensions and function for
use in echocardiographic practice: A guideline from the British Society of
Echocardiography. Echo Research and Practice 2020;7(1):G1–18.
13. Robinson S., Bushra R., Oxborough D, et al. Guidelines and recommendations.
A practical guideline for performing a comprehensive transthoracic
echocardiogram in adults: The British Society of Echocardiography minimum
dataset. Echo Research and Practice 2020;7(4):G59–93.
14. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber
quantification by echocardiography in adults: An update from the American Society
of Echocardiography and the European Association of Cardiovascular Imaging. Eur
Heart J CVI 2015;16(3):233–70.
15. Mitchell C, Rahko PS, Blanwet LA, et al. Guidelines for performing a
comprehensive transthoracic echocardiographic examination in adults:
Recommendations from the American Society of Echocardiography. J Am Soc
Echo 2019;32(1):P1–764.
16. Galderisi M, Cosyns B, Edvardsen T, et al. Standardization of adult transthoracic
echocardiography reporting in agreement with recent chamber quantification,
diastolic function, and heart valve disease recommendations: An expert consensus
document of the European Association of Cardiovascular Imaging. Europ Heart J
CVI 2017;18(12):1301–10.
13
Left Ventricular
Dimensions
and Function
2
The assessment includes:
● LV linear cavity dimensions
● LV wall thickness
● LV volumes—2D biplane Simpson’s or 3D full volume, when available
● LV function—systolic and diastolic
LV Linear Cavity Dimensions

● Measure at the base of the heart using 2D-guided measurements
(Figure 2.1).
● In patients with a sigmoid septum, measurements should be performed
slightly towards the apex, just beyond the septal bulge1.
● Commonly used normal ranges and grades of abnormality suggested by
ASE/EACVI are given in Table 2.1. Grades are useful for communication
with clinicians despite not necessarily correlating closely with outcomes.
Whether to use grades or a simpler classification as normal, dilated, or
severely dilated needs to be discussed by individual labs.
● The ASE/EACVI data are used in current ESC guidelines on diagnosis and
management, for example, in valve disease and cardiomyopathies.
● However, the BSE 2020 guidelines, derived from the NORRE dataset, give
larger end-systolic dimensions than in Table 2.1, for example, severely
dilated LVSD >46 mm in women, and >50 mm in men3. Individual labs need
to agree whether to use ASE/EACVI or NORRE ranges.
● ASE/EACVI recommend that chamber measurements should be indexed to
BSA (most commonly using the Dubois–Dubois formula)5. This is not done
routinely in clinical practice because:
● In mitral and aortic valve disease, outcomes and the timing of
interventions are related to absolute LV dimensions4.
● For a BMI >30 kg/m2, indexing may overcorrect an abnormally large dimension.
● However, indexing should be done to help identify borderline abnormalities

in patients, particularly at extremes of size (e.g. DCM family screening).
15
DOI: 10.1201/9781003242789-2
Left Ventricular Dimensions and Function
Figure 2.1 Sites for making 2D measurements. (a) Linear internal

measurements of the LV should be acquired in the parasternal long-axis view
perpendicular to the LV long axis and measured at the level of the mitral valve leaflet tips.
(b) In patients with sigmoid septum, LV cavity measurements should be performed slightly
towards the apex, just beyond the septal bulge. Guidelines suggest measuring from inner
to inner edge. Diastolic measurements are timed with the onset of the QRS complex, and
systolic measurements with the end of the T wave on the electrocardiogram.
Table 2.1 Grading of LV cavity diameters suggested by ASE/EACVI2
Mildly Moderately Severely

Normal
dilated dilated dilated
Women
LVDD (mm) 38–52 53–56 57–61 >61
LVSD (mm) 22–35 36–38 39–41 >41
Men
LVDD (mm) 42–58 59–63 64–68 >68
LVSD (mm) 25–40 41–43 44–45 >45
Abbreviations: LVDD, left ventricle end-diastolic diameter; LVSD, left ventricle end-systolic
diameter.
LV Wall Thickness
● Measurements should be taken at the base of the heart.
● A guide to grading thickness is given in Table 2.2.
● Patterns of hypertrophy are given in Table 2.3 and Figure 2.2.
● If the LV looks hypertrophied but the measured thickness is normal, this is
usually because of concentric remodelling. This is a precursor to hypertrophy
in pressure overload. It is defined by a relative wall thickness (RWT) >0.45.
16
LV Wall Thickness
Table 2.2 Grading LV wall thickness suggested by ASE/EACVI1, 2

Normal
thickened thickened thickened
Women
6–9 mm 10–12 mm 13–15 mm ≥16 mm
Men
6–10 mm 11–13 mm 14–16 mm ≥17 mm
Table 2.3 Patterns of hypertrophy
Symmetrical
Thick wall and reduced LV cavity size in response to pressure
Concentric load (e.g. aortic stenosis, systemic hypertension). Defined by
relative wall thickness >0.45.
Occurs to offset the high-wall stress resulting from LV dilata
tion (e.g. in volume load in aortic or mitral regurgitation).
Eccentric
Relative wall thickness <0.45.
Wall stress = LV pressure × (LVDD/wall thickness).
Asymmetrical Localised (e.g. LV apex or septum).
Figure 2.2 Patterns of LV hypertrophy.
17
Table 2.4 Grading LV mass suggested by ASE/EACVI using linear

dimensions*2
Mild Moderate Severe

Normal
hypertrophy hypertrophy hypertrophy
Women
LV mass (g) 67–162 163–186 187–210 >210
LV mass/
43–95 96–108 109–121 >121
BSA (g/m2)
Men
LV mass (g) 88–224 225–258 259–292 >292
LV mass/
49–115 116–131 132–148 >148
BSA (g/m2)
* LV mass = 0.83 × [(LVDD + IVS + PW)3 – LVDD3].
● RWT = (2 × posterior wall thickness)/LV diastolic diameter.

● Calculation of LV mass is not routinely necessary in clinical practice.
● A guide to grading LV mass is given in Table 2.4.
LV hypertrophy in obese patients (BMI >30 kg/m2) is a pathological process

and may be underestimated by indexing to BSA. Instead, LV mass should be
indexed to height with LV hypertrophy defined by LV mass >50 g/m in men and
>47 g/m in women6.
LV Volumes
● If the linear dimensions are abnormal or there is relevant pathology (e.g.
cardiomyopathy or valve disease), LV volume should be measured either by
2D or 3D and indexed to BSA.
● When ≥2 contiguous endocardial segments cannot be visualised in the
apical views, 3D calculations are not feasible and contrast agents should
be considered for 2D Simpson’s method if an accurate result is needed1.
● The BSE 2020 guideline, based on the NORRE dataset, gives a normal
range for LVEDVi of 30–79 mL/m2 for men and 29–70 mL/m2 for women3.
The cut point for severe dilatation is >91 mL/m2 for women and 103 mL/m2
for men3.
● Individual labs need to agree whether to report individual ASE/EACVI grades
(Table 2.5) or NORRE normal, abnormal, and severely dilated.
● International guidelines for cardiomyopathy still use ESC data.
18
LV Volumes
Table 2.5 ASE/EACVI grades for LV 2D-derived cavity volume2

Normal
dilated dilated dilated
Women
LVEDVi (mL/m2) 29–61 62–70 71–80 >80
LVESVi (mL/m2) 8–24 25–32 33–40 >40
LVEDV (mL) 46–106 – – >130

LVESV (mL) 14–42 – – >67
Men
LVEDVi (mL/m2) 34–74 75–89 90–100 >100
LVESVi (mL/m2) 11–31 32–38 39–45 >45
LVEDV (mL) 62–150 – – >200

LVESV (mL) 21–61 – – >85
Figure 2.3 LV 3D volume. 3D image acquisition focuses on including the entire left
ventricle within the pyramidal dataset. Volumetric measurements are based on tracings of
the interface between the compacted myocardium and the LV cavity. Use gated acquisition
full volume over two to six cardiac cycles.
19
● Normal ranges for 3D volumes vary widely but are larger than 2D volumes.
Suggested upper limits of normal for LVEDVi are 79 mL/m2 for men and 71 mL/m2
for women, and for LVESVi are 32 mL/m2 for men and 28 mL/m2 for women2.
● Serial comparison of 3D LV volumes and EF is useful in highly specialist
clinics (e.g. cardio-oncology, inherited cardiac conditions, valve clinics).
Measurements should be performed only when the 3D dataset is of good
quality, using the same equipment, ideally by the same operator, and
analysed on the same software.
LV Systolic Function
1. Regional LV wall motion
● Look at each arterial territory in every view.
● Describe wall motion abnormalities by segment (Figure 2.4) according
to their systolic thickening and phase (Table 2.6).
● Some centres assign a score to these descriptive categories. The most
common system is given in Table 2.6.
Figure 2.4 Arterial territories of the heart. The nomenclature of the

17-segment model is now established. Sometimes the apex is unreported if it is not seen
well. However, small apical aneurysms or apical thrombus may occur, and a stress test
may only be positive at the apex. The usual arterial territories are superimposed.
20
LV Systolic Function
Table 2.6 A commonly used wall motion scoring system
Wall motion Score

Normal 1
Hypokinesis (<50% normal movement) 2
Akinesis (absent movement) 3
Dyskinesis (movement out of phase with the rest of the ventricle) 4
Aneurysmal (paradoxical motion) 5
Table 2.7 Grading LV ejection fraction—biplane Simpson’s method3
Severely
Normal Borderline* Impaired
impaired**
≥55% 50–54% 36–49% ≤35%
* The values need to be interpreted with caution in individual cases. An EF 50–54% may be
normal in an athletic young subject, but may be abnormal if previously recorded as 60%
without changes in loading conditions or pre-chemotherapy.
** The cut point for severe impairment is either 30% or 35%, according to the published
guideline2, 3. Therapeutic decisions, for example, implantation of an AICD or CRT, usually
use 35% as the cut point. If EF is obtained using 3D imaging, these should be compared to
vendor-specific reference intervals.
2. Global LV systolic function

The minimum standard measurements are:
● LV ejection fraction (Table 2.7 for a guide to grading). LV systolic function
may still be impaired despite a normal LV ejection fraction if there are:
● Wall motion abnormalities
● Low VTIsubaortic
● Subtle abnormalities, for example, on Doppler tissue or GLS (see

page 22)
● Pulsed tissue Doppler systolic velocity (S’). Guidelines recommend
averaging the values at the lateral and septal mitral valve annulus in the
apical 4-chamber view. Some centres report just the septal value in the
text of the report. Methods of measurement and limitations are given
in Figure 2.5. Normal values are given in Table 2.8.
● Velocity time integral or stroke distance (VTIsubaortic). Measured
using pulsed Doppler in the LVOT outflow tract in the 5-chamber view.
● Stroke volume can be calculated using the LVOT radius (r):
● Stroke volume = πr2 × VTIsubaortic
● Cardiac output is stroke volume × heart rate

21
Figure 2.5 TDI S’ and E’. Peak systolic velocity of mitral annulus by pulsed TDI (cm/s)
is obtained by aligning the cursor to the direction of movement of the LV wall and placing the
sample volume at or within 10 mm of the insertion site of the mitral valve leaflets. Optimise the
velocity scale and baseline to demonstrate the full signal. Measurements are obtained at end-
expiration. Limitations: The S’, E’ velocities or E/E’ ratio should not usually be measured in the
presence of marked mitral annular calcification, prosthetic mitral valves, annuloplasty rings,
and severe mitral valve disease. The lateral site should not be used in pericardial constriction;
the septal site should be avoided in paced hearts. The site adjacent to the myocardial wall
infarction should not be used.
Table 2.8 Normal LV TDI average (lateral and septal) systolic velocity
according to age3
Parameter 20–40 years 40–60 years >60 years

S’ (cm/s) ≥6.4 ≥5.7 ≥4.9
● A normal VTIsubaortic is7:

● 17–23 cm with normal heart rate, 55–95 bpm.
● >18 cm with heart rate <55 bpm.
● <22 cm with heart rate >95 bpm to ensure a normal SV and CO.
● In acute decompensated heart failure or acute pulmonary

embolism, a VTIsubaortic <15 cm is associated with a poor prognosis7.
Other measures are used to detect subtle LV dysfunction in the

presence of normal or borderline LV ejection fraction:
● Global longitudinal strain (GLS) is used in cardio-oncology and
selected groups of patients with inherited cardiac conditions when
comparison with previous studies can be made using the same system
and analysed using the same software.
● Cut-off values from cardio-oncology guidelines are given in Table 2.9.
There are no agreed normal ranges for other clinical situations1–3.
● Left ventricular dP/dt is a relatively load-independent measure of the
development of LV pressure (Figure 2.6) and is used in LV disease and
valve disease.
22
LV Diastolic Function
● Normal is >1,200 mmHg/s, equivalent to a 25 ms delay between 1.0 and

3.0 m/s (Table 2.10).
Table 2.9 Cut-offs for adult GLS cardio-oncology clinics8
Normal GLS Borderline GLS Abnormal GLS

GLS <–18% –16% to –18% GLS >–16%
Figure 2.6 Estimating LV dP/dt. Measure the time (dt) between 1.0 m/s and 3.0 m/s
on the upstroke, which represents a pressure change of 32 mmHg [(4 × 3.0²) – (4 × 1.0²)]
using the short form of the modified Bernoulli theorem. dP/dt is then 32/dt.
Table 2.10 Guide to grading LV function by mitral regurgitant signal
Severely
Normal Abnormal
abnormal
dP/dt (mmHg/s) >1,200 800–1,200 <800
Time from 1 to
<25 25–40 >40
3 m/s (ms)
LV Diastolic Function
● The minimum standard study includes:
● Transmitral E and A peak velocity, E deceleration time, and E/A ratio.
23
● Peak E’ on the TDI signal at the level of the mitral valve annulus.
● LA volume using biplane method (apical 4-chamber and 2-chamber
views) indexed to BSA (see Chapter 6). Normal is <34 mL/m2. Dilatation
occurs in diastolic LV dysfunction.
● TR Vmax and estimated pulmonary pressure (see pages 43–45).
● Use these measures to describe the filling pattern as normal, slow-filling,
or restrictive (Table 2.11) and state if there is evidence of raised LV filling
pressures. Some labs grade LV diastolic dysfunction, but this carries the risk
of equating this with diastolic heart failure.
● In atrial fibrillation, diastole is already abnormal. It is still worth measuring
E, E deceleration, and E′ to look for restrictive filling.
● If the LV ejection fraction is <50%, the diagnosis of heart failure is
already made, but restrictive filling defines a group with a high risk of
decompensation or death.
Table 2.11 Definitions of filling patterns
MV E/A MV E LV filling
LV filling pattern E/E’ ratio
ratio (cm/s) pressure
Normal >0.8 >50 <10 Normal
Slow filling (grade I) ≤0.8 ≤50 <10 Normal
Pseudonormal (grade II) >0.8 but <2 >50 >14* Raised
Restrictive (grade III) E/A ≥2 >50 >14 Raised
* If E/E’ is between 10 and 14, use additional cut points: TR Vmax >2.8 m/s; LA vol indexed
>34 mL/m2; TDI E’ sep <7 cm/s or E’ lat <10 cm/s. The more of these are abnormal, the more
likely there is to be diastolic dysfunction9.
Figure 2.7 Left ventricular filling patterns. (a) Normal; (b) slow filling (low peak
E velocity, long deceleration time, high peak A velocity); (c) restrictive (high peak E velocity
with short E deceleration time with low or absent A wave).
24
LVEF >50%: Diastolic Heart Failure (HFpEF)?
● Restrictive filling is sometimes subdivided into reversible (normalises with

a fall in preload, for example, after a Valsalva manoeuvre) and irreversible.
Irreversible restrictive filling is associated with a particularly high risk of events.
LVEF >50%: Diastolic Heart Failure

(HFpEF)?
This is a clinical diagnosis which uses the TTE10 but cannot be made with the TTE
alone.
● The non-echocardiographic factors used are:
● Symptoms and clinical signs of heart failure
● Cardiovascular risk factors: body mass index >30 Kg/m2, hypertension,

atrial fibrillation
● Absence of other causes of breathlessness, including valve disease
● Raised level of B-type natriuretic peptide
● Other tests, including CMR, if amyloid is suspected; right heart catheter

with exercise to detect a rise in pulmonary capillary wedge pressure
● Suggestive TTE features include concentric LV remodelling or hypertrophy
and LA dilatation.
● TTE measurements suggesting diastolic dysfunction are given in Table 2.12.
● If LV diastolic function is indeterminate, assess pulmonary vein flow (Figure 2.8):
● The peak velocity of the pulmonary vein atrial flow reversal
● The duration of atrial flow reversal (PV Ar duration)
● The duration of the transmitral A wave (transmitral duration)
● The most reliable measure of diastolic dysfunction (Table 2.12) is the

pulmonary venous Ar reversal duration–transmitral A duration (Ar–A) >30 ms.
Table 2.12 Diastolic function using transmitral and pulmonary vein

pulsed Doppler11
Transmitral and PV Ar peak

Ar–A duration
TDI pattern velocity
Normal Normal Normal <0.35 m/s
Mild dysfunction Slow filling Normal <0.35 m/s
Moderate dysfunction Pseudo-normal Prolonged >30 ms >0.35 m/s
Severe dysfunction Restrictive Prolonged >30 ms >0.35 m/s
25
Figure 2.8 Pulmonary vein flow patterns. The systolic (S) and diastolic (D)
peaks of forward flow are marked. Atrial reversal (arrow) has a peak velocity of 0.35 m/s.
MISTAKES TO AVOID
● Incorporating a false LV tendon or RV trabeculation in the septal

measurement.
● Cutting the septum or LV cavity obliquely.
● Measuring the LV internal dimensions at the level of a sigmoid septum.
● Diagnosing diastolic heart failure from the echocardiographic filling
pattern alone.
● In a patient with clinical heart failure and preserved LV ejection fraction,
forgetting to consider pericardial constriction. Check for a dilated IVC
and septal bounce (Chapter 17).
● Diagnosing systolic dysfunction from a borderline LV ejection fraction in
an athletic subject (see page 63).
CHECKLIST FOR REPORTING LV FUNCTION

1. LV and LA dimensions.
2. Global and regional LV systolic function.
3. LV diastolic function +/– high filling pressure.
4. RV function and PA pressure.
26
LVEF >50%: Diastolic Heart Failure (HFpEF)?
References
1. Mitchell C, Rahko PS, Blauwet LA, et al. Guidelines for performing a
comprehensive transthoracic echocardiographic examination in adults:
Recommendations from the American Society of Echocardiography. J Am Soc
Echo 2019;32(1):1–64.
2. Lang R, Badano L, Mor-Avi V, et al. Recommendations for cardiac chamber
of Echocardiography and the European Association of Cardiovascular Imaging.
Europ Heart J CVI 2015;16(3):233–71.
3. Harkness A, Ring L, Augustine DX, et al. Guidelines and recommendations:
Normal reference intervals for cardiac dimensions and function for use
in echocardiographic practice: A guideline from the British Society of
4. Nishimura RA, Otto CM, Bonow RO, et al. AHA/ACC focused update of the 2014
ACC/ AHA guideline for the management of patients with valvular heart disease:
A report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines. Circulation 2017;135(25):e1159–95.
5. Ristow B, Ali S, Na B, Turakhia MP, Whooley MA & Schiller NB. Predicting heart
failure hospitalization and mortality by quantitative echocardiography: Is body
surface area the indexing method of choice? The heart and soul study. J Am Soc
Echocardiography 2010;23(4):406–13.
6. Singh M, Sethi A, Mishra AK, et al. Echocardiographic imaging challenges in
obesity: Guideline recommendations and limitations of adjusting to body size.
J Am Heart Assoc 2020;9(2):1–9.
7. Blanco P. Rationale for using the velocity–time integral and the minute distance
for assessing the stroke volume and cardiac output in point-of-care settings.
Ultrasound Journal 2020;12(1):21.
8. Liu J, Barac A, Thavendiranathan P & Scherrer-Crosbie M. Strain imaging in cardio-
oncology. J Am Coll Cardiol Cardio-oncology 2020;2(5):677–89.
9. Nagueh SF, Smiseth AO, Appleton CP, et al. ASE/EACVI guidelines and standards:
Recommendations for the evaluation of left ventricular diastolic function by
echocardiography: An update from the American Society of Echocardiography
and the European Association of Cardiovascular Imaging. J Am Soc Echo
2016;29(4):277–314.
10. Pieske B, Tschope C, de Boer RA, et al. How to diagnose heart failure with
preserved ejection fraction: The HFA–PEFF diagnostic algorithm: A consensus
recommendation from the Heart Failure Association (HFA) of the European Society
of Cardiology (ESC). Europ Heart J 2019;40(40):3297–317.
11. Redfield MM, Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR & Rodeheffer
RJ. Burden of systolic and diastolic ventricular dysfunction in the community:
Appreciating the scope of the heart failure epidemic. J Am Med Assoc
2003;289(2):194–202. 27
Acute Coronary
Syndrome 3
Echocardiography is indicated:
● To help determine whether a mildly raised troponin level is caused by a new
cardiac event or non-cardiac illness.
● After myocardial infarction to determine residual LV function and to look for
complications.
● In acute chest pain with suspected myocardial infarction (with non-
diagnostic ECG or ST segment changes), and when the scan can be
performed during pain, to aid the differentiation between myocardial
ischaemia and other causes (e.g. pericarditis or aortic dissection).
● As an emergency in cardiac decompensation, to look for acute complications,
for example, papillary muscle rupture or ventricular septal or free wall rupture1.
1. Assess regional LV systolic function

The working diagnosis is confirmed by a regional wall motion abnormality,
without scarring, in an arterial territory:
● Describe the segments affected (see Figure 2.4, page 20).
● Comment on the other regions. Compensatory hyperkinesis is a good
prognostic sign. Hypokinesis of a territory other than of the acute
ischaemia could suggest multivessel disease and is a poor prognostic sign.
● Are there thin segments implying previous coronary events?
● Consider enhancement with transpulmonary contrast if two or more
adjacent segments are not well seen or LV thrombus is suspected.
● A wall motion abnormality affecting the mid and apical LV segments,
with preserved or hyperdynamic function of the basal segments,
suggests Takotsubo cardiomyopathy (Table 3.1)2, 3, especially in women
aged >50 after an emotional shock.
2. Global systolic function

● Report global LV systolic function (Chapter 2).
● Report LV ejection fraction and LVOT velocity time integral, as both
have important prognostic information.
● If the LV ejection fraction appears impaired by eye, measure systolic
and diastolic volumes using biplane Simpson’s method or 3D when
available and feasible. The LV ejection fraction is used to guide medical
treatment and the decision for biventricular pacing and/or defibrillator.
29
DOI: 10.1201/9781003242789-3
Acute Coronary Syndrome
Table 3.1 Features of Takotsubo cardiomyopathy3
Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid-

segments with or without apical involvement.
The regional wall motion abnormalities extend beyond a single epicardial
vascular distribution.
Absence of significant obstructive coronary disease* or angiographic evidence
of acute plaque rupture.
New electrocardiographic abnormalities (either ST-segment elevation and/or T
wave inversion) or modest elevation in cardiac troponin.
Absence of phaeochromocytoma or myocarditis.
* May rarely coexist with obstructive coronary disease.
3. Right ventricle
● Assess RV size and regional and global systolic function (Chapter 4).
● Up to 30% of all inferior infarcts are associated with RV infarcts, and in
10%, the RV involvement is haemodynamically significant.
● Estimate pulmonary artery pressure (Chapter 5).
4. Describe the mitral valve

● Mitral regurgitation is common after myocardial infarction (Table 3.2).
● A restricted posterior leaflet causing a posteriorly directed jet is common
after an inferior or inferolateral (posterior) infarction (Figure 3.1).
● ‘Tenting’ of both leaflets leading to a central jet occurs when there is
dilatation of the mid and apical parts of the LV cavity (Figure 9.5, page 107).
● More complex situations can arise with restriction of some parts of the
leaflet and prolapse of other parts. This can be secondary to stretching
or rupture of minor chords or papillary muscle dysfunction.
● Grade the mitral regurgitation (Chapter 9, pages 114 and 115). Even moderate
mitral regurgitation affects mortality independent of other factors2 and may
influence the decision to offer surgery rather than coronary angioplasty.
● 3D TTE and, occasionally, 2D/3D TOE may be required for the detailed
evaluation of mitral valve morphology and the mechanism of regurgitation4.
Table 3.2 Causes of mitral regurgitation after myocardial infarction
Restricted posterior mitral leaflet (Figure 3.1)

LV dilatation leading to symmetrical ‘tenting’ of the mitral leaflets
Rupture of major chords
Dysfunction or rupture of papillary muscle
Mitral prolapse secondary to minor chordal dysfunction
30 Coexistent primary mitral valve disease
Figure 3.1 Restricted posterior mitral leaflet. Abnormal stresses on the posterior
mitral leaflet as a result of an inferior or inferolateral myocardial infarct cause systolic restriction
of the posterior leaflet (left), ‘asymmetric tenting’, with a posteriorly directed jet of regurgitation
(right).
And here’s an electronic link to a loop on the website or use

http://goo.gl/B5IO2h
And here’s an electronic link to 3 or 4 loops on the website or use

http://goo.gl/txLqiv
Table 3.3 Complications after myocardial infarction detected on TTE1
True aneurysm (Figure 3.2a) False aneurysm (Figure 3.2b)

Mitral regurgitation (Table 3.2) Papillary muscle dysfunction/rupture
Ventricular septal rupture Free-wall rupture ± tamponade
Thrombus (Table 18.6, page 206)
Heart failure/cardiogenic shock* Pericarditis*
* Clinical diagnosis supported by focused echocardiography.
5. Complications (Table 3.3)

● If there is a murmur, check for mitral regurgitation and ventricular septal
rupture. These may occasionally coexist. Off-axis views are often necessary.
● A ventricular septal rupture may initially be obvious from abnormal
systolic flow in the RV.
31
Figure 3.2 True and false aneurysm. A true aneurysm (a) is caused by the infarct
bulging outwards so that there is a wide neck, and the myocardium is often seen in the
border zone of the aneurysm. A false aneurysm (b) is a rupture of the infarcted myocardial
wall with blood contained by the pericardium so that the false aneurysm contains no
myocardial tissue.

http://goo.gl/wvoGQ4
● If there is mitral regurgitation, consider the causes in Table 3.2.

● All complications must be reported immediately to the clinician in
charge of the case.
● A true aneurysm complicates about 5% of all anterior infarcts and is a sign
of poor prognosis. It must be distinguished from a false aneurysm caused
by free wall rupture contained by the pericardium (Table 3.4) (Figure 3.2).
● Occasionally, a true aneurysm leaks and is associated with a false
aneurysm.
● Sometimes an aneurysm is found in the absence of an acute history.
The differential diagnosis is given in Table 3.5.
6. Consider stress echocardiography
Indications for stress echocardiography in an acute coronary syndrome1 include:
● Typical cardiac chest pain with normal or equivocal ECG changes (e.g.
LBBB, RBBB, paced rhythm) and normal troponin levels.
● Normal or minimal troponin rise, but clinically stable, and high risk for
32 contrast angiography (e.g. renal failure).
● Residual coronary stenosis in a non-culprit vessel, and decision for

intervention to be based on ischaemic burden.
● Low-dose viability assessment if this will affect intervention.
Table 3.4 Differentiation of true and false aneurysms
True aneurysm False aneurysm

(Figure 3.2a) (Figure 3.2b)
More commonly
Position More commonly apical
inferolateral
Neck Commonly wide Commonly narrow
Lining of aneurysm Myocardium Pericardium
Gradually thinning myocardium Punched-out edge to
Border zone
stretching into the aneurysm the myocardium
Into in systole, out in
Colour flow Absent or very slow flow
diastole
Table 3.5 Differential diagnosis of apical aneurysm as a presenting

feature
Coronary disease
Syphilis
Chagas disease
Iatrogenic (e.g. surgical vent)
Congenital
Tuberculosis
Hypertrophic cardiomyopathy (Chapter 7, page 67)
Arrhythmogenic RV cardiomyopathy with LV involvement
MISTAKES TO AVOID
● Failing to detect secondary mitral regurgitation and to determine its

aetiology.
● Missing inferior wall motion abnormalities with incomplete views.
● Missing a ventricular septal rupture by not using off-axis views.
● Not responding to a hyperdynamic LV, which may suggest a large
ventricular septal rupture or severe mitral regurgitation.
● Not looking for the other cardiac causes of chest pain when the
LV appears normal—aortic dissection and pulmonary embolism
(Tables 19.2 and 19.5, pages 214 and 215). 33
CHECKLIST REPORT IN ACUTE CORONARY

SYNDROME
1. LV size and function.
a. Dimensions.
b. Regional wall motion.
c. Global systolic function.
2. Complications (Table 3.3), including mitral regurgitation grade and
mechanism.
3. RV size, regional and global systolic function.
4. Estimated pulmonary artery systolic pressure.
5. Exclude other causes of acute chest pain, especially aortic dissection and
acute pulmonary embolism.
References
1. Chatzizisisa YS, Venkatesh L, Murthyb VL & Solomona S. Echocardiographic
evaluation of coronary artery disease. Coronary Artery Disease 2013;24:613–23.
2. Ghadri JR, Ruschitzka F, Luscher TF & Templin C. Takotsubo cardiomyopathy: Still
much to learn. Heart 2014;100:1804–12.
3. Prasad A, Lerman A & Rihal CS. Apical ballooning syndrome (Tako-Tsubo or
stress cardiomyopathy): A mimic of acute myocardial infarction. Am Heart
J 2008;155:408–17.
4. Doherty JU, Kort S, Mehran R, Schoenhagen P & Soman P. ACC/AATS/AHA/ASE/
ASNC/HRS/SCAI/SCCT/SCMR/STS 2019 appropriate use criteria for multimodality
imaging in the assessment of cardiac structure and function in nonvalvular heart
disease. J Am Coll Cardiol 2019;73:488–516.
34
The Right Ventricle
4
● RV function affects prognosis in all types of cardio-pulmonary disease.
● A basic scan is done for suspected pulmonary embolism or in COVID-19
looking for RV dilatation.
● For a minimum standard study, the assessment includes:
● Relative RV size in comparison with other cardiac chambers.
● Measurement of the basal RV inflow diameter (RVD1 in Figure 4.1).
● RV systolic function (TAPSE and DTI of TV annulus).
● A comprehensive assessment should be considered if it will change

management and there is:
● RV dilatation on the initial study
● Congenital heart disease
● Severe left-sided valve disease
● Right-sided valve disease
● Suspected RV cardiomyopathy
● Pulmonary hypertension
● Cardiac transplantation
1. Is the RV dilated?
● Use multiple views optimised for the RV:
● Parasternal long- and short-axis views at the aortic level for the
measurement of RVOT diameter.
● Parasternal short-axis views at basal, mid-, and apical RV levels
(obtained at corresponding levels for the LV short-axis views).
● The RV-focused apical 4-chamber view (Figure 4.1).
● The RV is significantly dilated when it looks the same size or larger

than the normal LV in the apical 4-chamber view (be careful when
the left heart is also dilated).
● As a guide, a diameter >41 mm at the base (RVD1) or >35 mm at
the mid-level (RVD2) (Figure 4.1) in the RV-focused view indicates
RV dilatation1.
● If the RV is dilated, multiple 2D diameters should be measured
(Table 4.1), as explained in Figure 4.1.
● The new NORRE recommendations2, 3 are significantly different from
the joint ASE/EACVI 2015 guidelines1 (Table 4.1). The clinical implications
have not been explored, but the ASE/EACVI 2015 values are still used
for current guidelines on managing pathology, for example, ARVC.
● We suggest using the ASE/EACVI values until a consensus emerges.
35
DOI: 10.1201/9781003242789-4
The Right Ventricle
Figure 4.1 2D RV measurements

in ARVC/D. These images show the
recommended RV measurements in
patients suspected of ARVC/D: (a) Dilated
RVOT at 52 mm in PLAX view; (b) dilated
RVOT in short-axis view, with proximal
dimension at 48 mm and distal dimension
at 31 mm; (c) dilated RV in apical
4-chamber view with RVD1 at 59 mm,
RVD2 at 55 mm, and RV length at 83 mm.
Table 4.1 Upper limit of normal RV dimensions (mm)
ASE/EACVI NORRE2, 3
RV dimensions
20151 Male Female
RVOT (P/S long-axis) 30 – –
RVOT proximal (P/S short-axis) 35 44 42
RVOT distal (P/S short-axis) 27 29 28
Basal (RVD1) 41 47 43
Mid (RVD2) 35 42 35
Length base to apex (RVD3) 83 87 80
RV areas (cm2/m2)
RVED area (men) ≤12.6 ≤13.6
RVED area (women) ≤11.5 ≤12.6
36
The Right Ventricle
Table 4.2 Suggested upper limit of normal for RV 3D volumes (mL/m2)1
RV 3D volumes
Male Female
(mL/m2)
RVEDV 87 74
RVESV 44 36
● Take care in measuring RV end-systolic and end-diastolic

measurements since major variability is caused by:
● Failure to optimise the RV-focused apical views.
● The presence of RV trabeculations and the moderator band.
● Limited visualisation of the endocardium.
● Sex-specific values and BSA indexing of 2D-derived values are included in all
recent recommendations1–3 but are not routinely used in clinical practice.
● If the RV is confirmed as dilated on 2D linear measurements and
systolic function is visually impaired, the measurement of RV volumes
on 3D is recommended.
● Normal 3D echo values for RV volumes are still to be established in
large population groups. The ASE/EACVI 2015 guidelines give the 3D
RV upper volumes in Table 4.2.
● RV 3D volumes are lower than by CMR, but the RV ejection fraction is
similar by both techniques1.
2. If dilated, is the RV active or hypokinetic?

● An active RV suggests volume overload caused by a left-to-right shunt at
atrial level or significant tricuspid or pulmonary regurgitation (Table 4.3).
Table 4.3 Causes of RV dilatation
Active RV
Left-to-right shunt above the RV (e.g. ASD)
Severe tricuspid or pulmonary regurgitation
Hypokinetic RV
RV pressure overload: acute or chronic pulmonary embolism, congenital heart
disease (with RV outflow obstruction), ARDS, severe left-sided heart disease
RV infarction
RV cardiomyopathy
End-stage pulmonary stenosis or regurgitation or tricuspid regurgitation
Post–cardiac surgery and lobectomy, pneumonectomy
Constrictive pericarditis and post-pericardiectomy
37
The Right Ventricle
Table 4.4 Thresholds for abnormal RV function1
Tissue Doppler systolic velocity <10 cm/s

TAPSE <17 mm
RV FAC <35%
RV 3D EF <45%
RV free wall strain (research use) >–19% (absolute value <19%)
● A hypokinetic RV suggests either pressure load or myocardial disease

(Table 4.3).
● Look for RV regional wall motion abnormalities and always check the
inferior wall of the LV, because about a third of inferior LV infarcts are
associated with RV infarction.
● A dilated RV with regional wall motion abnormalities (+/– aneurysms),
especially in the context of a family history of sudden cardiac death,
suggests ARVC (see page 75).
3. Quantification of RV systolic function (Table 4.4)

● Tissue Doppler imaging (TDI) measured as described in Figure 4.2a.
An S′ velocity <10 cm/s indicates RV systolic dysfunction.
● TAPSE (tricuspid annular plane systolic excursion) measured as
described in Figure 4.2b. TAPSE <17 mm is abnormal.
● RV 2D fractional area change (FAC) provides an estimate of global
RV systolic function. This can be performed manually in the apical
4-chamber view but otherwise is generated automatically from the RV
3D data (Figure 4.3). RV FAC < 35% indicates RV systolic dysfunction1.
Figure 4.2 Assessment of RV systolic function. (a) Peak TDI systolic velocity
of the tricuspid annulus. Place a pulsed Doppler tissue sample on the tricuspid annulus,
ensuring good alignment with the RV free wall motion. Record the peak systolic velocity.
(b) RV TAPSE. Place the M-mode cursor on the junction between the RV free wall and
tricuspid annulus in a 4-chamber view. Ensure it is exactly aligned along the direction
of the tricuspid lateral annulus, avoiding cutting through the RV basal lateral wall
38
myocardium. Measure the excursion as the vertical distance between the peak and nadir.
The Right Ventricle
● RV 3D ejection fraction (Figure 4.3)

● May be useful after cardiac surgery (in the absence of marked
septal shift), since conventional indices (TAPSE, S′) are no longer
representative.
● As a guide, RV ejection fraction <45% suggests abnormal RV
systolic function1.
4. Is there RV hypertrophy?
● Defined by a free wall thickness >5 mm. This is best measured in the
subcostal view level with the tips of the tricuspid valve.
● RV hypertrophy suggests:
● Pulmonary hypertension (page 45).
● Storage diseases—e.g. Fabry, Pompe.
● Infiltrative diseases—e.g. amyloidosis.
● Hypertrophic cardiomyopathy, Noonan’s syndrome.
Figure 4.3 RV 3D volumes. All four chambers of the heart must be included within
the pyramidal dataset to allow correct recognition of the RV. Use gated-acquisition full
volume over four to six cardiac cycles for the best results. 3D data analysis is performed
automatically and allows for manual correction of borders, both at end-diastole and
systole. The analysis results include all RV apical linear dimensions, RV volumes, RV
ejection fraction, FAC, and TAPSE from a single 3D volume dataset.
39
The Right Ventricle
Figure 4.3 (Continued)
5. Is there left-sided disease?

● RV dilatation secondary to pulmonary hypertension may complicate
severe mitral stenosis.
● It can also occur in end-stage aortic stenosis and, occasionally, mitral
regurgitation or severe LV dysfunction.
6. Is there evidence of a shunt above the RV?
● If the RV is dilated and active but no ASD is visible, injection of agitated
saline may help unmask it.
● Otherwise, consider TOE, CMR, or CT to detect a sinus venosus
defect or partial anomalous pulmonary venous drainage.
7. Is there tricuspid and pulmonary regurgitation (pages 121 and 125)?
8. Estimate pulmonary artery pressure (Chapter 5)
9. Other imaging modalities:
● CMR is the gold standard technique for assessing RV volumes
and should be considered for serial studies in patients with severe
pulmonary regurgitation to guide the timing of intervention.
40
The Right Ventricle
MISTAKES TO AVOID
● Overestimating RVOT dimensions by scanning from low parasternal

positions.
● Foreshortening the RV by scanning from a rib space too high, which can
lead to overestimating the transverse diameters.
● Including pericardial fat, trabeculations, or papillary muscles when
measuring RV wall thickness.
● Incorrect cursor alignment to include the RV basal free wall adjacent
to the tricuspid annulus when assessing TAPSE. This underestimates
values.
● Including trabeculations, papillary muscles, and moderator band when
tracing RV endocardium for measuring RV area or volume.
CHECKLIST REPORT FOR THE RV

1. RV size.
2. Global and regional RV systolic function.
3. Pulmonary pressures (Chapter 5).
4. Right-sided valve disease (Chapter 10).
5. Evidence of a shunt (Chapters 6 and 16).
6. Presence of left-sided disease.
References
1. Lang RM, Badano LP, MD, Mor-Avi V, et al. Recommendations for cardiac chamber
J Am Soc Echo 2015;28(1):1–39.
2. Lancellotti P, Badano LP, Lang RM, et al. Normal reference ranges for
echocardiography: Rationale, study design, and methodology (NORRE Study).
Europ Heart J CVI 2013;14(4):303–8.
3. Harkness A, Ring L, Augustine DX, et al. Guidelines and recommendations:
Normal reference intervals for cardiac dimensions and function for use
in echocardiographic practice: A guideline from the British Society of
41
5
Pulmonary Pressure
and Pulmonary
Hypertension
● An elevated pulmonary artery (PA) systolic pressure is a marker of a poor

clinical outcome, regardless of aetiology.
● The assessment of right-sided pressures is needed for two reasons:
● The estimation of PA systolic pressure, where this is needed to aid
clinical management, notably in mitral valve disease.
● The detection of pulmonary hypertension.
Estimating PA Systolic Pressure

1. Estimating the right ventricular (RV) to right atrial (RA) pressure difference
● Measure the TR Vmax.
● Ensure correct alignment with the direction of the jet.
● Obtain a full Doppler envelope. Inspiratory hold or bubble contrast

may be helpful for trivial jets of TR.
● If the signal varies, take the highest value.
● Estimate the RV–RA pressure difference (4 × TR Vmax)2.

● Estimate the RA pressure (see next section and Tables 5.1 and 5.2).
● The sum of the RV–RA pressure difference and RA pressure gives
an estimate of RV systolic pressure. This is the same as PA systolic
pressure, assuming that there is no pulmonary stenosis or other RV
outflow obstruction.
Table 5.1 Estimating RA pressure1*
Normal Intermediate High

0–5 mmHg 5–10 mmHg 10–20 mmHg
Mean Mean Mean
3 mmHg 8 mmHg 15 mmHg
IVC diameter (mm) ≤21 ≤21 >21 >21
Collapse with sniff >50% <50% >50% <50%
* Either a range or a mean value may be used, depending on local preference.
43
DOI: 10.1201/9781003242789-5
Pulmonary Pressure and Pulmonary Hypertension
Table 5.2 Secondary indices if the RA pressure estimate is intermediate
Restrictive right-sided filling pattern (tricuspid E/A >2.1, deceleration time <120 ms)
Tricuspid E/E’ >6
Diastolic flow dominance in the hepatic vein
RA dilatation with no other cause (e.g. tricuspid regurgitation or atrial
fibrillation)
Displacement of atrial septum to the left throughout the cycle
● This method has only moderate precision, and significant under- and
overestimation can occur. The measurement of TR Vmax should always be
used in conjunction with other TTE markers of pulmonary hypertension2, 3.
● In patients with severe free-flowing TR, the correlation between TR Vmax
and RV/PA systolic pressure is poor and an estimate should not be made.
● If there is any RV outflow obstruction (e.g. pulmonary stenosis), the RV
systolic pressure will not reflect the PA systolic pressure. It is important
to check the whole of the RV outflow (sub-pulmonary area, pulmonary
valve, main and branch pulmonary arteries) for evidence of obstruction4.
● Large left-to-right shunts (e.g. large VSD, aorto-pulmonary window,
PDA) will cause equalization of RV/PA pressure with LV/aortic pressure.
There is no need to measure the TR Vmax, as it will just reflect the
systemic systolic blood pressure4.
● A VSD ejecting into the region of the tricuspid valve may ‘contaminate’
the spectral Doppler trace, making it uninterpretable4.
2. Estimating right atrial (RA) pressure
● This is based on the diameter of the IVC (subcostal view) and response
to a sniff (Tables 5.1 and 5.2).
● The diameter should be measured at end expiration close to the
junction with the hepatic veins 10–20 mm from the ostium of the RA.
● Avoid the IVC moving out of the imaging plane during sniffing, which
can exaggerate the reduction in diameter.
● In acutely ill patients in whom the subcostal view is suboptimal, a
right anterior oblique mid-axillary view can be used instead5.
● Estimating RA pressure is semi-qualitative.
● When IVC diameter and response to a sniff are discordant
(intermediate in Table 5.1):
● Assign as ‘high’ if the IVC collapses <50%.
● Assign as ‘normal’ if there are no secondary indices (Table 5.2).
● Assign as ‘intermediate’ if the IVC collapses >50% but there are

some secondary indices (Table 5.2).
44
Assessing the Probability of Pulmonary Hypertension
3. Making the estimate of PA systolic pressure

RV systolic pressure is the sum of the RV–RA pressure difference plus the
estimated RA pressure, provided there is no RV outflow obstruction.
● In mitral stenosis, a PA systolic pressure >50 mmHg at rest is an
indication for balloon valvotomy, even in the absence of symptoms6.
● In severe aortic stenosis (AS), a PA systolic pressure >60 mmHg
indicates a high risk of dying, unless surgery or a TAVI is performed6, 7.
● This identifies the patient as having critical AS, meaning, that
intervention is needed as soon as possible.
● Inform the clinician in charge of the case.
● A rise in TR Vmax is a secondary sign of deterioration in any type of

valve disease and may aid the cardiologist to recommend intervention
in otherwise-equivocal cases.
Assessing the Probability

of Pulmonary Hypertension
● Pulmonary hypertension (PH) is defined as a mean pulmonary arterial
pressure (mPAP) ≥25 mmHg at rest by right heart catheterization.
● However, the probability of PH can be estimated from the TR Vmax at rest
(Table 5.3).
● If the TR signal is not analysable, the signal may be improved by bubble
contrast.
1. Estimating the probability of PH from the PA systolic signal
● A PA acceleration time >105 ms excludes pulmonary hypertension10,
and <80 ms makes pulmonary hypertension highly likely. This method
is not accurate enough to give an estimate of absolute pressure
(Figure 5.1a).
2. Estimating the probability of PH from the PR late-diastolic signal
● Optimise the continuous wave pulmonary regurgitant signal ideally to
capture the full waveform.
Table 5.3 Probability of PH based on TR Vmax
TR Vmax Probability of PH
≤2.8 m/s Low
2.9–3.4 m/s Check for other signs of PH (Figure 5.3)
>3.4 m/s High
45
Figure 5.1 Pulmonary artery velocity waveform and acceleration time.

A normal waveform with time to peak velocity 120 ms (a) and a recording in a patient with
pulmonary hypertension (b). The time to peak velocity is short and the signal is notched
because of increased wave reflectance.
46
Figure 5.2 Pulmonary regurgitation. Pulmonary artery end-diastolic pressure is

estimated using the end-diastolic velocity of the pulmonary regurgitant continuous wave
signal (arrow) added to an estimate of RA pressure: (a) is a signal from a patient with a
normal PA pressures, and (b) from a patient with pulmonary hypertension.
47
Figure 5.3 Signs suggesting pulmonary hypertension.
● Measure the end-diastolic velocity of the pulmonary regurgitant signal

(Figure 5.2) and estimate the pressure difference (4v2).
● An end-diastolic pressure difference >5 mmHg suggests PH8.
● To estimate PA end-diastolic pressure:
● Estimate the RA pressure (Tables 5.1 and 5.2).
● End-diastolic PA pressure = PR end-diastolic pressure difference +

RA pressure.
● This technique is not reliable if there is severe PR4.
48
3. Estimating the probability of PH from the PR early-diastolic

signal
● Measure the peak velocity of the pulmonary regurgitant signal. A Vmax
>2.2 m/s suggests PH.
● To estimate mean PA pressure:
● Calculate the pressure difference (4v2).
● Estimate the RA pressure (Tables 5.1 and 5.2).
● Mean PA pressure = PR peak diastolic pressure difference + RA

pressure.
● A summary of signs suggesting pulmonary hypertension is given
in Figure 5.3.
4. Assess RA and RV size and systolic function (Chapters 4 and 6)

● Flattening of the interventricular septum in systole causing a
‘D-shaped’ LV cavity is a clue that there could be PH.
● An RA area >20 cm2 is enlarged. One cause is PH.
5. Look for causes of pulmonary hypertension

● The cardiac causes will be seen on TTE (Table 5.4).
● Other causes may be suggested by the presence of valve thickening or
regurgitation (e.g. SLE, antiphospholipid syndrome, anorexic drugs) or
aortic dilatation (e.g. rheumatoid arthritis).
Table 5.4 Cardiac causes of pulmonary hypertension detectable on TTE9
Pulmonary venous hypertension

Valve disease
● Mitral valve disease (stenosis > regurgitation)
● Severe aortic stenosis (pulmonary hypertension in at least 25%)
Severe left ventricular impairment
● Cardiomyopathy
● LV failure of any cause
Congenital heart disease without shunts
● Coarctation
● Subaortic or supravalvar stenosis
Pericardial constriction
Left atrial obstruction
● Myxoma
● Cor triatriatum
(Continued)
49
Table 5.4 Cardiac causes of pulmonary hypertension detectable on

TTE9 (Continued)
Pulmonary venous hypertension (Continued)

Pulmonary vein obstruction
● Congenital vein stenosis
● Mediastinal pathology (fibrosis, tumour)
Chronic left-to-right shunts
ASD, VSD, patent ductus arteriosus, ruptured aortic sinus, aorto-pulmonary
window
6. Confirming pulmonary hypertension

● Proving the diagnosis and grading the severity of PH requires a right
heart catheter. The new haemodynamic definition of PH suggests a
mPAP>20 mmHg and PVR 2 WU as a means of early detection.11
MISTAKES TO AVOID
● Overdiagnosis of pulmonary hypertension when screening patients. The

TTE can only grade the probability of PH2.
● Over-reliance on the TR Vmax, which should always be used in
conjunction with other TTE markers.
● Overdiagnosis. Pulmonary pressures increase with age and weight, so
a pulmonary artery systolic pressure of 35–40 mmHg may be normal in
an elderly or obese patient1.
● Using IVC size and collapse in continuous mechanical ventilation since
these are unreliable. The pressure from a central line should be used
instead or judgements made using clinical observations.
CHECKLIST FOR REPORT IN PULMONARY

HYPERTENSION
1. Estimated pulmonary pressures or presence/absence of pulmonary
hypertension.
2. RV size and systolic function.
3. Tricuspid regurgitation grade.
4. Underlying cause.
50
References
1. McQuillan B, Picard M, Leavitt M & Weyman A. Clinical correlates and reference
intervals for pulmonary artery systolic pressure among echocardiographically
normal subjects. Circulation 2001;104(23):2797–802.
2. Augustine DX, Coates-Bradshaw LD, Willis J, et al. Echocardiographic assessment
of pulmonary hypertension: A guideline protocol from the British Society of
Echocardiography. Echo Res Pract 2018;5(3):G11–24.
3. Galie N, Humbert M, Vachieryc JL, et al. 2015 ESC/ERS guidelines for the diagnosis
and treatment of pulmonary hypertension. Europ Heart J 2016;37(1):67–119.
4. Skinner GJ. Echocardiographic assessment of pulmonary arterial hypertension for
pediatricians and neonatologists. Front Pediatr 2017;5:168.
5. Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA & Lester SJ.
Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol
2003;92(11):1373–6.
6. Baumgartner H, Falk V, Bax JJ, et al. 2017 ESC/EACTS Guidelines for the
management of valvular heart disease the task force for the management of
valvular heart disease of the European Society of Cardiology (ESC) and the
European Association for Cardio-Thoracic Surgery (EACTS). Europ Heart J
2017;38(36):2739–91.
7. Genereux P, Pibarot P, Redfors B, et al. Staging classification of aortic stenosis
based on the extent of cardiac damage. Europ Heart J 2017;38(45):3351–8.
8. Ristow B, Ahmed S, Wang L, et al. Pulmonary regurgitation end-diastolic gradient
is a Doppler marker of cardiac status: Data from the heart and soul study. J Am
Soc Echocardiogr 2005;18(9):885–91.
9. McLaughlin VV, Atcher SL, Badesch DB, et al. ACCF/AHA 2009 expert consensus
document on pulmonary hypertension. J Am Coll Cardiol 2009;53(17):1573–619.
10. Hoeper MM, Bogaard HJ, Condliffe R, et al. Definitions and diagnosis of
pulmonary hypertension. J Am Coll Cardiol 2013;62(52):D42–50.
11. Humbert M, Kovacs G, Hoeper MM et al. 2022 ESC/ERS Guidelines for the diagnosis
and treatment of pulmonary hypertension. Europ Heart J 2022;43(38):3618–3731.
51
The Atria and
Atrial Septum 6
Left Atrium
● Left atrial (LA) size is not accurately represented by a linear dimension or area.
● Left atrial diameter (measured on 2D in a parasternal long-axis view) is still used:
● In studies requested by electrophysiologists, since their literature still
uses this dimension.
● In hypertrophic cardiomyopathy, since the diameter is still part of the
formula used to estimate the risk of sudden death1.
● LA volume should always be measured in the following:
● Systemic hypertension (as a sign of chronically increased filling pressure).
● Atrial fibrillation (ant-post diameter and volume are both predictors of success
of electrical cardioversion, catheter ablation of AF, and thromboembolic risk).
● Suspected LV diastolic dysfunction.
● Mitral valve disease (thromboembolic risk, indirect marker of severity).
● Helping to discriminate an athletic heart from early cardiomyopathy (see

Chapter 7).
● Measuring LA volume:
● Planimeter the LA in optimised left atrial 4-chamber and 2-chamber
views, excluding the pulmonary veins and appendage. Use Simpson’s
method. Index to BSA if BMI <30 kg/m2.
Table 6.1 Upper limits of normal for left atrial size2, 3
Males Females
Ant-post dimension Absolute (mm) 43.3 40.6
Indexed (mm/m2) 22.7 24.0
Area Absolute (cm2) 20.3 22.0
Indexed (cm2/m2) 11.9 12.7
Volume* Indexed (mL/m2) 34 34
Note: Ant-post dimension measured in the anteroposterior plane in the parasternal long-axis view.
Area at end-systole in the apical 4-chamber view. Volume by Simpson’s biplane method at end-
systole in the apical 4- and 2-chamber views. Upper limit of normal (ULN) based on mean + 2 SD.
* ULN for indexed volume based upon expert consensus3, and corresponding absolute data not
available.
53
DOI: 10.1201/9781003242789-6
The Atria and Atrial Septum
● The upper limit of normal is 34 mL/m2 2, 3.

● Where suboptimal image quality permits measurement in only one
plane, values tend to be 1–2 mL/m2 smaller than the biplane equivalent.
There are no normal ranges for 3D LA measurements yet2.
● If there is a left atrial mass, see Chapter 18.
Right Atrium
● Right atrial area is measured in the minimum standard TTE. This is
particularly important if:
● It looks larger than the LA in the 4-chamber view.
● There is atrial fibrillation (likely success of cardioversion, thromboembolic risk).
● There is suspected RV or LV dysfunction.
● There is pulmonary hypertension.
● There is an ASD.
● There is tricuspid valve disease.
● Image the right atrium in the right heart apical 4-chamber view at end-systole.
● Volume can be measured using the single-plane Simpson’s method. Area is
then given automatically (Table 6.2).
● Atrial dilatation can give a clue to the diagnosis (Table 6.3).
● If there is a mass, see Chapter 18.
Atrial Septum
1. Is the septum thickened?
● Lipomatous hypertrophy is usually normal and occurs in a dumb-bell-
shaped distribution, sparing the fossa ovalis in the middle.
● An attached mass suggests a myxoma or, less commonly, a thrombus
caught in a PFO.
Table 6.2 Upper limits of normal for right atrial size3, 4*
Male Female
Area (cm2) 21.9 19.0
Indexed area (cm2/m2) 11.1 11.0
Volume (mL) 70.6 55.3
Volume (mL/m2) 35.5 31.4
* Although this is the most contemporaneous data range for the RA, it was measured using a
54
normal apical 4-chamber view. The upper limit is calculated as mean + 2 SD.
Atrial Septum
Table 6.3 Causes of atrial enlargement
Characteristically biatrial enlargement

Chronic atrial fibrillation
Restrictive cardiomyopathy
Rheumatic disease affecting mitral and tricuspid valves
Athletic heart (mild enlargement)
Pericardial constriction (mild or moderate enlargement)
Predominantly LA enlargement
Mitral stenosis or regurgitation
Left ventricular diastolic dysfunction
Predominantly RA enlargement
Tricuspid stenosis or regurgitation
Pulmonary hypertension
ASD
RV cardiomyopathy
2. Is the septum mobile or aneurysmal?

● An atrial septal aneurysm is defined5 (Figure 6.1) by:
● A mobile segment with base >10 mm wide.
● Excursion ≥10 mm between left and right atrium during spontaneous

respiration.
● A mobile septum is defined by an excursion of <10 mm and has no
pathological significance.
● An aneurysmal septum is often associated with a PFO. The presence
of both together is associated with a significantly higher recurrence
rate after cardioembolic stroke than with either alone6.
● Bowing of the whole septum may also occur as a result of severe TR or
MR or high RA or LA pressures.
● Sometimes, the aneurysm is fixed.
3. ASD or dropout?
● In the 4-chamber view, it is common to see dropout. The uncertainty is
usually resolved on other views and by the absence of abnormal flow
on colour mapping.
● If doubt remains, consider:
● A saline contrast injection, which may make the ASD obvious as a
void.
55
Figure 6.1 Atrial septal aneurysm. Maximum rightward (a) and leftward (b)
extent.
● Pulsed Doppler on the RA side of the septum. ASD flow has a peak
in late diastole and systole. For the superior vena cava, the peaks are
earlier.
● TOE or CMR: TOE gives superior imaging of the interatrial septum
and any defects. CMR provides accurate shunt quantification and
accurate ventricular volumes.
4. Is there a PFO?
● These occur on bubble contrast TTE in c15% of the normal population7
but may be more common and larger in:
● Young people with TIA or cerebral infarcts.
● Decompression sickness in divers.
● Disproportionate hypoxia in critically ill patients.
● The rarely seen patients who are normal lying down but become
breathless, with a drop in oxygen saturation, when they stand up
(platypnoea-orthodeoxia syndrome)8.
● A PFO may be seen on colour imaging, most frequently in a subcostal
view, with the colour scale reduced to maximise detection of
low-velocity flow.
● More usually, a bubble study is needed (Table 6.4). This is usually better
performed on TTE than TOE, since a Valsalva manoeuvre is easier in the
conscious patient. A PFO is usually taken to be present if bubbles appear in
the LA within three or fewer cardiac cycles after the contrast enters the RA.
56
Atrial Septum
Figure 6.2 Bubble contrast study. These show a moderate (a) and large
PFO (b).
Table 6.4 Performing a bubble contrast study
Allow adequate time. Practice the Valsalva manoeuvre at the start, ensuring
that image quality is minimally affected and there is good leftward deviation of
the atrial septum.
Ask the patient to breathe out then hold the breath and strain with the
abdomen against a closed glottis with minimal movement of the chest. Practice
instant release.
Place a 21 G cannula in an antecubital fossa vein and connect to a three-way
tap.
Fill a syringe with about 8.5 mL 0.9% saline. For each injection, leave
approximately 0.5 mL air in the syringe and withdraw approximately 1 mL
venous blood into the syringe.
Attach a dry syringe to the other port of the three-way tap and agitate between
the two syringes until a dense, uniform froth containing no large air bubbles is
produced.
For the initial injections, there may be no manoeuvre. With the Valsalva
manoeuvre, the injection should be timed to reach the right heart at release.
Other manoeuvres are asking the patient to cough or take a sharp sniff on right
heart opacification.
Multiple injections with Valsalva should be given until attaining at least one
with perfect synchronisation of all elements. Sometimes, several (up to 6) are
necessary.
Archive about eight to ten cycles capturing the contrast arriving in the right
heart and at least five cycles after this.
57
Table 6.5 Suggested methods of grading a patent foramen ovale9
Small A small number of individual bubbles

A few bubbles, but not sufficient to cause a bolus within the
Moderate
left atrium or to fill the whole of the left heart (Figure 6.2a)
Left atrial bolus of bubbles too numerous to count or
Large
bubbles filling the whole of the left heart (Figure 6.2b)
● Grading a PFO is controversial and subjective:

● Many thresholds for a large shunt appear in the literature based on the
number of bubbles crossing to the LA.
● However, counting individual bubbles is not usually easy in practice. We
use the grading system in Table 6.59.
● Individual studies should be discussed at an MDT concerning possible
closure.
● Pulmonary arteriovenous malformations are suggested by10, 11:
● Bubbles appearing after three cycles.
● Bubbles entering via the pulmonary veins.
● Slow clearance of the bubbles because of continuing replenishment.
MISTAKES TO AVOID
● Overdiagnosing atrial dilatation from a diameter in one plane.

● Missing LA dilatation by measuring only an anteroposterior dimension
without volume assessment.
● Failing to coordinate a Valsalva manoeuvre and the timing of the
contrast injection when looking for a PFO.
● Mistaking SVC flow for an ASD.
CHECKLIST FOR REPORTING THE ATRIA

1. Sizes of LA and RA.
2. If LA or RA dilated, is there an obvious cause (Table 6.3)?
3. Appearance of atrial septum.
4. Is there evidence of a shunt?
58
Atrial Septum
References
1. O’Mahony C, Jichi F, Pavlou M, et al. A novel clinical risk prediction model for
sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD). Eur Heart J
2014;35(30):2010–20.
2. Lang RM, Badano LP, Mor-avi V, et al. Recommendations for cardiac chamber
quantification by echocardiography in adults : An update from the American
Society of Echocardiography and the European Association of Cardiovascular
Imaging. J Am Soc Echocardiogr 2015;28(1):1–39.
3. Harkness A, Ring L, Augustine DX, et al. Normal reference intervals for cardiac
dimensions and function for use in echocardiographic practice: A guideline from
the British Society of Echocardiography. Echo Res Pract 2020;7(1):G1–18.
4. Kou S, Caballero L, Dulgheru R, et al. Echocardiographic reference ranges for
normal cardiac chamber size: Results from the NORRE study. Eur Heart J CVI
2014;15(6):680–90.
5. Gondi B, Nanda N. Two-dimensional echocardiographic features of atrial septal
aneurysms. Circulation 1981;63(2):452–7.
6. Snijder RJR, Luermans JGLM, de Heij AH, et al. Patent foramen ovale with
atrial septal aneurysm is strongly associated with migraine with aura: A large
observational study. J Am Heart Assoc 2016;5(12):1–7.
7. Rundek T, Elkind MSV, Di Tullio MR, et al. Patent foramen ovale and migraine:
A cross-sectional study from the Northern Manhattan Study (NOMAS). Circulation
2008;118(14):1419–24.
8. Cheng TO. Mechanisms of platypnea-orthodeoxia: What causes water to flow
uphill? Circulation 2002;105(6):e47.
9. Chambers J, Seed PT & Ridsdale L. Association of migraine aura with patent
foramen ovale and atrial septal aneurysms. Int J Cardiol. 2013;168(4):3949–53.
10. Rana BS, Thomas MR, Calvert PA, et al. Echocardiographic evaluation of patent
foramen ovale prior to device closure. J Am Coll Cardiol CVI 2010;3(7):749–60.
11. Freeman JA & Woods TD. Use of saline contrast echo timing to distinguish
intracardiac and extracardiac shunts: failure of the 3- to 5-beat rule.
Echocardiography 2008;25(10):1127–30.
59
Cardiomyopathies
7
● Cardiomyopathies are heart muscle diseases not caused by pressure or
volume overload or coronary artery disease1–3.
● They may be caused by primary familial (genetic) muscle disease, by
infiltrative processes (e.g. amyloid), by storage diseases (e.g. Fabry
disease), or by external agents (e.g. alcohol, radiation, anthracyclines).
● Their diagnosis is based on a balance of clinical factors (presentation, family
history, past medical history, examination), the ECG findings, and imaging.
● TTE is the first-line imaging technique and initially categorises as:
● Dilated LV, including dilated cardiomyopathy (DCM).
● Hypertrophied LV, including hypertrophic cardiomyopathy (HCM).
● Specific cardiomyopathies also have characteristic TTE features:

● Restrictive cardiomyopathy—non-dilated LV and RV with high filling
pressures and biatrial enlargement.
● Non-compaction—hypertrabeculation.
● Arrhythmogenic ventricular cardiomyopathy—RV dilatation, wall motion

abnormalities, +/– LV involvement.
The Dilated LV
● Secondary myocardial impairment and dilated cardiomyopathies may look
similar on TTE, but there may be clues to the aetiology (Table 7.1).
1. LV size and systolic function

● Is the LV large? Borderline cavity dimensions and volumes should be
indexed to BSA (Table 2.1, page 16).
● Is the LV hypokinetic (Table 7.1), normal, or hyperkinetic (Table 7.2)?
Borderline hypokinesis is normal in athletic hearts (Table 7.3).
2. General appearance
● Is there a regional abnormality suggesting an ischaemic aetiology
(Figure 2.4)?
● Are both ventricles dilated, suggesting a cardiomyopathy?
● Is there concentric LV hypertrophy, suggesting hypertension?
● Is there a valve abnormality which might have caused the myocardial
impairment?
61
DOI: 10.1201/9781003242789-7
Cardiomyopathies
Table 7.1 Causes of a dilated, hypokinetic LV
Common non-DCM cause

Regional wall abnormalities
Coronary artery disease
corresponding to coronary territories
Pressure overload
LVH, dilated aorta
Hypertension, severe AS
Volume overload Differentiating secondary from primary
End-stage MR, AR MR may be difficult (see Chapter 9)
LVH, valve calcifications, pericardial
Renal failure
effusion
DCM of acquired aetiology
Uncontrolled atrial tachyarrhythmia
Tachyarrhythmia
Very frequent ventricular ectopics
May recover after alcohol cessation
Alcohol
in 50%
Chemotherapeutic agents, verapamil,
Drugs
cocaine
Impaired LV relaxation, MR, pericardial
Autoimmune systemic diseases
effusion
Churg–Strauss syndrome
Valve thickening, non-bacterial
Systemic lupus erythematous
Libman–Sacks vegetations, pulmonary
(SLE)
hypertension, pericardial effusion
Thinning and dilatation crossing arterial
Sarcoidosis
territories
Last month of pregnancy and up to the
Peripartum cardiomyopathy
first five months after delivery
Early diastolic dysfunction with raised
Haemochromatosis (genetic
filling pressures and dilated LA
disorder of iron metabolism)
Arrhythmias (AF, VF)
Thalassaemia (inherited Biventricular DCM, restrictive filling (iron
haemoglobin disorder) overload), pulmonary hypertension
HIV (10% of asymptomatic cases),
Uncommon causes nutritional (thiamine), metabolic
(hypothyroidism)
Post myocarditis DCM
LV and RV increased wall thickness
Viral
Dilated and aneurysmal coronary arteries,
Other vasculitis—Kawasaki
LV regional wall motion abnormalities
62
The Dilated LV
Table 7.1 (Continued)
Genetically determined DCM (family history of HF, CM, SCD)

Muscular dystrophies
Duchenne and Becker muscular Inferolateral akinesia
dystrophy AV block, ventricular arrhythmias
LMNA cardiomyopathy
Idiopathic DCM
Unknown aetiology After excluding genetic factors
Specific preclinical DCM (new categories)4:
Familial history of SCD, ventricular
Arrhythmic DCM
arrhythmias
Normal size, hypokinetic LV, severe
Hypokinetic non-DCM
diastolic dysfunction
Table 7.2 Causes of a dilated, hyperkinetic LV
Valve disease
Severe aortic regurgitation
Severe mitral regurgitation
Moderate or worse mixed aortic and mitral regurgitation
Shunts
Ventricular septal defect
Ruptured sinus of Valsalva aneurysm
Persistent ductus
Table 7.3 Features of an athletic heart5, 6
Increased LV end-diastolic diameter (rarely >60 mm) may persist for >5 years
after stopping training. If associated with reduced LV ejection fraction and
abnormal diastolic function, suggests DCM.
Normal systolic function, occasionally borderline global hypokinesis.
Mild left ventricular hypertrophy, septum usually ≤13 mm.
Normal LV diastolic function.
Mild RV dilatation and hypertrophy.
63
Cardiomyopathies
Table 7.4 Echocardiographic findings in sarcoid7*
Dilated LV with global systolic dysfunction

Regional wall motion abnormalities not in a coronary artery distribution
Thin walls, most commonly the basal anterior septum (occasionally thickened
in early disease, becoming thin later)
LV aneurysms
Diastolic dysfunction—initially delayed relaxation, restrictive pattern in
advanced disease
Focal intracardiac mass caused by a large granuloma that may involve
papillary muscle, causing mitral regurgitation
RV dysfunction secondary to pulmonary disease
Pericardial effusion
Multisystem
* disorder characterised by the growth of tiny collections of inflammatory cells
(granulomas). High incidence of arrhythmias (AV block, BBB, SVT, VT) and SCD.
● Are there unusual features?

● Regional wall motion abnormalities crossing arterial territories (e.g.
sarcoid) (Table 7.4).
● Bright endocardial echoes (e.g. haemochromatosis).
● Apical echogenicity (consider thrombus, HCM, or non-compaction).
● Abnormal myocardial density (non-specific, but consider amyloid).
3. Quantify LV systolic function and assess LV diastolic function

See pages 20–25
4. Are there complications?
● LV thrombus
● Secondary mitral regurgitation (Table 7.5)
● Pulmonary hypertension (see Chapter 5)
5. Other imaging modalities:

● CMR8:
● Differentiation of ischaemia from other causes of LV dilatation by
the pattern of late gadolinium enhancement (transmural, patchy
subendocardial, global subendocardial, epicardial, mid-wall).
● Assessment of viability in ischaemic cardiomyopathy.
● Better than TTE for LV morphology, volumes, and ejection fraction if

image quality suboptimal.
● May help the diagnosis of myocarditis using T1 and T2-weighted
imaging to evaluate myocardial inflammation and oedema, and
gadolinium enhancement to assess diseased myocardium.
64
The Hypertrophied LV
Table 7.5 Differentiating primary and secondary mitral regurgitation

with a dilated LV
Favours secondary regurgitation

Mitral valve normal in appearance, with dilated annulus
Mitral valve tented
Review of echocardiograms showing LV function declining while mitral
regurgitation still mild
Favours primary regurgitation
Mitral valve abnormal in appearance (prolapsing, flail leaflet, or rheumatic)
Review of TTE shows severe mitral regurgitation with previously
hyperdynamic LV
● T2* imaging detects and quantifies iron deposits in the myocardium

in haemochromatosis.
● Detection of aneurysms in Chagas disease.
● CT coronary angiography: to look for coronary disease as a cause of
LV dilatation. Especially used instead of invasive coronary angiography
in young patients at low clinical risk of coronary disease.
● Invasive contrast coronary angiography: to look for coronary disease
as a cause of LV dilatation, especially in patients at high or intermediate
risk of coronary disease.
● PET: to identify myocardial viability.
MISTAKES TO AVOID
● Measuring LV obliquely, causing overdiagnosis of LV dilatation.

● Overdiagnosis of dilatation by not correcting for BSA in large individuals.
● Misdiagnosis of athlete’s heart as cardiomyopathy.
● Mistaking LV dilatation caused by primary mitral valve disease as
cardiomyopathy.
● The cause of LV hypertrophy may be obvious if there is aortic stenosis or
systemic hypertension.
● Often, it may be difficult to differentiate the effects of hypertension from
an athletic heart or hypertrophic cardiomyopathy or less-common causes
(Table 7.6).
65
Cardiomyopathies
Table 7.6 Causes of increased LV wall thickness9,10
Common
Hypertension
Aortic stenosis
Renal disease
African/Afro-Caribbean ethnicity
Obesity
Athletes (usually mild hypertrophy)
Cardiomyopathies
Hypertrophic cardiomyopathies (sarcomere)
Glycogen storage diseases (e.g. Pompe, Danon)
Lysosomal storage diseases (e.g. Anderson–
Metabolic genetic errors Fabry)
(storage disorders)
Carnitine disorders
AMP-kinase (PRKAG2)
Infiltrative disorders—amyloidosis (familial ATTR, senile TTR, AL)
Neuromuscular disease (e.g. Friedreich’s ataxia)
Malformation syndromes: Noonan, LEOPARD, Costello
Mitochondrial diseases
Drug-induced (e.g. tacrolimus, hydroxychloroquine, steroids)
1. Describe the pattern of hypertrophy

● Is it symmetrical or asymmetrical (Figure 2.2)?
● Does it affect RV as well as LV? Symmetrical LV and RV hypertrophy
suggests an infiltrative cardiomyopathy.
● Asymmetrical hypertrophy usually suggests HCM. Describe its
distribution, for example:
● Septal hypertrophy (reverse curvature).
● Apical (Figure 7.1).
● Septum and free wall, with sparing of the posterior wall.
● Papillary muscles hypertrophy +/– antero-apical displacement,

double-bifid papillary, direct insertion into the MV leaflets.
● Sigmoid septum or subaortic septal bulge. This is common in elderly
patients. It may be the first site of hypertrophy associated with
hypertension. If severe and in a young person with a family history,
it may also be consistent with HCM.
66
Figure 7.1 Apical hypertrophic cardiomyopathy. (a) Distal LV hypertrophy

involving apical segments; (b) LV apical colour flow acceleration.
2. If the hypertrophy is asymmetric, measure wall thickness at all levels.

● Measurements should initially be made in short-axis views perpendicular
to the circumference of the endocardium and epicardium.
● Exclude aberrant tendons and LV papillary muscles, RV papillary
muscles, or moderator band.
● Report the maximal wall thickness since this is used in the score to
estimate the risk of sudden cardiac death in HCM. A wall thickness
≥30 mm in any segment is a strong marker of sudden death.
● Measurements should be interpreted in the clinical context10:
● In first-degree relatives (50% risk of inheritance), maximal wall
thickness ≥13 mm is diagnostic of HCM.
● Apical hypertrophy ≥13 mm associated with marked T wave
inversion on the ECG is diagnostic of apical HCM.
● Wall thickness ≥15 mm in a young patient with abnormal ECG
and no previous medical history has a high probability of HCM.
Exceptions occur, for example, Afro-Caribbean athletes.
● Concentric hypertrophy 15–20 mm in African or Afro-Caribbean
people may be secondary to hypertension.
3. Quantify LV systolic and diastolic function.
● In HCM, LV radial systolic function is often preserved or increased, but
longitudinal systolic function is frequently impaired (GLS > –15%).
● A reduced LV ejection fraction <50% in HCM indicates a high risk for
sudden cardiac death.
● Impaired LV systolic function with significant concentric hypertrophy
suggests amyloid rather than HCM.
67
Cardiomyopathies
● In end-stage ‘burnt-out’ HCM, the LV may be dilated and hypokinetic, with

only mild hypertrophy. Review of older studies will validate the diagnosis.
● Impaired relaxation and pseudo-normal filling are the most common
patterns of diastolic dysfunction in HCM. Restrictive physiology may be
seen in advanced HCM but is more suggestive of amyloid.
4. Is there an apical aneurysm?
● Aneurysm formation (+/– thrombus) is uncommon in HCM (2% in HCM;
13–15% in apical HCM) but indicates a high risk for sudden death11.
● Contrast TTE or sometimes CMR are needed if image quality is suboptimal.
5. Measure LA size
● Measure LA linear dimension at end-systole in a 2D parasternal long-
axis view. This is used to calculate the risk of sudden cardiac death.
● Measure LA volume indexed to BSA (ideally on 3D, if available).
● LA dilatation (LA volume >34 mL/m2; LA diameter >48 mm)
predicts sudden cardiac death12 and indicates an increased risk of
thromboembolism.
6. Is there intra-LV or LVOT flow acceleration?
● Use colour and pulsed Doppler to locate the area of maximal flow
acceleration. Use CW Doppler to record the maximal velocity.
● Use pulsed Doppler to measure LVOT velocity at rest and CW if abnormal.
● Use CW before and after a Valsalva manoeuvre performed semi-supine
then sitting and, if no obstruction is provoked, on standing9,10.
● The measured peak LVOT gradient is used in the risk calculator of
sudden cardiac death. In addition:
● A peak gradient >50 mmHg, in symptomatic patients, is a threshold
for myomectomy or alcohol ablation.
● In patients with symptoms and resting or provoked LVOT gradient
<50 mmHg, consider exercise testing10 to look for worsening LVOT
acceleration.
7. Differential diagnosis of LVOT obstruction
● Look at the aortic valve and rule out AS or subaortic membrane as a
cause of LV hypertrophy and LV obstruction.
● Systolic anterior motion of the anterior mitral leaflet (SAM) causes a
dynamic, late-systolic peak velocity.
● AS and subaortic membrane cause a fixed obstruction with a velocity
peak in early or mid-systole.
● Do not forget the other haemodynamic and morphological changes
that can cause SAM and LVOT obstruction (Table 7.7). These can lead to
an overdiagnosis of HCM.
68
Table 7.7 Non-HCM SAM and LVOT obstruction
Haemodynamic changes Causes

Decreased preload Hypovolaemia
Fever, anaemia, inotropic drugs (e.g.
Increased LV inotropy
dobutamine)
Morphological changes Causes
Sigmoid septum Hypertension, elderly heart
Compensatory hyperkinesis of basal
Acute coronary syndromes
segments
Takotsubo cardiomyopathy Catecholamine effect
Annuloplasty ring with change in MV
Post–mitral valve repair
leaflet geometry
Transcatheter mitral valve in ring Change in native MV leaflet
implant orientation into LVOT
8. Assess the valves

Mitral valve:
● Look for SAM of the MV leaflets or of the chords alone.
● SAM more often involves the anterior leaflet but may occasionally
affect the posterior leaflet alone or, more rarely, both.
● Is SAM incomplete or complete (leaflet contacts the septum)?
● Mitral regurgitation is mostly directed posteriorly away from the point
of anterior motion but, in some cases, could be central or anteriorly
directed.
● Abnormal mitral valve appearance:
● Abnormally long anterior mitral valve leaflet (>16 mm).
● Mitral valve thickening from septal contact (with mirror thickening of

the basal septal endocardium).
● Associated intrinsic MV disease like mitral prolapse may be
present.
● Evidence of previous endocarditis (HCM is a risk factor).
● Abnormal mitral valve sub-apparatus:

● Papillary muscle hypertrophy.
● Antero-apical displacement of the papillary muscles.
● Double-bifid papillary muscles.
● Direct insertion of MV leaflets into the papillary muscles.
● Aberrant mitral valve chordae extending into LVOT.

69
Cardiomyopathies
Other valves:
● Mid-systolic closure of the aortic valve indicates LVOT obstruction.
● Look for sub-pulmonary valve stenosis, frequently seen in Noonan syndrome.
● Measure tricuspid regurgitation velocity and estimated pulmonary
systolic pressure (see Chapter 6).
9. Hypertrophic cardiomyopathy (HCM) vs hypertension
● The diagnosis of cardiomyopathy is made using all available clinical data.
● The TTE alone should never be used to make a new diagnosis but can
suggest HCM (Table 7.8).
10. Hypertrophic cardiomyopathy (HCM) vs athletic heart
● Endurance or resistance training usually causes an increase in cavity
size, but only mild septal thickening (≤13 mm) (Table 7.9).
11. Hypertrophic cardiomyopathy (HCM) vs phenocopies
● HCM (sarcomeric) and phenocopies cannot be reliably differentiated
based on imaging alone.
● It is crucial to distinguish and correctly diagnose HCM phenocopies at
an early stage, because prognosis and management differ significantly
from HCM.
● Table 7.10 shows features suggestive of HCM phenocopies.
Table 7.8 Features in favour of HCM rather than hypertensive disease
Asymmetrical hypertrophy most frequently affecting the septum

Hypertrophy affecting both ventricles
Septal hypertrophy ≥15 mm (Caucasian) and ≥20 mm (African/Afro-Caribbean)
Abnormally long mitral valve leaflet
Complete systolic anterior motion of the anterior mitral leaflet and severe LVOT
flow acceleration (both may also be present in hypertension with sigmoid septum)
Severe diastolic dysfunction
No regression in hypertrophy after good blood pressure control
Large QRS voltages and T wave changes on ECG
Family history of HCM
Table 7.9 Features in favour of cardiomyopathy rather than athletic

heart5, 6, 10
Asymmetric hypertrophy mainly affecting septum

Wall thickness:
● >15 mm or 13–15 mm with no change after three months’ detraining.
● In athletic heart (power athletes), the wall thickness is usually ≤12 mm.
70
Involvement of both RV as well as LV.
LV cavity dimension <45 mm.

Significant LA enlargement. In athletic heart, there is mild LA enlargement.
Early markers of LV systolic dysfunction:
● TDI S’ <9 cm/s and reduced GLS.
● In athletic heart, the LV ejection fraction may be low at rest, but TDI S’
>9 cm/s and GLS normal.
Diastolic dysfunction E/A <1, prolonged E deceleration time, and low E’.
In athletic heart, diastole is normal or supranormal, E/A >2, A velocity is low, E’
lateral and septal increased, and E/E’ low.
Associated SAM or mid-systolic aortic valve closure.
Eccentric RV remodelling particularly involving RV inflow tract. ARVC involves
both inflow and outflow.
Female gender or family history of hypertrophic cardiomyopathy.
Abnormal ECG.
Table 7.10 Features in favour of HCM phenocopies
Diagnoses TTE features9, 10

Concentric LVH
Ground-glass appearance of the myocardium
Thickened valves and interatrial septum
Cardiac
Thickened RV wall
amyloidosis
Markedly reduced GLS with apical sparing
Low ECG voltages
LV hypertrophy mostly symmetrical, but may be asymmetrical
Global hypokinesia +/− dilated LV
Fabry disease Inferolateral mid-wall scarring
Thickened valves
Thickened RV wall
Danon, Pompe Extreme concentric LVH
Noonan syndrome RV hypertrophy with RVOT obstruction
Other imaging modalities:

CMR may be used to:
● Improve the description of the hypertrophy, particularly looking for RV
involvement and apical LV involvement
● Identify LV apical aneurysms +/– thrombus
● Detect and quantify myocardial fibrosis
71
● Exclude differential diagnoses (amyloid, Anderson–Fabry, myocarditis)
Cardiomyopathies
MISTAKES TO AVOID
● Making a new diagnosis of HCM from the TTE alone. This is a clinical
diagnosis based on past medical and family history, blood tests and
ECG, genetic screening, and CMR.
● Incorrect measurements of the LV wall thickness by inclusion of
accessory tendons and chords, papillary muscles, or trabeculae.
● Over-reporting a subaortic septal bulge in hypertensive patients, and the
elderly as HCM.
● Overdiagnosis and reporting of moderate to severe concentric LVH as
HCM without excluding other potential causes (Table 7.6).
● Overdiagnosing and reporting HCM in all patients with SAM and LVOTO.
● Misdiagnosis of apical HCM as acute coronary syndrome when
apical wall endocardium is poorly visualised and may appear akinetic.
Transpulmonary contrast will help confirm the diagnosis.
● Failing to search for LV apical aneurysm in patients with apical HCM and
mid-cavity obstruction. Modified views, such as: very low LV parasternal
short-axis (fourth to fifth left intercostal space) and laterally displaced
apical 4-chamber and 3-chamber views (at posterior axillary line) may
help identify very distal LV apical aneurysms.
● Missing a subaortic membrane as a cause of non-valve LV outflow
acceleration and LV hypertrophy.
● Mistaking mitral regurgitation for the LV outflow jet on continuous-wave
Doppler.
● Failing to perform provocation manoeuvres to uncover dynamic SAM,
LVOTO, and mitral regurgitation.
● Failure to recognise and report specific features of conditions that
mimic HCM (Table 7.10).
Restrictive Cardiomyopathy
● In a patient suspected of heart failure with no obvious LV hypertrophy or
dilatation, restrictive cardiomyopathy is defined by:
● Restrictive LV filling (mitral deceleration time <140 ms, mitral E/A >2.5,
average E/E’ >14)4.
● Normal or mildly reduced LV systolic function.
● The causes are given in Table 7.11. An important differential diagnosis is

pericardial constriction (see page 197).
72
Restrictive Cardiomyopathy
Table 7.11 Common restrictive cardiomyopathies13
Examples
Infiltrative Amyloidosis (Table 7.10), sarcoidosis
Storage disease Fabry (Table 7.10), Pompe, mucopolysaccharidosis
Haemochromatosis (endocardial hyperechogenicity)
Non-infiltrative Idiopathic, scleroderma, inherited myopathies
Endomyocardial Endomyocardial fibrosis (Table 7.12)
Cancer therapy Cancer and cancer therapies (e.g. anthracycline)
Table 7.12 TTE features of endomyocardial fibrosis
Echogenicity at RV or LV apex (Figure 7.2)

Sub-valve LV or RV thickening
LV or RV thrombus
Tricuspid or mitral regurgitation
Figure 7.2 Endomyocardial fibrosis. There is thrombosis at the apex of both left
and right ventricle.

http://goo.gl/hA9Ueh
73
Cardiomyopathies

● CMR is used for the detection of amyloidosis and haemochromatosis and
99mTc-DPD scintigraphy for amyloidosis.
MISTAKES TO AVOID
● Mistaking the presence of restrictive physiology for restrictive

cardiomyopathy. Restrictive physiology occurs in any situation with a
high filling pressure and rapid cessation of flow (e.g. post–myocardial
infarction, pericardial constriction).
Non-Compaction
● The fetal heart is heavily trabeculated but becomes compacted during
development. Non-compaction arises either from interruption of this
process or the new growth of trabeculations later in life.
● New trabeculation can occur in other cardiomyopathies (dilated or
hypertrophic) or physiological stimuli (e.g. exercise training).
● The presentation is classically with heart failure, ventricular arrhythmia, or
systemic emboli, but the diagnosis may be made on family screening.
● The TTE shows numerous (>3), prominent trabeculations (Figure 7.3)
(Table 7.13). Look for thrombus in the recesses.
● Assess LV size and function. Systolic function is often reduced initially at the
area of hypertrabeculation.
● Other congenital cardiac abnormalities are commonly associated with non-
compaction (e.g. ASD, VSD, transposition, tetralogy of Fallot).
Figure 7.3 Non-compaction. (a) Parasternal short-axis view showing posterior

trabeculation, and this is illustrated diagrammatically in (b). A ratio of non-compacted:
compacted wall >2 (x/y) at end-systole is the commonly used Jenni diagnostic criterion15.
74
Arrhythmogenic
Non-Compaction
Right Ventricle
Table 7.13 Features of isolated ventricular non-compaction14
>3 large trabeculae (usually at apex, mid-inferior, or lateral wall), with deep
intertrabecular recesses (confirmed on colour mapping)
Ratio of non-compacted:compacted myocardium >2 on an end-systolic
parasternal short-axis view14 (Figure 7.3)
Absence of congenital causes of pressure load (e.g. LV outflow obstruction)
Associated features
Hypokinesis of affected segments
Dilatation and hypokinesis of unaffected segments, usually at the base of the LV
Abnormal ECG (LBBB, poor R wave progression, pathological Q waves)
● The differential diagnosis for hypertrabeculation15 is:

● Normal trabeculation in Afro-Caribbean people.
● Trabeculation associated with athletic training, especially in Afro-Caribbean

people.
● Trabeculation in hypertrophic cardiomyopathy.
● Trabeculation in dilated or peripartum cardiomyopathy.
● False tendons.

● CMR may be useful, especially if TTE image quality is suboptimal. The
diagnosis is suggested by a non-compacted:compacted ratio >2.3 at
end-diastole.
Arrhythmogenic Right Ventricle

Cardiomyopathy/Dysplasia
(ARVC/ARVD)
● The diagnosis is based on a combination of histology, imaging (echo and
magnetic resonance), ECG, arrhythmias, and family history.
● TTE is part of the initial evaluation of a patient with suspected ARVC and for
follow-up at one- to two-year intervals, based on age, genetic status, and
clinical features.
● TTE changes include RV dilatation, reduced RV systolic function, and regional wall
motion abnormalities, such as akinesis, dyskinesis, or aneurysms (Figures 4.1
and 7.4) (Table 7.14).
● The most commonly affected regions of the RV are the infundibulum, apex,
inferolateral wall, and peri-tricuspid annulus16.
75
Cardiomyopathies
● LV involvement is common and may sometimes dominate with:

● Non-dilated and globally hypokinetic LV.
● Regional wall motion abnormalities often starting inferolaterally.
● Other causes of RV dilatation and dysfunction that should be considered are:

● RV infarct.
● Dilated cardiomyopathy confined to the RV.
● Pulmonary artery hypertension.
Table 7.14 Echocardiographic features of arrhythmogenic RV

cardiomyopathy/dysplasia17, 18*
Major criteria
PLAX RVOT ≥32 mm (≥19 mm/m2)
PSAX RVOT ≥36 mm (≥21 mm/m2)
RV fractional area change** ≤33%
Minor criteria
PLAX RVOT ≥29 mm to <32 mm (≥16 ≤18 mm/m2)
PSAX RVOT ≥32 mm to <36 mm (≥18 ≤20 mm/m2)
RV fractional area change** >33% to ≤40%
* Regional RV akinesia, dyskinesia, or aneurysm and RV dilatation shown by one of the
following (end-diastole).
** Measured by tracing the RV endocardium in systole and diastole in the 4-chamber view. Subtract
the systolic area from the diastolic area and divide by the diastolic area, then multiply by 100.
76 Figure 7.4 ARVC/D. On the left is a short-axis view, and on the right, a modified RV
apical view, showing a markedly dilated RV with aneurysms.
Cardio-Oncology: Evaluation of Patients on Chemotherapy
● Congenital heart diseases, for example, ASD, Ebstein’s anomaly.

● Severe pectus excavatum.
● CMR is the most accurate imaging modality for the detection of early ARVC16.
● The peri-tricuspid area and the LV inferolateral wall may be the only
affected regions16.
Cardio-Oncology: Evaluation
of Patients on Chemotherapy
● Echocardiography is used for the evaluation of patients in preparation for,
during, and after cancer therapy.
● Choice of TTE protocol:
● Baseline imaging requires a comprehensive TTE.
● A focused study may be sufficient for surveillance during potentially

cardiotoxic cancer treatments (internally agreed with oncology team).
1. LV and RV systolic and diastolic function

● Accurate and reproducible assessment of LV systolic function is critical for
patients exposed to potentially cardiotoxic chemotherapeutic agents2, 4.
● A cut point <53% is used for a reduced LV ejection fraction in cardio-oncology
protocols2, 4. However, in practice it is nearly impossible to provide this level
of accuracy.
● Recommended methods for the assessment of LV systolic function:
● 3D volume–derived LV ejection fraction and 2D GLS (FR 50–80 Hz)
when images are of good quality. Ideally, use vendor-neutral software
for all 3D data analysis. Otherwise, use the same dedicated system for
serial studies, and strongly consider a single operator.
● For 3D data analysis, use multibeat acquisition (4–6 cycles) and frame
rates >20 Hz.
● 2D Simpson’s biplane LV ejection fraction and 2D GLS. If GLS is not
possible, use TDI S′ lateral.
● Have a low threshold for using a contrast agent if images are of
suboptimal quality.
● LV diastolic function and RV dysfunction have not been found to be
prognostic of cardiotoxicity.
● Immediately report any of the following to the cardio-oncology team18
(Figure 7.5):
77
Cardiomyopathies
Figure 7.5 Role of GLS in cardio-oncology. (a) Bull’s-eye representation of GLS

in a normal LV; (b) Bull’s-eye representation of an impaired LV with significantly reduced
GLS in a patient having Herceptin.
Table 7.15 Frequency of TTE according to chemotherapeutic agent2, 4, 19
Drugs
Toxicity type Measurements F/U TTE
examples
LVEF >53% End of treatment
Type I GLS <–16% and six months
Permanent damage Doxorubicin Troponin negative later
Cumulative dose Epirubicin
Risk of heart failure Idarubicin LVEF <53%
Guided by
and death GLS >–16%
cardiology review
Troponin positive
LVEF >53% Every three
Type II GLS <–16% months during
Reversible effects Trastuzumab Troponin negative treatment
Not dose-related Lapatinib
No apparent Pertuzumab LVEF <53%
Guided by
structural damage GLS >–16%
cardiology review
Troponin positive
● 10% reduction in serial LV ejection fraction to below the lower limit of

normal (50–55%).
● 15% reduction in GLS.
● GLS of >–16% (absolute value <16%) regardless of interval change.
● Guideline frequencies for serial TTE are given in Table 7.15.
2. Look at the valves and pericardium

● Heart valve disease may precede the cancer or may arise as a result of
radiotherapy, LV dysfunction, or infective or thrombotic non-infective endocarditis.
● Patients with baseline or changing valve abnormalities should have serial
TTE during and after treatment4.
78
Cardio-Oncology: Evaluation of Patients on Chemotherapy
● Pericardial disease may be secondary to cardiac metastases or a

consequence of radiotherapy or chemotherapy (see Chapter 17).
CHECKLIST REPORT IN CARDIOMYOPATHY

1. LV dimensions, wall thickness (location of any hypertrophy), and
morphology, including trabeculation.
2. LV regional and global systolic and diastolic function.
3. LV thrombus?
4. In suspected HCM—systolic anterior motion of the mitral valve with
secondary LVOT acceleration +/– mitral regurgitation (including changes
with Valsalva and standing).
5. In suspected HCM—echocardiographic risk factors for sudden death:
wall thickness ≥30 mm, LA >48 mm, LA volume >34 mL/m2, LV ejection
fraction <50%, LVOT obstruction >50 mmHg.
6. RV size and function. RVOT dilatation in ARVC.
7. Pulmonary pressure.
8. Valve function as a cause of LV dilatation, but also secondary mitral
regurgitation as a complication.
References
1. Elliott P, Andersson B, Arbustini E, et. al. Classification of the cardiomyopathies:
A position statement from the European Society of Cardiology Working Group on
Myocardial and Pericardial Diseases. Eur Heart J 2008;29(2):270–76.
2. Merlo M, Cannatà A, Gobbo M, Stolfo D, Elliott PM & Sinagra G. Evolving
concepts in dilated cardiomyopathy. Europ J Heart Failure 2018;20(2):228–39.
3. Pinto YM, Elliott PM, Arbustini E, et al. Proposal for a revised definition of dilated
cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for
clinical practice: A position statement of the ESC Working Group on Myocardial
and Pericardial Diseases. Eur Heart J 2016;37(23):1850–58.
4. Plana JC, Galderisi M, Barac A, et al. Expert consensus for multimodality imaging
evaluation of adult patients during and after cancer therapy: A report from
the American Society of Echocardiography and the European Association of
Cardiovascular Imaging. Europ Heart J 2014;15:1063–93.
5. Galderisi M, Cardim N, D’Andrea A, et al. The multi-modality cardiac imaging
approach to the athlete’s heart: An expert consensus of the European Association
of Cardiovascular Imaging. Europ Heart J CVI 2015;16(4):353a–t.
6. Richand V, Lafitte S, Reant P, et al. An ultrasound speckle tracking (two-dimensional
strain) analysis of myocardial deformation in professional soccer players
compared with healthy subjects and hypertrophic cardiomyopathy. Am J Cardiol
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2007;100(1):128–32.
Cardiomyopathies
7. Houston B & Mukherjee M. Cardiac sarcoidosis: Clinical manifestations,

imaging characteristics, and therapeutic approach. Clin Med Insights in Cardiol
2014;8(Suppl 1):31–7.
8. Marques. JS & Pinto FJ. Clinical use of multimodality imaging in the assessment
of dilated cardiomyopathy. Heart on Line 2015;101(7):565–72.
9. Elliott PM, Anastasakis A, Borger MA, et al. 2014 ESC Guidelines on diagnosis and
management of hypertrophic cardiomyopathy. Europ Heart J 2014;35(39):2733–79.
10. Turvey L, Augustine DX, Robinson S, et al. Transthoracic echocardiography of
hypertrophic cardiomyopathy in adults: A practical guideline from the British
Society of Echocardiography. Echo Research and Practice 2021;8(1):G61–86.
11. Rowin EJ, Maron BJ, Haas TS, et al. Hypertrophic cardiomyopathy with left
ventricular apical aneurysm: Implications for risk stratification and management. J
Am Coll Cardiol 2017;69(7):761–73.
12. Hiemstra YL, Debonnaire P, Bootsma M, et al. Global longitudinal strain and
left atrial volume index provide incremental prognostic value in patients with
hypertrophic cardiomyopathy. Circulation: CVI 2017;10(7):e005706.
13. Muchtar E, Blauwet LA & Gertz MA. Restrictive cardiomyopathy genetics,
pathogenesis, clinical manifestations, diagnosis, and therapy. Circ Res
2017;121(7):819–37.
14. Jenni R, Oechslin E, Schneider J, Attenhofer JC & Kaufmann PA.
Echocardiographic and pathoanatomical characteristics of isolated left ventricular
non-compaction: A step towards classification as a distinct cardiomyopathy. Heart
2001;86(6):666–71.
15. Nagueh SF, Smiseth AO, Appleton CP, et al. ASE/EACVI Guidelines and standards.
Recommendations for the evaluation of left ventricular diastolic function by
echocardiography: An update from the American Society of Echocardiography
and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr
2016;29(4):277–314.
16. Corrado D, Van Tintelen PJ, J. McKenna WJ, et al. Arrhythmogenic right ventricular
cardiomyopathy: Evaluation of the current diagnostic criteria and differential
diagnosis. Europ Heart J 2020;41(14):1414–27.
17. Marcus FI, McKenna WJ, Sherill D, et al. Diagnosis of arrhythmogenic right
ventricular cardiomyopathy/dysplasia. Proposed modifications of the task force
criteria. Circulation 2010;121(13):1533–41.
18. Towbin JA, McKenna WJ, Abrams DJ, et al. HRS expert consensus statement on
evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy.
Heart Rhythm 2019;16(11):e301–72.
19. Dobson R, Ghosh AK, Ky B, et al. British Society for Echocardiography and British
Cardio-Oncology Society guideline for transthoracic echocardiographic assessment
of adult cancer patients receiving anthracyclines and/or trastuzumab. Echo
Research and Practice 2021;8(1):G1–8.
80
Aortic Valve Disease
8
Aortic Stenosis
1. Appearance of the valve and aorta
● Describe the valve in detail. Look at the number of cusps, pattern of
thickening, and mobility on zoomed views. These may give a clue to
the aetiology (Table 8.1).
● A bicuspid aortic valve may only be obvious in systole (Figure 8.1).
● If the valve is bicuspid:
● Is it anatomical or functional (two cusps fused either partially or fully
with a median raphe).
● Which cusps are fused? Fusion of right and left cusps is the most
common pattern and more likely to be associated with aortic
dilatation and coarctation1.
● Is the valve thickened and restricted or thin and normally
functioning? More than mild thickening and restriction predicts
faster progression to surgery2.
● Assess the aorta at all levels (see page 161).
● With a bicuspid aortic valve, the sinus, sinotubular junction, or
ascending aorta may be dilated.
● If the ascending aorta cannot be imaged adequately even after moving
the probe a space higher than for the parasternal views or in a right
intercostal space, consider CMR or CT scanning.
Table 8.1 Clues to the aetiology in aortic stenosis
Systolic Associated
Closure line
bowing features
Calcification of mitral
Calcific disease No Central
annulus or aorta
Bicuspid Yes Often eccentric Ascending aortic
dilatation, coarctation
Rheumatic Yes Central Mitral involvement
81
DOI: 10.1201/9781003242789-8
Figure 8.1 Bicuspid aortic valve in systole and diastole. In diastole,

(a) the valve may look tricuspid if there is only mild fusion and no raphe. Only in systole
(b) with the valve open will it be obvious that two cusps are partly fused. The fusion may
affect only a small length of the cusp edge adjacent to the commissure.
● The aorta may be replaced at a diameter of 45 mm if aortic valve

surgery is independently indicated3, 4.
● About 5% of bicuspid valves are associated with coarctation.
2. Doppler measurements
● The minimum dataset5 is Vmax, mean gradient and effective orifice area
using the continuity equation (Figure 8.2).
● Your laboratory should agree a convention for the site of measuring the
LV outflow diameter. Most centres aim as high in the LVOT as close to
the base of the aortic cusps as possible while avoiding annular calcium.
● Check that the measured LVOT diameter is the same as last time. If
not, we suggest:
● Use the better of the two measurements (taking into account image
quality and measurement technique).
● In your summary, report the EOA, calculated using the optimal
diameter for your own and the previous study for consistency.
● This is particularly important if you are measuring the diameter at the
base of the aortic cusps when previously a point was taken within
the cylindrical part of the LVOT.
82
Aortic Stenosis
Figure 8.2 Continuity equation. Measure the LVOT diameter from inner to inner
edge (a) as high as possible towards the base of the cusps avoiding annular calcification.
(b) Record the pulsed signal in the centre of the LVOT as flow accelerates, moving the
pulsed sample up and down until a stable signal is obtained. Record the continuous wave
signal using a stand-alone probe from the apex (c) and right intercostal space (d) and use
the optimal signal, in this case (d). Trace the modal or dense part of the signal, avoiding
artefact.
● Record the continuous waveform using the stand-alone probe from

the apex and at least one other approach (usually suprasternal or right
intercostal), unless the aortic valve disease is obviously mild, shown by
all of:
● Mobile cusps
● Vmax <3.0 m/s
● Normal LV ejection fraction
3. Assess severity
● If the aortic valve is thickened with a Vmax <2.5 m/s and normal LV
ejection fraction, report ‘aortic valve thickening with no stenosis’.
● If the Vmax ≥2.5 m/s, grade as in Table 8.2 if all measurements agree. If
there is disagreement, see Section 3.1 or 3.2.
83
Table 8.2 Severity in aortic stenosis: Main criteria5

Transaortic Vmax (m/s) 2.6–2.9 3.0–4.0 >4.0
Peak gradient (mmHg) <40 40–65 >65
Mean gradient (mmHg) <20 20–40 >40
EOA (continuity equation) (cm2) >1.5 1.0–1.5 <1.0
Table 8.3 Severity in aortic stenosis: Extra criteria

Waveform shape (Figure 8.3) Dagger Dagger Arch
Indexed EOA (cm2/m2) >0.85 0.60–0.85 <0.60
Dimensionless index >0.50 0.25–0.50 <0.25
3.1 If the Vmax suggests severe (>4.0 m/s) but the EOA suggests only
moderate (>1.0 cm2)
This arises because of:
● High flow (aortic regurgitation, anaemia, anxiety)
● Errors of measurement
You need to:
● Check your measurements. Was the pulsed sample too close to the
valve? Check the LV outflow diameter against previous measurements.
● Consider the dimensionless index (Table 8.3). If the LV outflow
diameter is unreliably large, the dimensionless index gives a guide to
severity. It should be calculated as VTIsubaortic/VTIav. Do not use the ratio
of subaortic to aortic Vmax.
● Look again at the valve appearance. Is the valve calcified and
immobile, suggesting severe AS, or are the tips mobile, suggesting
more moderate AS?
● Look at the waveform shape5 (Figure 8.3 and Table 8.3). A dagger
shape suggests moderate stenosis, and an arch shape suggests
severe stenosis.
● Correct for body surface area (Table 8.3). Correction for BSA should
not be done routinely, because it will tend to categorise too many
people as having severe aortic stenosis, but it is helpful in uncertain
cases. If the patient is large, a corrected EOA may be in the severe
range despite a moderate uncorrected EOA (Box 8.1).
84
Aortic Stenosis
Figure 8.3 Continuous waveform shape. (a) Left panel. In moderate aortic
stenosis, the upstroke is relatively quick, giving a dagger-shaped signal in which the mean
gradient is approximately half the peak. Right panel. In severe stenosis, the ejection time
lengthens and the acceleration time to peak velocity also lengthens. This causes an arch
shape in which the mean gradient is approximately 2/3 the peak gradient. (b) shows a
waveform in moderate disease, and (c) a waveform in severe disease.
Box 8.1 Correcting effective orifice area for

body surface area (BSA)
Assuming an EOA 1.3 cm2:
● If the patient is 6 ft tall and weighs 120 kg, the BSA is 2.4 m2, giving
EOAi 0.54 cm2/m2, indicating severe AS.
● If the patient is 5 ft tall and weighs 50 kg, the BSA is 1.45 m2 and the
EOAi is 0.9 cm2/m2, indicating mild AS.
85
3.2 If the Vmax suggests moderate (<4.0 m/s), but the EOA suggests
severe (<1.0 cm2)
This can be for a number of reasons:
● The cut points between the grades are, to a degree, arbitrary, and an EOA
0.8–1.0 cm2 may be moderate, especially in smaller people6 (Box 8.1).
● Low flow causes a fall in Vmax despite severe aortic stenosis.
● Errors of measurement.
You need to:
● Check your measurements. The likeliest errors are in placing the
pulsed sample too far towards the LV apex and in underestimating
LVOT diameter (check the value found in previous studies).
● Look again at the valve appearance. Is the valve calcified and fixed,
suggesting severe AS, or are the tips mobile, suggesting moderate AS?
● Look at the waveform shape5 (Figure 8.4 and Table 8.3). A dagger
shape suggests moderate stenosis, and an arch shape suggests severe.
● Correct for body surface area if the patient is small.
● Consider measuring the area of the LV outflow tract on 3D since
it may not be circular and may be underestimated from the linear
diameter.
● Consider low-gradient, low-flow AS (see 3.3).
3.3 Low-gradient, low-flow aortic stenosis

This occurs if:
● The LV ejection fraction is low, usually <50% (‘classical low-flow, low-
gradient AS’).
● The low LV ejection fraction is likely caused solely by the AS and,
unless very low, will improve after intervention.
● The LV cavity is small despite a normal ejection fraction >50%
(‘paradoxical low-flow, low-gradient AS’). Even with a normal or high LV
ejection fraction, the volume of blood ejected is small.
● There may be LV disease (e.g. from hypertension, or amyloid)
separate from the AS, and the differentiation of these can be
difficult and require further tests.
● Conventionally, a stroke volume index <35 mL/m2 is used to define
this entity, although this is not a measure of flow.
● Occasionally, true flow, calculated as (stroke volume)/(systolic ejection
time), may be low despite a normal stroke volume index. A flow < 200
mL/s is usually taken as low.
● Or there is severe mitral stenosis or regurgitation or a VSD.
86
Aortic Stenosis
4. If the diagnosis is not clear, discuss the case to consider further action:
4.1 Consider low-dose dobutamine stress echocardiography
● This is indicated for a Vmax <3.5 m/s with an LV ejection fraction <40%.
● It is not usually indicated if:
● The Vmax is >3.5 m/s, especially if the LV ejection fraction is <40%,
since this is almost certainly severe aortic stenosis7.
● The LV cavity is small and the LV ejection fraction is normal,
since severe LV outflow acceleration may occur, making accurate
measurement impossible and risking cardiac arrhythmia.
● It requires medical supervision because of the risk of cardiac arrhythmia:
● Give 5 then 10 μg/kg/min dobutamine (occasionally 20 μg/kg/min,
especially if prior beta blockade).
● Stop the infusion if the VTIsubaortic rises >20% or the heart rate
increases.
● Judge the severity of AS and whether there is LV contractile reserve
(Table 8.4). If the VTIsubaortic fails to rise by >20%, consider calculating
the change in flow (see 3.3 or Appendix for calculation).
● In the absence of contractile reserve, the risk at aortic valve
replacement is high8.
Table 8.4 Stress echocardiography in low-flow aortic stenosis8
Is there severe aortic stenosis?

Mean gradient >40 mmHg and EOA <1.0 cm2 at any time during stress
Is there LV contractile reserve?
Subaortic velocity time integral (or ejection fraction or flow) rises by >20%
4.2 Consider CT calcium scoring

This is useful in ‘paradoxical low-flow, low-gradient AS’ when the valve is
calcified and the LV ejection fraction is normal.
4.3 Clinical correlates
A review of the case correlating clinical characteristics, imaging, and
biomarkers is often needed (Table 8.5), unless the grade is clear.
5. General
● Assess aortic regurgitation (page 90).
● Assess the aorta.
87
Table 8.5 Differentiating moderate and severe aortic stenosis with

mean gradient <40 mmHg and EOA <1.0 cm2 and EF >50%4
Likely moderate Likely severe

EOA (cm2) 0.8–1.0 <0.8
Vmax (m/s) <3.5 3.5–3.9
Continuous wave signal shape Dagger Arch
Heavily calcified
Valve appearance Cusp tips still open
and immobile
Patient characteristics Small and asymptomatic Symptoms
SVi (mL/m2) >35 <35
<1,600 for men, >2,000 for men,
CT calcium score (A units)
<800 for women >1,200 for women
● If the ascending aorta cannot be imaged by TTE, a CT scan or CMR

should be requested. These can also assess the whole of the rest of
the aorta.
● If there is apparent heavy aortic calcification, then a CT scan is
indicated to look for a ‘porcelain aorta’, which may contraindicate
surgical valve replacement.
● Assess the other valves. Secondary (functional) mitral regurgitation
may develop in severe aortic stenosis if the LV is dilated. Mitral surgery
is likely to be necessary if:
● The mitral valve is anatomically abnormal (e.g. prolapsing).
● The secondary mitral regurgitation is moderate to severe or severe.
● Estimate pulmonary artery pressure (see Chapter 5).

● Pulmonary hypertension is no longer included as an indication for
intervention in asymptomatic severe AS.
● However, pulmonary hypertension is common (usually taken as a PA
systolic pressure >60 mmHg) and carries a poor prognosis without
aortic valve intervention9.
● A rise in tricuspid regurgitation Vmax from the last study alerts to a
change and may be used to help decide the need for intervention if
other measures are equivocal.
● Note LV outflow hypertrophy, which has a number of possible
consequences:
● It may contribute to high flow velocities across the aortic valve.
● It may affect a TAVI procedure (see 7).
88
Aortic Stenosis
● If severe, it increases risk at surgery.

● Post-operatively, it can cause HCM-like physiology with low cardiac
output, especially with excessive inotropes and diuretic therapy.
● If there is a discrepancy in the pressure difference and the appearance
of the valve, check for a subaortic membrane.
6. Is surgery indicated on TTE?4, 5
Aortic valve surgery is most clearly indicated for severe AS and symp-
toms. However, in asymptomatic patients or patients having CABG, the
TTE can aid the decision for surgery (Table 8.6).
Table 8.6 Echocardiographic and other indications for surgery in

asymptomatic aortic stenosis3, 4
Echocardiographic indications Class

Moderate or severe AS having CABG or aortic replacement I
Severe AS and LV ejection fraction <50% with no other cause I
Severe AS and LV ejection fraction <55%4 or 2a
a progressive decrease to <60% on three successive studies3 2b
Transaortic Vmax >5.0 m/s or EOA <0.6 cm2 2a
Severe coexistent aortic dilatation (see page 165) I
Increase in Vmax ≥0.3 m/s in one year associated with severe
2a
calcification4
Non-echocardiographic indications
Symptoms on exercise test I
Fall in BP >20 mmHg on exercise 2a
B-type natriuretic peptide level raised by >3 times normal4 2a
7. Transcatheter valve (TAVI) workup (Table 8.7)

● Measure the echocardiographic ‘annulus’ taken from inner to inner
edge at the base of the cusps10. This is needed for sizing the valve.
● The annulus may be oval. Further assessment of the annulus size and
shape may be performed at the TAVI centre using 3D TOE at the time
of the procedure or beforehand if there is significant uncertainty11.
● CT is routine for assessing: the annulus (area, perimeter, diameters,
shape, and calcification), the height of the coronary ostia above the
annulus, the whole thoracic aorta and peripheral arteries.
89
Table 8.7 Echocardiographic features in the TAVI workup
Aorta
Confirms TAVI more suitable than
Heavy calcification
surgical replacement
Annulus diameter Used for sizing
Dilatation (>45 mm) may
Diameter at sinus and STJ
contraindicate CoreValve
Left ventricle
If small, contraindicates transapical
LV cavity size
approach
Severe subaortic bulge May contraindicate SAPIEN
Valves
Bicuspid valve Caution with some types of device
Caution re-occlusion of left main stem
Heavy calcification of left cusp
during the procedure
Severe mitral regurgitation May favour conventional surgery
Abbreviation: STJ is sinotubular junction.
MISTAKES TO AVOID
● Mistaking the continuous wave signal from an eccentric jet of mitral

regurgitation for aortic stenosis.
● Failing to recognise severe aortic stenosis if the Vmax or mean gradient
is in the moderate range but the EOA is low.
● Underestimating the degree of aortic stenosis by not using a stand-
alone probe from at least two windows.
● Failing to detect dilatation of the ascending aorta, which is common if
there is a bicuspid aortic valve.
● Missing a subaortic membrane. Recheck if the valve looks relatively
mildly affected but the velocities are high.
Aortic Regurgitation
1. Appearance of the valve and aorta

● Describe the valve in detail. Look at the number and mobility of the
cusps on zoomed views (see Figure 8.1 for bicuspid aortic valve).
90
● Measure the aorta at every standard level (see page 161).

● This may allow you to determine the aetiology (Table 8.8).
2. Colour flow mapping

● Measure the jet height 5–10 mm below the cusps (on 2D or colour
M-mode) (Figure 8.4) and express as a percentage of the diameter of
the LVOT at the same level.
● If the jet is eccentric, the width must be taken perpendicular to its axis.
If it is so eccentric that it impinges on the septum or anterior mitral
leaflet, do not make the measurement.
● The width of the narrowest portion of the jet (the vena contracta) can
also be used (Table 8.8) even if the jet is eccentric.
Figure 8.4 Regurgitant jet. Parasternal long-axis view. The position for measuring
the height of the colour flow map as a percentage of the outflow tract height is at (a). The
vena contracta or neck is at (b).
91
Table 8.8 Aetiology of aortic regurgitation
Dilatation of root or ascending aorta

(Table 15.1)
Valve
Common Bicuspid, rheumatic, calcific disease, endocarditis
Uncommon Prolapse, irradiation, drugs,* antiphospholipid syndrome, carcinoid
* Cabergoline, pergolide, fenfluramine, benfluorex.
3. Continuous wave signal

● Record either from the apex or, if the jet is directed posteriorly, from
the parasternal position.
● Measure the pressure half-time and note the density of the signal
compared with the density of forward flow.
4. Flow reversal at the arch
● From the suprasternal notch, describe:
● Whether flow reversal is holodiastolic, fills approximately half of
diastole, or is only seen at the start of diastole using colour M-mode
(Figure 8.5) and pulsed Doppler (Figure 8.6).
● How far down the aorta can flow reversal be detected on colour
mapping.
Figure 8.5 Flow reversal on colour mapping in the upper descending

thoracic aorta. Using a suprasternal position colour M-mode in a patient with mild
regurgitation (a) illustrates localised and short-lived flow reversal. In severe regurgitation,
(b) flow reversal is holodiastolic across the whole aortic lumen and seen well down the
92
descending thoracic aorta.
Figure 8.6 Flow reversal on pulsed Doppler in the distal arch. Using
a suprasternal position, mild regurgitation causes (a) short-lived low-velocity reversal,
while in severe regurgitation, (b) the reversal is holodiastolic, with a relatively high
93
velocity at the end of diastole (e.g. ≥ 0.2 m/s)12.
5. Grade the severity of regurgitation

● Make an assessment based on all modalities. The height of the colour
jet in the LVOT and flow reversal beyond the arch are the most reliable
modalities (Table 8.9).
● The PISA technique is not routinely used for aortic regurgitation.
Table 8.9 Criteria of severity in aortic regurgitation13

Colour/LVOT height (%) <25 25–64 ≥65
Vena contracta
<3 3–6 >6
width (mm)
Flow reversal in Not
None Holodiastolic
descending aorta holodiastolic
Pressure
>500 200–500 <200*
half-time (ms)
Faint or incomplete Dense as
CW signal intensity Intermediate
waveform forward flow
*
The pressure half-time depends on LV diastolic pressure and systemic vascular resistance and
may be short with LV dysfunction even if the aortic regurgitation is mild or moderate.
94
6. The left ventricle

● Is the LV hyperdynamic (suggesting severe aortic regurgitation)?
● Chronic severe regurgitation usually causes LV diastolic dilatation. In
acute regurgitation, the LV diastolic volume may be normal.
● Measure LV volumes. The LV becomes more spherical in severe aortic
regurgitation, and linear dimensions may then be unrepresentative of
LV size. No guideline cut point for surgery exists, but a progressive
increase in volume may still be clinically useful.
● LV TDI or GLS can corroborate a decline in other measures of LV
function but cannot be used alone as indications for surgery.
7. Are there echocardiographic criteria for surgery?3, 4
See Table 8.10. In individual cases, two or more of these indications may summate.
Table 8.10 Echocardiographic and other indications for surgery in

asymptomatic aortic regurgitation3, 4
Indications for surgery Class

Moderate or severe AR having CABG or aortic replacement I
Severe AR and LV ejection fraction ≤50%4 or ≤55%3 with no
I
other cause
LV systolic diameter >50 mm or 25 mm/m2 I4 2a3
Low-risk surgery, severe AR, and progressive fall in LV ejection
2b
fraction to <60% on ≥3 serial studies3
Low risk for surgery and LV systolic diameter >20 mm/m2 if
2b
the patient is small or LV ejection fraction ≤55%4
Progressive increase in LV diastolic diameter to >65 mm3, 4 or
2b
fall in LV ejection fraction to <60% on ≥3 serial studies3
Severe coexistent aortic dilatation (see page 165) I
8. Assess the other valves and right heart

● Mitral regurgitation may occur secondary to LV dilatation.
● Pulmonary hypertension is much less common than in severe aortic
stenosis.
Other techniques in aortic stenosis and regurgitation
● CMR
● Shows valve morphology if TTE windows are suboptimal.
● Shows the rest of the aorta if only the root can be imaged adequately
on TTE.
95
● Estimates the regurgitant fraction if the grade of regurgitation is uncertain

on TTE.
● Calculates LV volume and function if image quality is suboptimal on TTE.
● CT
● Shows the whole aorta for dimensions and the presence of excess
calcification.
● Images coronary arteries in selected patients before valve intervention.
● TAVI workup (see Table 8.7).
Acute Aortic Regurgitation

This is caused mainly by infective endocarditis. The LV and general circulation
have not had time to adapt, and the LV may be hyperdynamic but not yet
dilated. The risk of decompensation and death is high:
● Measure transmitral E deceleration time (Figure 8.7).
● Use continuous wave Doppler across the mitral valve to look for
diastolic mitral regurgitation (Figure 8.7). This is a sign of immediate LV
decompensation and an indication for emergency surgery15.
● Inform the clinician in charge of the case immediately if the E deceleration
time is <150 ms or if there is diastolic mitral regurgitation.
MISTAKES TO AVOID
● Placing the pulsed sample in the distal arch too close to the aortic wall.
This produces signal artefacts late in diastole (signal symmetrical above
and below the baseline), which can be mistaken for flow reversal.
● Missing a transmitral deceleration time <150 ms as a sign of imminent
decompensation in acute aortic regurgitation.
● Overestimating AR using AR pressure half-time shortened by a high
LVEDP as a result of coexistent LV disease.
● Using vena contracta cut points to assess the jet width in the LVOT.
● Measuring pressure half-time when not fully aligned to the regurgitant
jet. The AR jet initial peak velocity is usually about 4 m/s with a normal
blood pressure. If much lower, especially with a bidirectional signal, use
other methods to evaluate the degree of regurgitation.
96
Figure 8.7 Spectral Doppler signals in acute aortic regurgitation. These

signals were recorded soon before decompensation and death in a patient with acute
severe aortic regurgitation caused by endocarditis. In (a), the E deceleration time is
shortened to 151 ms, and in (b), there is prolonged diastolic mitral regurgitation.
97
CHECKLIST REPORT IN AORTIC

VALVE DISEASE
1. Appearance and movement of the aortic valve.
2. Grade of stenosis and regurgitation.
3. Size of aorta and check for coarctation.
4. LV dimensions and systolic function.
5. RV size and function and PA pressure (for aortic stenosis).
6. Other valves, particularly the mitral valve.
References
1. Schaefer BM, Lewin MB, Stout KK, Gill E, Prueitt A, Byers PH & Otto CM. The
bicuspid aortic valve: An integrated phenotypic classification of leaflet morphology
and aortic root shape. Heart 2008;94(12):1634–8.
2. Michelena HI, Desjardins VA, Avierinos JF, et al. Natural history of asymptomatic
patients with normally functioning or minimally dysfunctional bicuspid aortic valve
in the community. Circulation 2008;117(21):2776–84.
3. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the
management of patients with valvular heart disease: A report of the American
College of Cardiology/American Heart Association Joint Committee on Clinical
Practice Guidelines. Circulation 2021;143(5):e72–227.
4. Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the
management of valvular heart disease. Eur Heart J 2022;43(7):561–632.
5. Baumgartner H, Hung J, Bermejo J, et al. Recommendations on the
echocardiographic assessment of aortic valve stenosis: A focused update from
the European Association of Cardiovascular Imaging and the American Society of
Echocardiography. Europ Heart J CVI 2017;18(3):254–75.
6. Minners J, Allgeir M, Gohlke-Baerwolf C, Kienzle RP, Neuman FJ & Jander N.
Inconsistencies of echocardiographic criteria for the grading of aortic stenosis.
Europ Heart J 2008;29(8):1043–8.
7. Kellermair J, Saeed S, Chambers J, Kammler J, Blessberger H, Kiblboeck D, Grund
M, Lambert T & Steinwender C. Predictors of true-severe classical low-flow low-
gradient aortic stenosis at resting echocardiography. Int J Cardiol 2021;335:93–7.
8. Monin J-L, Quere J-P, Moncho M, et al. Low-gradient aortic stenosis. Operative
risk stratification and predictors for long-term outcome: A multicenter study using
dobutamine stress hemodynamics. Circulation 2003;108(3):319–24.
9. Cam A, Goel SS, Agarwal S, Menon V, Svensson LG, Tuzcu EM & Kapadia SR.
Prognostic implications of pulmonary hypertension in patients with severe aortic
stenosis. J Thorac Cardiovasc Surg 2011;142(8):800–8.
98
10. Zamorano JL, Badano LP, Bruce C, et al. EAE/ASE Recommendations for the use
of echocardiography in new transcatheter interventions for valvular heart disease.
Europ Heart J 2011;32(17):2189–4.
11. Rajani R, Hancock J & Chambers J. Imaging: The art of TAVI. Heart 2012;98
(Suppl 4):iv14–22.
12. Tribouilloy C, Avinee P, Shen WF, et al. End-diastolic flow velocity just beneath the
aortic isthmus assessed by pulsed Doppler echocardiography: A new predictor of
the aortic regurgitant fraction. Brit Heart J 1991;65(1):37–40.
13. Lancellotti P, Tribouilloy C, Hagendorff A, et al. European Association of
Echocardiography recommendations for the assessment of valvular regurgitation.
Part 1: Aortic and pulmonary regurgitation (native valve disease). Europ J Echo
2010;11(3):223–44.
14. Detaint D, Messika-Zeitoun D, Maalouf J, et al. Quantitive echocardiographic
determinants of clinical outcome in asymptomatic patients with aortic
regurgitation. A prospective study. J Am Coll Cardiol CVI. 2008;1(1):1–11.
15. Hamirini YS, Dietl CA, Voyles W, Peralta M, Begay D & Raizad V. Acute aortic
regurgitation. Circulation 2012;126(9):1121–6.
99
Mitral Valve Disease
9
Mitral Stenosis
1. Appearance of the valve, annulus and chords

● Mitral annulus calcification is increasingly common in our aging
population. It usually causes no more than moderate stenosis. It may
be misdiagnosed as severe mitral stenosis because:
● The extensive annular calcification may be mistaken for valve
calcification.
● It may be hard to image the relatively thin and mobile mitral leaflets.
● Stenosis of the mitral valve leaflets is usually rheumatic (Table 9.1). In

early chronic disease, there is:
● Commissural fusion (‘fish mouth’ appearance on the parasternal
short-axis view).
● Thickening of the leaflet tips (‘drumstick’ appearance) but thin and
mobile leaflets.
● In established rheumatic disease, there is progressive scarring and
calcification. Describe:
● The commissures. Are both fused? Is there calcium at the
commissures? If so, is it in the outer part or the whole of the fused
edge?
● Leaflet thickening. Is it just at the tips, or does it extend over the
whole leaflet or only a part?
● Leaflet mobility. Often, the posterior leaflet is immobile, but the
anterior leaflet still bows fully. Is the anterior leaflet less mobile or
completely immobile?
● The degree of chordal thickening and shortening. Are individual
chords still visible? Are chords partially matted together? Do the
chords form a secondary orifice, causing deviation or splitting of
the colour profile within the LV? Is it impossible to see where the
papillary muscles end and the chords begin?
Table 9.1 Causes of mitral stenosis
Common Rheumatic disease, mitral annulus calcification

Uncommon Radiation, systemic lupus erythematosus, congenital
101
DOI: 10.1201/9781003242789-9
Figure 9.1 Pseudo-severe mitral stenosis. In patients with mitral annulus

calcification, it is uncommon for the mitral stenosis to be severe. However, there may
be a large A wave as a result of underlying LV diastolic dysfunction. This can increase
the estimated transmitral gradient to levels suggesting severe stenosis despite a mild or
moderate orifice area (b). In this example, the mean gradient is 9 mmHg (a) despite an
orifice area 2.5 cm2 (c).

http://goo.gl/EDsYfs
102
Mitral Stenosis
Figure 9.2 Planimetry of the mitral orifice. Care must be taken to section the
tips of the mitral leaflets perpendicularly. This is aided by 3D. A common mistake is to
section towards the base of the leaflets or across thickened chords.
2. Planimeter the orifice area

● Make sure that the section is not oblique. This is aided by 3D
(Figure 9.2).
● Use colour Doppler as a guide to the extent of the orifice if this is not
obvious on imaging.
● Take care not to include the chords, which, if thickened, can mimic the
orifice.
● If there is significant thickening with reverberation artefact, the
measurement may be inaccurate and should not be made.
● In mitral annulus calcification, planimetry is not valid or feasible.
If colour flow through the valve is wide in all views with no major
aliasing, then there is no significant stenosis.
● Average the pressure half-time and mean gradient over three cycles.
Choose cycles with an instantaneous heart rate close to 60–90 bpm if
there is atrial fibrillation.
● There is little point in averaging many cycles if the heart rate is so high
as to reduce mitral valve flow. Better to wait for rate control.
● The Hatle formula (orifice area = 220/pressure half-time) is an
approximate guide to severity in moderate or severe stenosis.
103
● In mitral annulus calcification in sinus rhythm, a large transmitral

A wave (Figure 9.1) causes overestimation using the grading
thresholds derived from patients in atrial fibrillation. Some labs
measure the gradient omitting the A wave, but individual cases may
need MDT discussion using all TTE modalities, including qualitative
assessment by colour Doppler.
4. Assess mitral regurgitation (see page 115)
● Anything more than mild mitral regurgitation means that the valve is
not suitable for balloon valvotomy.
● The transmitral pressure half-time will be shortened disproportionate to
the orifice area if there is severe mitral or aortic regurgitation.
● The mean transmitral gradient will increase if there is significant mitral
regurgitation (see Chapter 11).
5. Grade the mitral stenosis (Table 9.2)
● The planimetered orifice area is the most reliable measure in rheumatic
disease if performed accurately. The gradient and pulmonary artery
pressure are flow-dependent.
● Intervention is increasingly dominated by balloon valvotomy, which is
usually more successful when the orifice area is <1.5 cm2 and before
the valve is severely calcified.
6. Examine the right heart
● The pulmonary artery pressure (see Chapter 5) has a loose relationship
with the severity of mitral stenosis. A pulmonary artery systolic
pressure >50 mmHg at rest is a criterion for balloon valvotomy2, 3.
● RV dilatation with hypokinesis is a more important predictor of poor
outcome at mitral valve surgery than the pulmonary artery pressure,
which may fall after mitral valve replacement.
Table 9.2 Criteria of severity in mitral stenosis1
Significant*
Measurement Mild Moderate Severe
Orifice area by planimetry (cm2) >1.5 1.0–1.5 <1.0
Pressure half-time (ms) <150 150–220 >220
Mean gradient (mmHg) <5 5–10 >10+
PA pressure (mmHg) <30 30–50 >50**
* ‘Significant’ is a term in the new guidelines2, 3 meaning moderate or severe mitral stenosis.
+ >15 mmHg after exercise.
** The relationship with valve stenosis is not tight.
104
Mitral Stenosis
● Tricuspid rheumatic involvement is common but easily missed.

● More than mild tricuspid regurgitation with a tricuspid annulus
diameter ≥40 mm (≥21 mm/m2) is currently an indication for tricuspid
annuloplasty at the time of mitral valve replacement4.
7. Assess the other valves
● Significant aortic valve disease may mean that double valve
replacement rather than balloon mitral valvotomy is indicated.
● Aortic stenosis can be underestimated because of low flow caused by
severe mitral stenosis (or regurgitation).
8. If the patient has symptoms but the orifice area is >1.5 cm2
Symptoms occur on exertion, but the TTE so far has been at rest.
● Ask the patient to exercise until breathless. This can be done on a bicycle
or treadmill or, more simply, by walking around the echocardiography
department then immediately getting back on the couch.
● A mean gradient >15 mmHg after exercise is an indication for
considering balloon valvotomy2, 3 (Table 9.3).
Table 9.3 Guideline indications for intervention in mitral stenosis2, 3
Orifice
Symptoms Extra Intervention Class
area
Y ≤1.5 Suitable for balloon Balloon I
Y ≤1.5 Not suitable Surgery I
PA pressure at rest
N ≤1.5 Balloon 2a
>50 mmHg
Need for non-cardiac
N ≤1.5 Balloon 2a
surgery or pregnancy
New AF (or dense
N ≤1.5 contrast, prior Balloon 2b
embolism)
Exercise mΔP
Y >1.5 >15 mmHg or resting Balloon 2b
wedge >25 mmHg
Not suitable for
Y ≤1.5 surgery and not ideal Balloon 2b
for balloon
LA volume >60 mL/m2
N ≤1.5 Warfarin 2a
and sinus rhythm
105
Table 9.4 Markers of successful balloon valvotomy
Good mobility of the anterior leaflet

No more than minor chordal involvement (Figure 9.2)
No more than mild mitral regurgitation
No commissural calcification (Figure 9.2)
No left atrial thrombus (on TOE)
9. Risk of atrial thrombus

● TTE is insensitive for detecting thrombus. A TOE should always be
performed before balloon valvotomy.
● A dilated left atrium (volume >60 mL/m2) is a criterion for
considering warfarin in moderate or severe mitral stenosis and sinus
rhythm2, 5.
10. Is the valve suitable for balloon valvotomy?
● The most reliable characteristics of the valve for predicting success
without developing severe mitral regurgitation are given in Table 9.4.
● Some centres use the Wilkins system of scoring 1 to 4 for valve mobility,
thickening, calcification, and subvalvular involvement6 (Appendix
Table A.6), with a score ≤8 suggesting that balloon valvotomy will be
successful. This system does not focus on some important markers
(Table 9.4), notably the site of commissural calcification.
MISTAKES TO AVOID
● Off-axis planimetry of the mitral valve.

● Failing to take account of the effects of severe MR or AR on transmitral
pressure half-time.
● Overestimating the degree of stenosis in patients with a heavily
calcified annulus in sinus rhythm because of a large A wave.
Mitral Regurgitation
1. Appearance and movement of the valve
● MR is either primary (caused by an abnormality of the valve) or
secondary (caused by LV dysfunction) (Table 9.5). In primary MR, the
valve looks abnormal, while in secondary MR, the valve looks normal but
is restricted (‘tented’) in systole (Table 9.5).
106
Table 9.5 Causes of mitral regurgitation
Valve Jet
Cause Movement
appearance direction
Primary (organic) (i.e. abnormal mitral valve)
Variable
Away from
Floppy mitral valve myxomatous Prolapse in systole
prolapse
change
Rheumatic disease Thickened tips Bowing in diastole Usually central
Sections of valve
Vegetation,
Endocarditis may move out of Variable
destruction
phase
Generalised
Other: SLE, drugs Systolic restriction Usually central
thickening
Secondary (functional) (i.e. abnormal LV)*
Inferior or Posterior
Normal Posterior
inferolateral infarct restriction
Inferior and Symmetrical
Normal Central
anterior infarcts restriction
Usually symmetrical
Global LV dilatation Normal Central
restriction
* Papillary muscle rupture is usually considered separately as acute ischaemic mitral regurgitation.
‘Ischaemic mitral regurgitation’ is used for secondary mitral regurgitation caused by
myocardial infarction.
● The mitral valve apparatus consists of the leaflets, chords, annulus, and
adjacent myocardium. However, the main clues to the aetiology are in
the leaflets themselves (Table 9.5).
Appearance of the valve
● Thickened leaflet tips are typical of rheumatic disease, often with rigid
posterior leaflet, commissural fusion, and chordal thickening and matting.
● Generalised thickening occurs in antiphospholipid syndrome or late after
high-dose radiation or after drugs (e.g. cabergoline, pergolide, phentermine).
● A floppy valve may only look thickened as prolapse develops in systole
and is often associated with lax chords and a dilated mitral annulus.
● A discrete mass attached to the leaflet suggests a vegetation.
● In the context of an acute coronary syndrome, consider a ruptured
papillary muscle tip.
● A ruptured chord is usually a thin whip-like structure associated with
prolapse.
107
Figure 9.3 Mitral prolapse. In this image, the anterior leaflet prolapse (a) and the
regurgitant jet is directed posteriorly (b), away from the abnormal leaflet.
Movement of the valve

● Mitral prolapse is defined as:
● Movement of part of either leaflet >2 mm behind the plane of the
annulus in the parasternal or apical long-axis views.
● Displacement of the point of coaptation behind the plane of the
annulus in the 4-chamber view.
● However, prolapse of the medial or lateral parts of the leaflets may
only be seen in other views:
● Prolapse of A3, P3, or the medial commissure may be seen in
the apical 2-chamber view, the parasternal short-axis view, or the
parasternal long-axis view tilted towards the RV.
● Prolapse of A1, P1, or the lateral commissure may be seen in
the apical 2-chamber view, the parasternal short-axis view, or the
parasternal long-axis view tilted towards the pulmonary artery.
● Is there evidence of prolapse? (Figure 9.3)
● anterior or posterior leaflets or both?
● Which segments are involved using the Carpentier classification

(Figure 9.4)?
● Does prolapse affect the leaflet tip, the whole leaflet (like a bucket
handle), or is it flail (moving through 180º and often with a visible
ruptured chord)?
● Is there restriction of opening in diastole?
● Restriction of both leaflet tips with doming of the rest of the leaflets
occurs in rheumatic disease.
● Confusion occasionally arises because of reduced opening of the
whole of both leaflets (not just the tip) as a result of low cardiac
output or of the anterior leaflet alone because of an impinging jet of
aortic regurgitation.
108
Figure 9.4 Mitral valve segments on transthoracic examination.
● Is there restriction of both leaflets during systole (symmetrical

tenting)? (Figure 9.5)
● This is usually associated with severe LV systolic dysfunction either
a globally dilated and hypokinetic LV or myocardial infarction in both
inferior and anterior territories.
● The MR jet is directed centrally.
● Is there restriction of the posterior leaflet during systole

(asymmetrical tenting)? (Figure 3.1)
● This is usually associated with an inferior or inferolateral (posterior)
infarction, sometimes affecting only a small section of myocardium,
making it difficult to detect. Occasionally, it is caused by fibrotic
shortening of the chords.
● The restriction may be subtle.
● The MR jet is directed posteriorly.
● If the leaflets look and move normally:

● Check the annulus diameter. A diameter >35 mm in women and
>40 mm in men raises the suspicion of dilatation7. Isolated annulus
dilatation can cause severe MR even without leaflet prolapse or LV
dysfunction.
109
Figure 9.5 Secondary mitral regurgitation. In secondary regurgitation, as a

result of symmetrical tenting of the leaflets, the regurgitant jet is central; if one leaflet is
slightly more restricted than the other, the jet will be directed towards that leaflet.
Table 9.6 Restricted leaflet motion
Both leaflets
Tenting (point of apposition above the plane of the annulus in the 4-chamber
view)
Centrally directed jet of regurgitation (Figure 9.5)
Dilated LV causing abnormal papillary muscle function
Restriction of posterior leaflet motion
Tip of leaflet held in LV during systole (best seen in a long-axis view)
(Figure 3.1)
Jet directed posteriorly (Figure 3.1)
Inferior or inferolateral (posterior) infarct
● Check for a perforation or cleft.

● Check for commissural prolapse:
● The jet origin will be to the medial or lateral part of the orifice in
the parasternal short-axis view.
● A jet from the commissure imaged in the parasternal long-axis
110 view may be mistaken for a perforation.
● Angling from the parasternal long-axis view medially towards

the RV will bring prolapse of the medial commissure into view.
Angling laterally towards the PA will bring prolapse of the lateral
commissure into view.
● The abnormality may be more obvious on 3D. If image quality is
suboptimal, consider TOE.
2. Colour flow mapping
The following should be assessed7:
● The origin of the jet (e.g. medial, central, or lateral part of the orifice).
● The direction of the jet:
● Away from a prolapsing leaflet (Figure 9.3b).
● Behind a restricted leaflet (Figure 3.1b).
● Centrally in symmetrical ‘tenting’ of the leaflets (Figure 9.5).
● The width of the jet at the level of the orifice using either:
● The vena contracta width averaged from two orthogonal views,
usually 4- and 3-chamber (or parasternal long-axis view) (Figure 9.6).
● The PISA method (Figure 9.7).
● The size of the flow convergence zone within the left ventricle is
assessed by eye.
Figure 9.6 Vena contracta. An average diameter should be given from orthogonal
views as many jets are oval in cross-section rather than circular. 111
Figure 9.7 The PISA method.

1. Lower the image depth to increase the size of the area of interest.
2. Reduce the Nyquist limit to 15–40 cm/s.
3. Measure the radius of the first aliasing shell at mid-systole (Va) (Figure 9.7a).
4. Measure the peak velocity (Vcw) and velocity time integral (VTIcw) of the continuous wave
mitral regurgitant signal (Figure 9.7b).
5. The formulae are:
● EROA = 10 (2πr2Va/Vcw)
● R Vol = (EROA × VTIcw)/100
112
● The duration of the jet using colour M-mode:

● Is it holosystolic or present only in part of the systole, usually the
latter part, as prolapse develops in bileaflet prolapse?
● The quantification of a jet based on jet width or PISA has to be
downgraded according to common-sense judgement if it is non-
holosystolic.
● Look at the shape and density of the signal. A signal as dense as
forward flow suggests severe regurgitation. A low-intensity or
incomplete signal suggests mild regurgitation and an intermediate
signal moderate regurgitation.
● Rapid depressurisation causes a ‘dagger-shaped’ signal and is a sign of
severe regurgitation.
4. Pulsed Doppler
● Severe mitral regurgitation is suggested by:
● A high transmitral E wave velocity (>1.5 m/s) in the absence of
mitral stenosis.
● A ratio of VTImitral/VTIsubaortic >1.4.7
● A pulsed sample in a pulmonary vein at a distance from the jet can

aid quantification, although this is most useful on TOE. Blunting of the
systolic signal occurs in moderate and severe regurgitation and flow
reversal in very severe regurgitation.
● The estimation of filling pressures using the E/E′ ratio is not valid in the
presence of severe mitral regurgitation.
5. LV function
● Measure linear dimensions at the base of the heart. The systolic dimension
is particularly important and should be averaged over several cycles.
● In regurgitation caused by a floppy valve, surgery can be considered
even in the absence of symptoms if the systolic dimension is ≥40 mm
or the LV ejection fraction ≤60% and the valve is repairable at low risk.
● LV shape may often change in severe MR, making linear dimensions
unrepresentative of the whole LV. LV systolic volumes (biplane Simpson’s
method or 3D) then aid the detection of progressive LV dilatation on serial
studies. There are no agreed cut points for surgery based on volumes.
6. General
Assess the left atrium

● A dilated LA is a non-specific sign of chronic severe MR but also occurs
in atrial fibrillation, systemic hypertension, or LV diastolic dysfunction.
113
● Progressive LA dilatation reaching an indexed volume >60 mL/m2 is

a secondary indication for surgery in an asymptomatic patient with a
repairable mitral valve2. However, in practice it is almost never used
alone.
Assess the right heart
● Pulmonary hypertension may complicate severe MR.
● A PA pressure >50 mmHg at rest is an indication for surgery in
asymptomatic severe MR2.
Assess the other valves
● The significance of aortic stenosis may be underestimated from the
transaortic velocities as a result of low forward flow in severe mitral
regurgitation.
● Tricuspid annuloplasty may be considered at the time of mitral valve
surgery if there is mild or more tricuspid regurgitation and a tricuspid
annulus diameter >40 mm.
7. Grading regurgitation (Table 9.7)
● Use all TTE modalities to grade the regurgitation.
● Multiple jets may be hard to quantify using jet characteristics alone.
Use the indirect signs:
● A hyperdynamic LV.
● Pulmonary vein flow.
● LA size (non-specific).
● Pulmonary hypertension.
8. Acute mitral regurgitation

This is usually caused by papillary muscle rupture in acute myocardial
infarction but can also occur after deceleration injury or chordal rupture in
endocarditis.
It causes hypotension and pulmonary oedema, but there may be no murmur:
● The hyperdynamic LV is the major clue (but also occurs with post-
infarct VSD).
● Because of the low LV pressure and high LA pressure, the jet
momentum may fall quickly, resulting in a short colour flow signal,
which may be missed. However, it will be broad and may fill the whole
mitral annulus.
● There will be a to and fro signal throughout the cardiac cycle at the
mitral annulus on a continuous wave or pulsed Doppler.
● A TOE (once the patient is ventilated) is often needed to confirm the
diagnosis.
114
Table 9.7 Grading mitral regurgitation7
Measurement Mild Moderate Severe

Neck width (mm) <3 3–6.9 ≥7
Flow convergence zone Absent Moderate Large
PISA Quantities
Measurement Mild Mild-mod Mod-severe Severe

EROA (mm2) <20 20–29 30–39 ≥40
Regurgitant volume (mL) <30 30–44 45–59 ≥60
RF % <30 30–39 40–49 ≥50
Note: EROA effective regurgitant orifice area using PISA method.
MISTAKES TO AVOID
● A hyperdynamic LV suggests severe MR, so think twice before

reporting mild or moderate MR.
● Missing early LV dysfunction because LV ejection fraction is in the low
normal range for a LV with normal loading (Table 2.7).
● Missing papillary muscle rupture in haemodynamic deterioration after
myocardial infarction.
● Mistaking posterior restriction for anterior prolapse (both cause a
posteriorly directed jet of regurgitation).
● Excessive use of TOE when the information needed is obtainable on TTE.
CHECKLIST FOR REPORT IN MITRAL VALVE

DISEASE
1. Detailed description of the valve appearance and movement, including
mechanism of mitral disease (and, if possible, the cause).
2. Grade of stenosis and regurgitation.
3. LV dimensions, volume, and systolic function.
4. RV size and function, pulmonary artery pressure.
5. Tricuspid annulus diameter.
6. Left atrial size.
7. Presence of other valve disease.
8. For isolated mitral stenosis, is the valve suitable for balloon valvotomy?
115
Specialist Pre- and Post-Operative

Assessment
1. Surgery in primary (organic) mitral regurgitation
● In asymptomatic patients with severe primary MR, the indications for
surgery (Table 9.8) depend on LV systolic size and function and the
likelihood of repair:
Table 9.8 Indications for surgery in asymptomatic patients with

severe primary mitral regurgitation2, 3
Indications for surgery Class

LVSD ≥40 mm or EF ≤ 60% I
PA systolic pressure at rest >50 mmHg 2a
LA volume ≥60 mL/m2 2a
LVSD <40 mm and LVEF >60% if repair near certain
2a
at a ‘valve centre of excellence’
● Likely—localised prolapse, especially P2, or A2 (middle portion of

posterior or anterior leaflets) or medial commissure or localised
perforation.
● Hard—involvement of the whole of the posterior leaflet, destruction
after endocarditis, rheumatic disease with pliable anterior leaflet,
moderate or severe annular calcification, bileaflet prolapse.
● Not likely—extensive prolapse involving the anterior leaflet;
rheumatic disease, especially with a rigid anterior leaflet; extensive
destruction after endocarditis; extensive annular calcification.
● A tricuspid annuloplasty is usually performed at the time of mitral valve
surgery if there is:
● ≥ Moderate tricuspid regurgitation.
● A combination of ≥ mild tricuspid regurgitation and a tricuspid

annulus diameter ≥40 mm (≥21 mm/m2).
● Patients unfit for surgery may be considered for a transcatheter edge
to edge repair procedure (TEER) in the absence of adverse features7
(Table 9.9).
2. Surgery in secondary (functional) mitral regurgitation
● Management decisions are far harder than for primary mitral
regurgitation because the underlying LV dysfunction may not improve
after intervention and will also increase surgical risk.
● Intervention is only considered if the patient remains unwell after full
116 medical therapy, including CRT, if appropriate.
Specialist Pre- and Post-Operative Assessment
Table 9.9 Unfavourable features for TEER in primary and secondary MR
Primary MR Secondary MR
Severe tenting (coaptation depth
Leaflet perforation or large cleft
>11 mm)
Coaptation length <2 mm, large
Rheumatic disease
coaptation gap
Large flail gap >10 mm Posterior leaflet length <7 mm
LVDD >70 mm; LVEDV >200 mL or
Large flail width >15 mm
LVEDV index >96 mL/m2
More moderate MR, EROA <30 mm2*
Mitral valve opening area ≤4.0 cm²
Leaflet calcification in the grasping area
* The COAPT trial showed good results in patients with a mean indexed LV volume 101 mL/m2
and MR EROA 41 mm2, while the MITRA-FR trial had poor results in patients with a mean
indexed LV volume 130 mL/m2 and MR EROA 31 mm2.
Table 9.10 Adverse features for surgical repair7 for secondary mitral
regurgitation
Left ventricle Mitral valve

● LVDD >65 mm ● Broad, eccentric, or
● LVSD >51 mm complex jet
● LV systolic volume >140 mL ● Small or normal MV
● Interpapillary muscle distance annulus, as a guide
>20 mm <35 mm
● Distance between base of posterior ● Tenting height >10 mm
papillary muscle and fibrosa >40 mm (area >1.6 cm2) or posterior
● Sphericity index >0.7 angle >45o
● Lateral wall motion abnormality ● Heavy annular calcification
● A heart team must integrate the clinical features and echocardiogram. The
decision is determined by LV function, the presence of myocardial viability
(meaning, that LV function might improve after PCI or CABG), and the
grade of MR and morphology of the mitral valve (Table 9.10) (Figure 9.8).
● Patients unsuitable for surgical repair may still benefit from valve
replacement, and this is sometimes preferable to a repair since it
needs a shorter operation and guarantees elimination of the MR.
● Stress echocardiography may be considered. Patients with leaflet
tenting and ischaemic disease are more likely to increase the degree of
mitral regurgitation on exercise8.
117
Figure 9.8 Markers of a low likelihood of repair in secondary mitral

regurgitation.
● Exercise echocardiography is indicated for:

● Patients with breathlessness out of proportion to the grade of
MR or LV dysfunction.
● Patients with mild or moderate MR about to have CABG.
● Acute pulmonary oedema with no known cause.
● Dobutamine stress echocardiography is indicated for patients with an

impaired LV to determine whether there is evidence of viability.
● If a patient is judged too high risk for surgery, they may be considered
for transcatheter edge-to-edge repair (TEER) in the absence of adverse
characteristics (Table 9.9).
3. Echocardiography after mitral valve repair
A checklist after surgical repair and TEER is given in Table 9.11.
118
Specialist Pre- and Post-Operative Assessment
Table 9.11 Echocardiography after mitral valve repair or TEER
Appearance of the mitral valve, chords and annuloplasty ring

or clips
Residual regurgitation
● Grade
● Localisation (middle, medial, lateral)
● Through the valve or around the annuloplasty ring after surgical repair?
Presence and degree of mitral stenosis
Systolic anterior motion of the anterior leaflet?
LV outflow acceleration
LV size and function
RV size and function and PA pressure
Left atrial size
3.1 Appearance
Surgical repairs may involve:

● Resection of valve tissue with reduction in the height of the leaflet.
A shortened thickened immobile posterior echogenic structure is
normal after P2 repair.
● Annuloplasty ring. Echogenic structure at the base of the leaflets.
● Artificial chords. These show as more dense than natural chords.
● Alfieri stitch. This is uncommon but is a stitch placed in the middle of
the orifice, producing a double-orifice mitral valve.
After TEER, appearances include:
● Highly echogenic clips.
● For secondary MR, a single central clip may be placed, causing a
double-orifice mitral valve.
Adverse features to assess:
● Stenosis of the native mitral valve.
● Systolic anterior motion of the anterior mitral leaflet causing LV outflow
flow acceleration.
● Unsuccessful or partially successful procedure with residual MR.
References
1. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of
valve stenosis: EAE/ASE Recommendations for clinical practice. Europ J Echo
2009;10:1–25.
119

4. Dreyfus GD, Corbi PJ, Chan KM & Bahrami T. Secondary tricuspid regurgitation
or dilatation: Which should be the criteria for surgical repair? Ann Thorac Surg
2005;79(1):127–32.
5. Keenan NG, Cueff C, Cimidavella C, Brochet E, Lepage L, Detaint D, Himbert
D, Iung B, Vahanian A & Messika-Zeitoun D. Usefulness of left atrial volume
versus diameter to assess thromboembolic risk in mitral stenosis. Am J Cardiol
2010;106(8):1152–6.
6. Wilkins GT, Weyman AE, Abascal VM, Block PC & Palacios IF. Percutaneous balloon
dilatation of the mitral valve: An analysis of echocardiographic variables related to
outcome and the mechanism of dilatation. Brit Heart J 1988;60(4):299–308.
7. Lancellotti P, Pibarot P, Chambers J, et al. Multimodality imaging assessment of
native valvular regurgitation: An EACVI and ESC Council of valvular heart disease
position paper. Europ Heart J CVI 2022;23(5):e171–232.
8. Lancellotti P, Troisfontaines P, Toussaunt AC & Pierard LA. Prognostic importance of
exercise-induced changes in mitral regurgitation in patients with chronic ischaemic
left ventricular dysfunction. Circulation 2003;108(14):1713–7.
120
Right-Sided Valve
Disease 10
The right-sided valves are assessed in the minimum standard TTE. Pay
particular attention if there is:
● Left-sided disease.
● RV dilatation, especially if the RV is hyperdynamic.
Tricuspid Regurgitation
Trace or mild tricuspid regurgitation (TR) is normal and seen in 80% of studies.
Steps to take if there is more than minor TR:
1. Describe the appearance and movement of the valve
● Pathological TR is usually secondary (caused by dilatation of the RV or
RA or by pulmonary hypertension), but it may be primary (caused by an
abnormal valve) (Table 10.1).
● Primary and secondary TR may coexist. Primary TR causing severe RV
dilatation can lead to tethering of the valve and worsening TR.
● Examine the valve in all views (Figure 10.1).
● The normal apical displacement of the septal leaflet from the mitral
annulus is up to 15 mm (indexed 8 mm/m2).
● The annulus is dilated if its diameter is ≥40 mm (21 mm/m2) in the
4-chamber view1.
● Imaging all three leaflets is aided by 3D2. Preliminary 3D normal ranges
for the annulus3 are:
● Long-axis 28–44 mm.
● Short-axis 22–38 mm.
● Progressive RV dilatation causes:

● Initially, annular dilatation with failure of leaflet coaptation.
● Further RV dilatation causes restriction of the leaflet tips.
2. Grading TR
● Use all modalities available (Table 10.2). The most useful are the colour
width and density of the continuous wave signal. Systolic flow reversal
in the hepatic vein and IVC is specific for severe TR.
121
DOI: 10.1201/9781003242789-10
Right-Sided Valve Disease
Figure 10.1 The normal tricuspid valve. The 4-chamber view (a) shows the
anterior (left) and septal (right) leaflets. The parasternal long-axis view (b) shows the anterior
(right) and either septal or posterior leaflet (left), depending on whether the septum or
posterior LV wall is imaged. The short-axis view (c) shows the septal or anterior leaflet (right)
and the anterior or posterior leaflet (left), depending on the cut.
Table 10.1 Causes of tricuspid valve disease
Cause Notes
Primary
Doming without significant thickening.
Rheumatic disease Commissural fusion may be more obvious on 3D.
Associated left-sided rheumatic disease.
Eccentric jet directed away from the prolapsing
Floppy valve leaflet.
Often associated with mitral prolapse.
May occur without prolapse.
Associated with RA dilatation.
Annular dilatation
The normal annulus diameter is <40 mm
(<21 mm/m2).
May complicate IV drug use or indwelling venous
Endocarditis
cannulae.
122
Tricuspid Regurgitation
Cause Notes
Associated with pulmonary valve involvement.
Carcinoid
Fibrotic, stubby rigid leaflets.
Congenital Ebstein’s anomaly (see Table 16.8).
Drugs (e.g. pergolide) General thickening and tenting.
The electrode causes perforation, interferes with closure,
Pacemaker
adheres to the leaflet, or causes leaflet thickening.
Trauma Prolapse with ruptured chords after blunt chest injury.
Iatrogenic Endocardial biopsy can damage the valve or chords.
Secondary
Initially causes annular dilatation with failure
RV myopathy/RV of leaflet coaptation. If severe, causes leaflet
infarct restriction. Look for associated left-sided myocardial
abnormalities.
Pulmonary May be no abnormality of the leaflets, unless there is
hypertension secondary RV dilatation.
Left-to-right shunts An ASD causes RV volume overload.
Chronic AF can cause tricuspid annulus dilatation as
RA dilatation
part of general RA dilatation.
Table 10.2 Grading tricuspid regurgitation4
Mild Moderate Severe**

Usually none, but
Colour neck (mm) <7 ≥7**
always <3
PISA radius (mm) <6 6–9 >9
EROA (mm2) – – ≥40*
R vol (mL) – – ≥40*
Dense and may
Low or mod
Continuous wave Incomplete be triangular
intensity
(Figure 10.2)
Maybe systolic
Hepatic vein flow Normal Systolic reversal
blunting
* Not routinely performed.
** New grades are now established4, 5: severe 7–13 mm, massive 14–20 mm, and torrential
≥21 mm. These make clinical sense and help demonstrate the benefit of transcatheter
techniques, which improve the grade of TR from torrential down to severe. This change
would not register on the traditional grading scheme.
123
Figure 10.2 Tricuspid regurgitation. Mild regurgitation causes a dagger-shaped,

low-intensity signal (a). Moderate regurgitation causes a large intratrial jet on colour mapping
with a complete continuous wave signal (b). Severe regurgitation has a dense signal
which initially retains its usual shape but, when very severe, may be dagger-shaped (c).
● Trivial or mild TR could be noted in the text but should not appear in the
conclusion of the report. This might suggest significant valve disease
to a non-echocardiographer.
3. Describe RV size and function (Chapter 4)
● Progressive RV dilatation or reduction in systolic function are
indications for surgery even without symptoms2 in severe primary TR.
● Early repair is recommended with a flail tricuspid leaflet after trauma
if the RV is significantly dilated at the initial assessment but no
thresholds are available6.
5. Echocardiography and surgery

● Indications for surgery are in Table 10.3.
● The type of surgery is guided by echocardiography.
● Annular dilatation usually responds to annuloplasty.
124
Tricuspid Stenosis
Table 10.3 Echocardiographic indications for surgery in severe

tricuspid regurgitation2
Primary tricuspid regurgitation

Severe TR and symptoms
Consider if severe TR and progressive dilatation and reduced function of the RV
even with no symptoms
Having left-sided surgery
Moderate or worse TR
Mild TR and tricuspid annulus diam ≥40 mm (≥21 mm/m2)
● Severe systolic restriction usually requires more advanced repair

techniques or valve replacement.
● Tricuspid prolapse may be repairable.
● Severe thickening usually suggests replacement rather than repair will
be needed.
Tricuspid Stenosis
1. Appearance of the valve
● TS is usually rheumatic but may also be congenital (Ebstein, tricuspid
atresia) or occur in carcinoid or as a result of dense fibrosis secondary
to SLE or multiple pacemaker electrodes.
2. Recognising tricuspid stenosis
● Restriction of the leaflets (Figure 10.3) may not be obvious on imaging.
Tricuspid stenosis is suggested if:
● Vmax >1.0 m/s (or more specific >1.5 m/s)8
● Mean gradient >2 mmHg9,10
● Signs suggesting severe stenosis are2:

● Mean gradient ≥5 mmHg
● Pressure half-time ≥190 ms
● Another clue to severe tricuspid stenosis is a small RV (because of

underfilling) and large RA (because of high back pressure).
3. Surgery
● Surgery is indicated for severe tricuspid stenosis and symptoms or is
performed at the time of surgery for coexistent left-sided disease.
125
Figure 10.3 Tricuspid stenosis. Tricuspid stenosis may be missed because, unlike
the situation with the mitral valve, there may be little thickening or calcification.
MISTAKES TO AVOID
● A rheumatic tricuspid valve is easily missed because the leaflets can be

thin. It rarely occurs alone, so always check the tricuspid valve if there is
left-sided rheumatic disease.
CHECKLIST FOR THE REPORT IN TRICUSPID

VALVE DISEASE
1. Tricuspid valve appearance and movement. Annulus diameter.
2. Grade of regurgitation.
3. Trans-tricuspid gradient if valve-restricted.
4. RV size and function and PA pressure.
5. Left-sided valves.
Pulmonary Stenosis and Regurgitation

● Pulmonary stenosis is almost always congenital (Table 10.4)11. It may be part of
more complex cardiac lesions, especially tetralogy of Fallot, or associated with
other lesions, for example, ASD. It may also be associated with more general
126 congenital syndromes (Noonan, Williams, LEOPARD; see Table 16.1, page 172).
Table 10.4 Causes of pulmonary valve disease
Pulmonary
Pulmonary regurgitation
stenosis
Congenital Prior intervention for congenital stenosis
Carcinoid Endocarditis
Secondary
● Pulmonary hypertension
● PA or annular dilatation
Carcinoid
● The obstruction is at valve level in 90%, subvalvar in 5%, supravalvar in 1%,

and in a branch in 5%.
● An initial clue to the presence of stenosis is turbulent flow in the RV
outflow tract during systole on colour Doppler.
● A stenotic valve is either:
● Dysplastic and thickened (e.g. in Noonan syndrome)
● Relatively thin, but with systolic bowing, and therefore visible in

systole as well as diastole
2. Is there pulmonary regurgitation?
● Trace or mild regurgitation is normal. A jet originating near the edge of
the orifice should not be mistaken for coronary artery flow.
● Severe regurgitation is suggested by the findings in Table 10.5.
3. What is the pressure difference across the valve?

The main method of grading is by the transpulmonary Vmax (Table 10.6)11, 12.
Table 10.5 Factors suggesting severe pulmonary regurgitation4
A wide colour jet (e.g. >7.5 mm or >65% of the annulus diam)

Diastolic flow reversal visible in the distal main pulmonary artery or branches
(Figure 10.4)
A steep dense continuous wave signal (pressure half-time <100 ms and
deceleration time <260 ms) (Figure 10.5)
Ratio of PR duration:diastolic duration <0.77
Dilated, active RV
127
Figure 10.4 Pulmonary regurgitation—colour map. Mild regurgitation is

shown on the left with a narrow jet originating at the valve level. Severe regurgitation
on the right has a jet filling the RV outflow tract with flow reversal as far as the right
pulmonary artery branch.

http://goo.gl/eQmasZ
4. Check the level of the obstruction

● A muscular obstruction in the RV outflow tract (infundibulum) or mid-
cavity (double-chamber RV) may be mistaken for or be associated with
pulmonary valve stenosis.
● The continuous Doppler waveform may have a late-systolic peak but
may also be identical to obstruction at valve level.
● Pulsed Doppler may identify the level of obstruction.
● The diagnosis commonly needs CMR if TTE image quality is

suboptimal.
● A pulmonary artery membrane may be mistaken for valve obstruction
but is rare.
5. What is pulmonary artery pressure? (See Chapter 5)
● Dominant PR may be caused by pulmonary hypertension.
● PS protects the pulmonary circulation against the effect of high flow
from a left-to-right shunt.
128
Figure 10.5 Pulmonary regurgitation—continuous wave signal. In normal

mild PR, the signal has a slow descent (a), while in severe regurgitation (b), the pressure
half-time is <100 ms, 78 ms in this example.
129
Table 10.6 Grading pulmonary stenosis

Vmax <3.0 m/s 3.0–4.0 m/s >4.0 m/s
Peak gradient <36 mmHg 36–64 mmHg >64 mmHg
Table 10.7 Guide to upper limit of normal pulmonary artery dimensions13
RV outflow diameter (mm) 34

PV annulus (mm) 22
Main pulmonary artery (mm) 29
Right pulmonary branch (mm) 17
Left pulmonary branch (mm) 14
6. Assess the pulmonary artery

● Look for dilatation of the main and branch pulmonary arteries. Little
modern data exist, and Table 10.7 gives information on upper limits from
1984 as a guide.
7. Assess RV size and function (See Chapter 4)
8. Other imaging modalities

Once severe pulmonary valve disease is detected by echocardiography, CMR
is used to:
● Quantify the degree of PR. A regurgitant volume of >40 mL/beat and a
regurgitant fraction >35% are thresholds for severe.
● Measure RV volumes for serial studies.
● Differentiate double-chamber RV (mid-cavity) from infundibular (RVOT)
stenosis.
● Assess branch pulmonary artery stenoses and lung perfusion.
9. Are there indications for invasive intervention?

● If balloon valvotomy is feasible this can be considered if Vmax >4.0 m/s
even in the absence of symptoms11.
● If surgical valve replacement is needed, intervention should be discussed
at an MDT if there is severe (or moderate) PS11 or severe PR and:
● Symptoms or reduced exercise tolerance.
● A serial decrease in RV systolic function and progression of TR to ≥

moderate.
● RV systolic pressure >80 mmHg (in PS).
● Right-to-left shunting via an ASD or VSD (in PS).

130
MISTAKES TO AVOID
● Do not use the TR Vmax alone to calculate PA systolic pressure if there is

PS or other RV outflow obstruction. Subtracting the 4V2pulm from 4V2tr
will give a better estimate.
● Missing severe PR because the diastolic jet may be wide and low
momentum.
CHECKLIST FOR THE TTE IN PULMONARY

VALVE DISEASE
1. Appearance and motion of the pulmonary valve.
2. Vmax and mean gradient.
3. Grade of PR.
4. RV size, morphology and systolic function.
5. Diameter of pulmonary artery and estimated PA systolic pressure, if
possible.
References
2. Badano LP, Agricola E, de Isla LP, Gianfagna P & Zamorano JL. Evaluation of
the tricuspid valve morphology and function by transthoracic real-time three-
dimensional echocardiography. Europ J Echo 2009;10(4):477–84.
3. Addetia K, Muranu D, Veronesi F, et al. 3-Dimensional echocardiographic analysis
of the tricuspid annulus provides new insights into right ventricular geometry and
dynamics. J Am Coll Cardiol CVI 2019;12(3):401–12.
4. Lancellotti P, Pibarot P, Chambers J, et al. Multimodality imaging assessment of
native valvular regurgitation: An EACVI and ESC Council of valvular heart disease
position paper. Europ Heart J CVI 2022;23(5):e171–232.
5. Hahn RT, Zamorano JL. The need for a new tricuspid regurgitation grading scheme.
Europ Heart J CVI 2017;18(12):1342–43.
6. Messika-Zeitoun. Medical and surgical outcome of tricuspid regurgitation caused
by flail leaflets. J Thorac Cardiovasc Surg 2004;128(2):296–302.
131

8. Parris TM, Panidis JP, Ross J & Mintz GS. Doppler echocardiographic findings in
rheumatic tricuspid stenosis. Am J Cardiol 1987;60(16):1414–6.
9. Ribeiro PA, Al Zaibag M, Al Kasab S, Hinchcliffe M, Halim M, Idris M, et al.
Provocation and amplification of the transvalvular pressure gradient in rheumatic
tricuspid stenosis. Am J Cardiol 1988;61(15):1307–11.
10. Fawzy ME, Mercer EN, Dunn B, Al-Amri M & Andaya W. Doppler echocardiography
in the evaluation of tricuspid stenosis. Europ Heart J 1989;10(11):985–90.
11. Baumgartner H, de Backer J, Babu-Narayan SV, et al. 2020 ESC Guideline for the
management of adult congenital heart disease. Europ Heart J 2021;42(6):563–645.
12. Stout KK, Daniel CJ, Abdoulhosu JA, et al. 2018 AHA/ACC Guidelines
for the management of adults with congenital heart disease. Circulation
2019;139(14):e698–800.
13. Triulzi MO, Gillam LD & Gentile F. Normal adult cross-sectional echocardiographic
values: Linear dimensions and chamber areas. Echocardiography 1984;1(4):403–26.
132
Mixed Valve Disease
11
● This is increasingly common and was seen in 25% of patients in the 2017
European Heart Valve Survey1.
● If one valve lesion is severe and the other only mild or moderate, then the
severe lesion dominates management (see Chapters 8 and 9).
● Tricuspid regurgitation combined with left-sided disease is discussed in
Chapter 10.
● For moderate mixed valve lesions, the key to assessment and management is:
● The effect on the LV
● The presence of symptoms
● If you are uncertain, bring the case to an MDT discussion.
Mixed Moderate Aortic Valve Disease

● The transaortic Vmax gives a better assessment of overall severity than EOA.
● A Vmax >4.0 m/s implies severe mixed disease even if the EOA is >1.0 cm2.
● Surgery is indicated for symptoms.
● In the absence of symptoms, surgery should be considered if the LV
ejection fraction is <50% or has reduced progressively on serial studies. No
formal guideline thresholds exist2.
Mixed Moderate Mitral Valve Disease

● Mixed disease occurs in rheumatic disease and increasingly as a result of
mitral annulus calcification.
● A high transmitral gradient, whether caused by severe pure MS or mixed
moderate disease, is still haemodynamically important. Management
should be judged on symptoms and the haemodynamic effects on the RV
and PA pressure.
● More than mild MR is a contraindication to balloon mitral valvotomy.
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Mixed Valve Disease
Mixed Mitral and Aortic Valve Disease

● Causes of confusion to guard against are:
● Severe AR causes shortening of the transmitral pressure half-time in MS.
● The jet of severe AR impinging on the anterior mitral leaflet can cause
functional MS in the presence of an otherwise-normal mitral valve.
● An eccentric jet of MR directed parallel to the LVOT can cause a CW
signal similar to severe AS.
● Reduced flow to the LVOT as a result of severe MS or MR is a cause
of low-flow, low-gradient AS leading to potential underestimation of the
severity of AS (see page 86).
● Moderate AR and moderate MR together can cause severe LV volume
load. Management is guided by symptoms and LV geometry and
function and should be discussed at an MDT.
● The assessment of MR in patients with severe AS is described on
page 88. In general, mitral valve intervention is indicated by:
● Primary disease of the mitral valve, for example, prolapse.
● Moderate to severe or severe secondary MR.
References
1. Iung B, Delgado V, Rosenhek R, et al. Contemporary presentation and
management of valvular heart disease. The Eurobservational Research Programme
Valvular Heart Disease II Survey. Circulation 2019;140(14):1156–69.
134
Prosthetic Heart
Valves 12
● The core information to be gathered1–3 is:
● Appearance of the valve
● Colour Doppler forward flow and regurgitation
● Spectral Doppler
● The types of valve and their TTE features are given in Table 12.1 (see also
Figure 12.1).
Core Information
● On imaging, prosthetic valves can be classed as normal (thin and
mobile biological cusps) or failing (thick and restricted cusps or
mechanical occluder):
● The cusps of an AVR or TAVI are often best imaged from the apical long-
axis view and a tricuspid prosthetic valve from a modified parasternal
long-axis view.
● The cage of an aortic caged-ball valve is also best seen in the apical
long-axis view. A tilting disc or ball may both appear as an indistinct
mass in a parasternal long-axis view and may be difficult to tell apart.
● If image quality is suboptimal, colour Doppler filling the whole orifice in
all views suggests normal opening.
● Some appearances in a mitral valve which are normal but can cause
confusion are:
● The leaflets of a bileaflet mechanical valve may shut at slightly
different rates.
● Cavitations (bubbles) in the LV which occur with all types of valve
but especially bileaflet mechanical valves.
● Fibrin strands attached to the valve (seen best on TOE) are far
thinner than vegetations and have no pathological significance.
● If the surgeon has retained the posterior leaflet, a normal prosthetic
mitral valve may rock slightly. In other positions, rocking suggests a large
paraprosthetic leak. The diagnosis is established with colour Doppler.
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Prosthetic Heart Valves
Table 12.1 Types of prosthetic valves
Types Makes Common TTE features

SURGICALLY IMPLANTABLE BIOLOGICAL
Stented animal tissue (‘xenograft’)
Three ‘crowns’ of the stent
Duraflex, Mosaic, Epic,
and echogenic sewing ring,
Hancock, Abbot (previously
Porcine three thin and mobile cusps,
St Jude Medical), Biocor/
trivial regurgitation through is
Labcor Porcine
normal.
Edwards Perimount/
Magna/Inspiris, Mitroflow,
Labcor Pericardial, Biocor
Pericardial Ditto.
Pericardial, Trifecta, C-E
Biophysio, Sorin More,
Sorin Soprano
Perceval S, Edwards Intuity,
Sutureless Ditto.
3F Enable, Trilogy
Stentless
Toronto, Medtronic Some designs have prominent
Freestyle, Cryolife-O’Brien,* sewing cuffs, three thin
Porcine Koehler Elan, Labcor and mobile cusps, trivial
Stentless, Edwards Prima, regurgitation through is
Biocor normal.
Three thin and mobile cusps,
Pericardial Freedom Solo, Pericarbon
trivial regurgitation.
May look like a normal native
Homograft
valve.
Autograft may look like a
Ross normal native valve.
procedure Homograft in pulmonary
position.
SURGICALLY IMPLANTED MECHANICAL
Cage may be hard to image in
aortic position best seen in
apical long-axis. Obvious in
mitral position.
Caged ball Starr-Edwards
Prominent reverberations from
ball into LA.
Mild central regurgitation is
normal.
136
Core Information
Stentless (Continued)
Single disc obvious in MVR, may
Bjork-Shiley,* Medtronic
be mistaken for a mass in AVR.
Hall, Sorin Allcarbon,
Tilting disc Regurgitation from major and
Omnicarbon, Koehler
minor orifices (through the
Ultracor
disc for Medtronic-Hall).
Visualisation of both leaflets easy
in MVR and AVR depending on
surgical orientation.
Abbot (previously St Jude),
Minor regurgitation at both
Carbomedics, On-X, Sorin
Bileaflet pivots and occasionally
Bicarbon, ATS, Medtronic
around leaflets.
Advantage, Edwards Mira
Large ‘bubbles’ normal in the LV
with MVR.
Fibrin strands normal.
TRANSCATHETER
Short echogenic stent. Cusps
difficult to image except in
Balloon- Edwards SAPIEN, SAPIEN
apical views.
expandable XT, SAPIEN3
Mild regurgitation through is
common.
Medtronic CoreValve and Long echogenic stent. Cusps
Engager, Boston Scientific best imaged in apical views.
Self-
Lotus, Abbot Portico, Mild regurgitation through
expandable
Symetis Acurate, Direct and around the valve is
Flow, Jena common.
Abbreviation: C-E Carpentier-Edwards.
* Now withdrawn.
2. Colour Doppler
● All mechanical valves have ‘physiological’ regurgitation through the valve
(Figure 12.2). These are narrow, with little or no aliasing. Regurgitation
across the valve also occurs in about 10% of normal biological valves and
is common in transcatheter valves.
● Paraprosthetic regurgitation is abnormal:
● Mild paraprosthetic regurgitation (best seen on TOE) can cause
haemolysis. If asymptomatic, should be followed at least once after
the baseline TTE to exclude progression.
● In the mitral and tricuspid positions, an easily seen jet is usually
paraprosthetic since normal transprosthetic regurgitation tends to
be hidden by flow shielding (unless the LA is very large).
● The intraventricular flow recruitment region of paraprosthetic
regurgitation can usually be seen even when the intra-atrial jet is 137
Figure 12.1 Images of prosthetic heart valves. Stented biological valves:

(a) Magna-Ease (bovine pericardial), (b) Epic (porcine). Stentless biological valve:
(c) Medtronic Freestyle. Bileaflet mechanical mitral valve: (d) OnX, (e) Abbot Master HP.
Single tilting disc: (f) Medtronic-Hall. Transcatheter: (g) Edwards SAPIEN, (h) Medtronic
Corevalve.
138
Core Information
Figure 12.2 Patterns of normal regurgitation.
invisible. This allows the regurgitation to be localised using the

sewing ring as a clockface.
● If there is doubt about the origin or size of a jet, TOE is indicated.
3. Spectral Doppler
● Steerable CW from the apex is sufficient if the patient is well and the
valve clearly normal, but if there is doubt, the stand-alone probe should
be used in at least two windows for an AVR.
● It is important not to position the pulsed sample too close to the AVR
or TAVI, which results in an artefactually high EOA.
● The minimum dataset1 is:
● Aortic: Vmax, mean gradient, and EOA using the continuity equation.
139
● Pulmonary: Vmax and mean gradient.

● Mitral and tricuspid: Mean gradient, pressure half-time.
● For prosthetic mitral valves:
● The Hatle formula (220/pressure half-time) is not valid.
● The EOA and DVI are not routinely calculated but are used if
uncertainty remains after imaging and basic spectral Doppler:
● Mitral EOA is CSAAo × VTIsubaortic/VTImitral.
● Mitral DVI is VTImitral/VTIsubaortic (ratio rises with obstruction).
● For aortic prosthetic valves, the aortic DVI may be useful as an adjunct
if the LVOT diameter is hard to measure:
● Aortic DVI is VTIsubaortic/VTIAo (ratio falls with obstruction).
Is There Dysfunction of the Prosthetic

Valve?
Patients may present with symptoms as a result of:
● Dysfunction of the prosthetic valve, causing regurgitation or obstruction
(Table 12.2).
● Other structural cardiac disease: LV or RV dysfunction or other valve
disease.
Table 12.2 Complications of prosthetic heart valves
Echocardiographic
Complication Mechanical Biological
effect
Structural valve Thickened cusps with
– ++++
degeneration (SVD) regurgitation >> obstruction
Thrombosis ++ + Obstruction
Thromboembolism +++ +++ Nil
Infective Vegetations, abscess, new
++ ++
endocarditis dehiscence
Obstruction of closure or
Pannus + + opening of leaflet; may be
intermittent.
Dehiscence ++ ++ Paraprosthetic regurgitation
Bleeding +++ ++ Nil
Note: + rare, ++ uncommon, +++ common, ++++ universal in long-lived patients, and – almost
140
never occurs.
Is There Dysfunction of the Prosthetic Valve?
Echocardiography is important in differentiating these causes.

The key questions as you scan are:
1. Is the valve normal, or are there signs of early failure?
2. If the Vmax is high, is it from patient–prosthesis mismatch or obstruction?
3. Is there regurgitation, and is it pathological?
4. Is there other disease?
1. Is the valve normal, or are there signs of early failure?

● Failure (structural valve deterioration or SVD) is inevitable in all
biological valves and TAVI, if the patient lives sufficiently long, but
almost never occurs in mechanical valves.
● Early failure starts with thickening of the cusps and usually progresses
gradually to cause obstruction or regurgitation. Occasionally, a tear in
the base of the cusp can extend suddenly.
● In practice, mild thickening and regurgitation is a prompt to consider
annual echocardiograms. Moderate SVD (Tables 12.3 and 12.4) might
prompt more frequent reassessment, depending on the clinical situation.
● Re-intervention is indicated mainly for symptoms. In routine clinical
practice, changes in valve morphology and haemodynamic function
from baseline should be highlighted. Severe valve failure should
be highlighted to the clinician in charge of the case (Tables 12.3 for
surgical and transcatheter aortic valves and 12.4 for mitral valves).
2. High Vmax. Patient–prosthesis mismatch vs obstruction
● All prosthetic valves are obstructive compared with a normal native
valve because of the presence of a stent and sewing ring and the
reduced compliance of the leaflet tissue.
● Mild patient prosthesis mismatch is therefore normal, but severe
mismatch may affect outcomes and cause symptoms5.
Table 12.3 Guideline grading structural valve deterioration4 in aortic

surgical and transcatheter valves compared to a baseline study 1–3
months after surgery

Morphology Thickening of the leaflets
↑ mean gradient
↑ mean gradient ≥20
≥10 mmHg to
mmHg to ≥30 mmHg
No significant ≥20 mmHg and
Obstruction and
change ↓ EOA ≥0.3 cm2
↓ EOA ≥0.6 cm2 or ≥50%
or ≥25% (or ↓ DVI
(or ↓ DVI ≥0.2 or ≥40%)
≥0.1 or ≥20%)
Regurgitation No significant ↑ by ≥1 grade to ↑ by ≥2 grades to
through the valve change ≥ moderate severe 141
Table 12.4 Guideline grading structural valve deterioration4 in biological

mitral valves compared to a baseline study 1–3 months after surgery

Morphology Thickening of the leaflets
↑ mean gradient ≥10
↑ mean gradient
mmHg and ↑ DVI ≥0.8
≥5 mmHg and ↑
or ≥40%, resulting in
No significant DVI ≥0.4 or ≥20%,
Obstruction a DVI ≥2.7
change resulting in a
(or EOA ≥1.0 cm2 or
DVI ≥2.2 (EOA ≥
≥ 50% resulting in
0.5 cm2 or ≥25%)
EOA <1.0 cm2)
Regurgitation No significant ↑ by ≥1 grade to ↑ by ≥2 grades to
through the valve change ≥ moderate ≥ moderate-severe
● The key features of patient–prosthesis mismatch are (Table 12.5 and

Figure 12.3):
● Normal valve appearance.
● Vmax, gradient, and EOA in normal range for valve design and size
(Appendix Tables A.8-A.10).
● No significant change in spectral Doppler from baseline study.
● Low EOA indexed to BSA (Table 12.5).
● If the cusps or leaflets are not imaged well on TTE, consider:

● TOE, but the leaflets of a mechanical valve may still be difficult to image.
● Fluoroscopy.
● CT, which may also image pannus.
Table 12.5 Differentiating patient–prosthesis mismatch from

obstruction in aortic prosthetic valves
Patient–prosthesis
Key features Obstruction
mismatch
Cusps or disc thickened
Thin mobile cusps
or reduced opening
Appearance of the valve Colour fills orifice in all
Restricted colour across
views
the valve
Normal range spectral Within for size and type
Outside
Doppler of valve
Change from baseline
● Mean gradient ≤10 mmHg* >10 mmHg
● EOA No change ↓ >0.3 cm2
* Mean gradient may rise if LV systolic dysfunction recovers after surgery, but the EOA should
stay approximately constant.
142
Figure 12.3 Flow diagram to differentiate patient–prosthesis mismatch

from obstruction in an aortic valve.
Table 12.6 Grading of patient–prosthesis mismatch by indexed

effective orifice area (cm2/m2)5
Moderate Severe
BMI <30
Aortic 0.66–0.85 ≤0.65
Mitral 0.9–1.2 <0.9
BMI >30
Aortic 0.56–0.70 ≤0.55
Mitral 0.8–1.0 <0.8
● If there are no baseline or other earlier studies, Table 12.7 suggests

when to suspect obstruction.
● Pressure half-time does not reflect orifice area in normally functioning
prosthetic mitral valves, but it lengthens significantly when the valve
becomes obstructed (Figure 12.4).
3. Is there regurgitation, and is it pathological?
If regurgitation is detected, it must be categorised as normal or pathological
based on its origin and grade.
3.1 Origin of the jet
● How many jets, and are they through the valve (Figure 12.2),
paraprosthetic, or both? Localisation can only be certain if the base
or neck of the jet can be imaged in relation to the sewing ring.
143
Table 12.7 When to suspect significant prosthetic valve obstruction

with an isolated study1, 2
Symptoms
Thickened or immobile cusps or occluder
Narrowed colour map across the valve
Measurements outside normal values (Appendix Tables A.8– A.10)
Aortic position:
● Vmax >4.0 m/s (see also Figure 12.3 if Vmax >3.0 m/s)
● Mean pressure difference >35 mmHg
● EOA <0.8 cm2
● Acceleration time >100 ms*
Mitral position:
● Pressure half-time >200 ms and Vmax >2.5 m/s
● Mean gradient >10mmHg
● DVI (VTImitral/VTIsubaortic) >2.5
Pulmonary position:
● Vmax >2.0 m/s for homograft or >3.0 m/s for any other valve type
Tricuspid position:
● Pressure half-time >230 ms
● Mean gradient >6 mmHg
● Vmax >1.6 m/s
Indirect signs:
● Rise in TR Vmax
● Dilatation of RV (any valve, but especially pulmonary)
● Dilatation or hypokinesis of LV (aortic)
* Acceleration time is the time from the onset to the peak of the transaortic CW signal.
● For a mechanical valve, the jets through the valve should match the
typical pattern expected of the design (Figure 12.2).
● Regurgitation through the valve in bileaflet mechanical valves
(‘pivotal washing jets’) begins close to the edge of the orifice and
must not be mistaken for paraprosthetic jets.
● The site and extent of a paraprosthetic aortic jet can be described
on the sewing ring as a clockface in the parasternal short-axis view.
3.2 Severity of regurgitation
● Normal regurgitation through a mechanical valve is usually low in
momentum (relatively homogeneous colour), with an incomplete or
very low-intensity continuous wave signal.
● For larger jets, use the same methods as for native regurgitation (see
Chapters 8–10). Assessing the height of a jet relative to LVOT diameter
144 may be difficult since paraprosthetic jets are often eccentric.
Figure 12.4 Obstruction in a mitral prosthetic valve. The transmitral Doppler

signal is shown soon (a) after implantation with a pressure half-time 50 ms, and (b) after
stopping warfarin when the patient was admitted with pulmonary oedema and a pressure
half-time 350 ms.
145
● The circumference of the sewing ring occupied by the jet is another

approximate guide. For a surgical valve in the aortic position, a jet
occupying >20% of the circumference on TTE is likely severe. 3D TOE
is required for the mitral position.
● TAVI may have multiple jets, and these may occur both through
and around the valve. Quantification is often difficult using
echocardiography. If accurate quantification is needed, consider CMR.
● Severe paraprosthetic MR may be obvious from:
● A large region of flow convergence within the LV.
● A broad neck.
● A hyperdynamic LV.
● A dense continuous wave signal, especially with early

depressurisation (dagger shape).
4. Is there other disease?
● Assess all other valves, LV and RV function, and PA pressures.
● A hyperdynamic LV is a clue that there may be severe prosthetic aortic
or mitral regurgitation.
● A rise in pulmonary artery pressure can be a sign of prosthetic mitral
valve obstruction.
When is TOE indicated?

TTE and TOE are complementary, and TOE is rarely used without initial TTE
(Table 12.8). Although TOE is usually necessary to image vegetations and
posterior root abscesses, anterior root abscesses may be better seen on TTE.
Table 12.8 Indications for TOE
Endocarditis clinically likely

Obstruction suggested by TTE to:
● Image leaflets
● Detect thrombus, pannus, or vegetations
To image leaflet opening to differentiate patient prosthesis mismatch from
pathological obstruction in an aortic valve prosthetic
Haemolysis (small regurgitant jet often not detected on TTE)
Symptomatic patient and suboptimal TTE imaging
Paraprosthetic mitral regurgitation of uncertain severity
Thromboembolism despite therapeutic INR (to detect pannus or thrombus)
146
MISTAKES TO AVOID
● Mistaking normal regurgitant jets in bileaflet mechanical valves, which

begin close to the edge of the orifice for paraprosthetic jets.
● Overdiagnosing obstruction with a single high Vmax.
● Failing to use off-axis views to detect flow convergence and the neck of
a paraprosthetic mitral regurgitant jet.
● Not responding to a hyperdynamic LV as an indirect sign of severe
paraprosthetic aortic or mitral regurgitation.
● Not doing a TOE to look for a small paraprosthetic jet if there is clinically
severe haemolysis.
CHECKLIST FOR ECHOCARDIOGRAPHY OF

PROSTHETIC VALVES
1. Appearance of the valve.
2. Vmax, mean gradient, and effective orifice area (aortic) and pressure half-
time (mitral and tricuspid).
3. Presence, location, and grade of regurgitation.
4. If velocities and gradients high: Is there evidence of pathological
obstruction? Is there patient prosthesis mismatch?
5. LV size and function.
6. RV size and function and pulmonary pressure.
7. Aorta:
a. Size of ascending aorta.
b. Evidence of coarctation if the valve prosthetic was for a bicuspid aortic
valve.
References
1. Lancellotti P, Pibarot P, Chambers J, et al. Recommendations for the imaging
assessment of prosthetic heart valves. A report from the European Association
of Cardiovascular Imaging endorsed by the Chinese Society of Echocardiography.
Europ Heart J CVI 2016;17(6):589–90.
2. Zoghbi WA, Chambers JB, Dumesnil JG, et al. American Society of
Echocardiography recommendations for evaluation of prosthetic valves with two-
dimensional and Doppler echocardiography. J Am Soc Echo 2009;22(9):975–1014.
147
3. Zamorano JL, Badano LP, Bruce C, et al. EAE/ASE Recommendations for the use
of echocardiography in new transcatheter interventions for valvular heart disease.
JASE 2011;24:937–65 and Europ Heart J 2011;32(17):2189–214.
4. Pibarot P, Hermann HC, Changfu W, et al. Standardized definition of bioprosthetic
valve dysfunction following aortic or mitral valve replacement. J Am Coll Cardiol
2022;80(5):545–61.
5. Pibarot P & Dumesnil JG. Valve prosthesis-patient mismatch, 1978 to 2011: From
original concept to compelling evidence. J Am Coll Cardiol 2012;60(13):1136–9.
148
Endocarditis 13
● Infective endocarditis is uncommon1 but important because the mortality is
up to 20%, and about 50% need inpatient cardiac surgery2.
● Echocardiography is essential for:
● Aiding the diagnosis when clinically suggested by contributing
vegetations or local complications to the Duke criteria (Appendix Table
A.7) as major criteria. TTE should not be done for fever alone.
● Assessing the resulting valve regurgitation.
● Planning surgery.
1. Is there a vegetation?
● This is typically a mass attached to the valve and moving with a different
phase to the leaflet. However, there may sometimes be new thickening
integral to the leaflet.
● It may be difficult to differentiate from other types of masses (e.g.
calcific or myxomatous degeneration, a fibrin strand, or flail chord). This
is a particular problem if TTE has been requested with a low clinical
likelihood of endocarditis. Choose a descriptive term that will not lead
to overdiagnosis of endocarditis (Table 13.1).
● Note the size and mobility of the vegetation. Highly mobile masses
longer than 10 mm have a relatively high risk of embolisation and may
affect the decision for and timing of surgery3. Vegetations longer than
15 mm are an indication for surgery in their own right.
● Vegetations usually occur on valves but also at the site of jet lesions or
around the orifice of a VSD or on pacing leads.
2. Is there a local complication?
● A new paraprosthetic leak (dehiscence) is a reliable sign of replacement
valve endocarditis, provided there is a baseline post-operative study
showing no leak.
● Perforation, fistula.
● An abscess usually suggests that surgery will be necessary.
● TTE is good for showing anterior root abscesses (Figure 13.1); TOE
better for posterior root abscesses.
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Endocarditis
Table 13.1 Suggested terms for describing a mass
● ‘Typical of a vegetation’
● ‘Consistent with a vegetation’
● ‘Consistent but not diagnostic of a vegetation’
● ‘Consistent with a vegetation but more in keeping with calcific degeneration’
● ‘Most consistent with calcific degeneration’
Figure 13.1 Aortic abscess. Parasternal short-axis view showing cavities between
the pulmonary artery and aorta and in the anterior aorta. The aortic valve cusps are
thickened because of endocarditis.
3. Is there valve destruction?

● This may show as:
● Disruption of the leaflet tissue with unusual patterns of movement,
‘dog-legs,’ or small flail segments (Figure 13.2).
● A perforation.
● New prolapse.
● New or worsening regurgitation.
4. Check the other valves

● Multiple valve involvement is particularly likely with invasive organisms,
e.g. Staphylococcus aureus.
● The jet of AR may impinge on the anterior mitral leaflet to seed a
vegetation or cause local infection leading to an aneurysm or perforation.
150
Endocarditis
Figure 13.2 Valve destruction.
5. Grade regurgitation
● This is as for regurgitation from any cause (Chapters 8–10).
● The colour jet and spectral Doppler may be difficult to interpret because
of artefact caused by the vibration of a vegetation, ruptured chord, or torn
leaflet (Figure 13.3). A hyperdynamic LV is a clue to severe regurgitation.
● The presence of severe regurgitation is an indication for surgery.
6. Assess the LV
● Progressive systolic dilatation of the LV suggests the need for urgent
surgery.
● If there is acute severe AR, look for (Figure 8.7):
● A transmitral E deceleration time <150 ms on pulsed Doppler.
● Diastolic mitral regurgitation.
● These are ‘red flag’ signs of a raised LV end-diastolic pressure and an

indication for urgent or emergency surgery.
● If you see these ‘red flag’ signs, immediately inform the clinician in
charge of the case.
7. Detect a predisposing abnormality
● About one-half of cases develop on previously normal valves. For the
others, predisposing abnormalities are given in Table 13.2.
● Pacemaker and implantable defibrillator endocarditis is increasingly
151
common.
Endocarditis
Figure 13.3 Comb artefact. This is caused by the vibration of a vegetation attached
to the posterior mitral leaflet and leads to colour filling the left atrium and extending
outside the heart.

http://goo.gl/0kP3od
Table 13.2 Predisposing abnormalities1, 4
Prior endocarditis
Replacement or repaired heart valve
Native heart valve disease
Unrepaired cyanotic heart disease (or residual shunt)
Congenital disease repaired with a prosthetic valve
Hypertrophic cardiomyopathy
Implantable pacemaker or defibrillator
8. TTE normal despite a clinical suspicion of endocarditis

● This requires clinical discussion and depends on the clinical likelihood of
endocarditis, how ill the patient is, and the quality of the TTE images.
● If the clinical likelihood is low or an alternative diagnosis emerges,
further echocardiography is not indicated.
● If the clinical likelihood is moderate or high, choices include immediate
TOE or a further TTE ± TOE after five to seven days2.
152
Endocarditis
Table 13.3 Indications for TOE in endocarditis
● Prosthetic valve, especially mechanical, if diagnosis not established

● Pacemaker or implantable defibrillator (pre- or intra-extraction procedure)
● Suspicion of abscess on transthoracic study or clinically (e.g. long PR interval)
● Normal or equivocal transthoracic study and moderate or high clinical
suspicion of endocarditis
9. When is TOE necessary?

● Established indications are given in Table 13.3.
● TOE is commonly necessary if there is a prosthetic valve or pacemaker
or defibrillator, because the yield of vegetations and complications is
far higher than with TTE.
● Guidelines2 suggest a low threshold for requesting TOE even if the
diagnosis has been established by TTE. The rationale is to refine the
assessment of vegetation size and exclude abscesses. In clinical
practice, TOE is not usually necessary if the results are not expected to
change management (e.g. decision for surgery already made).
10. Other imaging modalities
● Echocardiography, even with TOE, may fail to show evidence of
endocarditis in replacement valves or infected pacing systems. This
is partly because of shielding and partly because vegetations or
local complication may not occur.
● If the diagnosis remains clinically likely, PET CT should be considered.
● A CT scan may be requested before cardiac surgery to avoid the
need for invasive coronary angiography. CT may better define a
complication like a para-aortic aneurysm or occasionally show
complications not obvious on TTE and TOE.
Table 13.4 Red flag signs on the echocardiogram in endocarditis
Severe AR, especially with E deceleration time <150 ms and diastolic mitral
regurgitation
Severe MR, especially if the LV is hyperdynamic (confirming severe MR) or
hypodynamic (end-stage)
Abscess
Large (>15 mm), mobile vegetations
Rocking replacement valve
153
Endocarditis
MISTAKES TO AVOID
● Using TTE as part of a fever screen, since it then has a very low yield
and risks detecting ‘innocent bystander’ abnormalities (e.g. coincidental
valve thickening).
● Reporting innocent bystander findings as vegetations.
● Missing progressive valve regurgitation as a sign of endocarditis.
● Overusing TOE when it will not change management.
● Assuming that the absence of a vegetation refutes the diagnosis.
● Not alerting the clinician in charge of the case to positive findings and
particularly red flag signs (Table 13.4).
CHECKLIST REPORT IN ENDOCARDITIS

1. Is there a vegetation? How long and how mobile?
2. Is there a local complication or evidence of valve destruction?
3. Grade of regurgitation?
4. Presence and severity of predisposing disease (e.g. valve stenosis or
VSD).
5. LV dimensions and function (or RV for tricuspid valve endocarditis).
6. Is there a mitral E deceleration time <150 ms or diastolic MR as evidence
of high LV filling pressures?
7. Have you informed the clinician in charge of the case if there is evidence
of endocarditis, severe valve regurgitation, and/or a restrictive LV filling
pattern?
References
1. Thornhill M, Jones S, Prendergast B, et al. Quantifying infective endocarditis risk in
patients with predisposing cardiac conditions. Europ Heart J 2018;39(7):586–95.
2. Habib G, Lancellotti P, Antunes MJ, et al. 2015 ESC Guidelines for the
management of infective endocarditis. Europ Heart J 2015;36(44):3075–128.
3. Thuny F, Disalvo G, Belliard O, Avierinos JF, Pergola V, Rosenberg V, et al.
Risk of embolism and death in infective endocarditis: Prognostic value of
echocardiography: A prospective multicenter study. Circulation 2005;112(1):69–75.
4. Verheugt CL, Uiterwaal CSPM, van der Velde ET, et al. Turning 18 with congenital
heart disease: Prediction of infective endocarditis based on a very large population.
Eur Heart J 2011;32(15):1926–34.
154
The Heart Valve Clinic
14
A heart valve clinic is the best practice method of assessing new patients with
valve disease and following them during ‘watchful waiting’1, 2.
● The arrangements needed beyond a normal TTE list3 are given in Box 14.1.
● A guide to setting up a new clinic is available on the British Heart Valve
Society website3.
● The visit comprises a clinical assessment with or without TTE.
● The usual frequency of follow-up is given in Table 14.1. This can be modified
for individuals according to clinical need or the exigencies of COVID-193,
including virtual assessment as appropriate.
● The components of the TTE can be individualised. A comprehensive study is
needed on the first visit, but thereafter, the cardiologist or clinical scientist
can sometimes focus the study. For example, it is not necessary to study
the pulmonary valve repeatedly if known to be normal. Points to cover in
the history are given in Box 14.2.
Box 14.1 Organisational requirements for a

valve clinic
● Experienced staff with specialist valve competencies.
● Agree types of patients to be seen and link with staff, for example, nurse
to see cases post-intervention not requiring TTE, senior physiologist or
clinical scientist to see patients with asymptomatic moderate and severe
native valve disease, cardiologist for new and complex patients.
● Multidisciplinary meetings for difficult decisions and quality assurance.
● Referral links to: cardiac surgery and valve interventional services, other
cardiac services (e.g. heart failure and electrophysiology), and non-
cardiac services (e.g. dental, elderly care).
● Links to other tests, e.g., BNP, exercise testing, stress echo, TOE, CMR,
CT, lung function.
● Inward referral, e.g., alerts in echocardiography lab, murmur clinic4, links
to open-access or community echocardiography services.
● Agreed set of criteria for referral from nurse or physiologist to the
cardiologist (Figure 14.1).
● One-stop echocardiography.
● ‘Hotline’ for GPs and patients to report new symptoms.
● Patient information resources4, 5.
155
DOI: 10.1201/9781003242789-14
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Mitral Stenosis Mitral Regurgitation Mitral & Tricuspid Valve R
Mitral Stenosis Mitral Regurgitation
Severe: every 6 months (ETT annually) Severe: every 6 months + annual ETT – Echo at 12 months –
Moderate: every 1-2
Severe: every years
6 months (ETT annually) Moderate: every 1-2 years every 6 If repair, competent, continue clinical
– surve
Ech
Severe: months + annual ETT
Mild: every 2 years Mild: not followed nurse-led clinic.
Moderate: every 1-2 years Moderate: every 1-2 years If repa
Mild: every 2 yearsalerts: Mild: not followed nurse-
If repair impaired, continue echo surveillan
Echocardiographic Echocardiographic alerts:
 New PA hypertension or rise in PA systolic pressure towards dysfunction.
 LVSD approaching 40 mm
Echocardiographic
50 mmHg alerts: If repa
Echocardiographic
 LV EF approaching 60% alerts: Echocardiographic alerts:

 RV dysfunction
New PA hypertension or rise in PA systolic pressure
 towards
PA systolic pressure approaching 50mmHg dysfun
 LVSD approaching 40 mm  Worsening regurgitation – see MR/TR
Other50alerts:
mmHg  LV EF approaching 60%  Systolic anterior motion
RV dysfunction
 Symptoms
Other alerts: Echo
 Symptoms  PA systolic pressure approaching 50mmHg
 INR > 4.0 or < 1.5 in last 6 months Other alerts:  W
 New arrhythmia
 New atrial fibrillation  Spontaneous symptoms
Other alerts:  Patient request  Sy
Suggestion of Other alerts:
TIA or stroke  New arrhythmia
Symptoms
 Patient request  endocarditis  Patient request
 Symptoms
INR > 4.0
 Suggestion or < 1.5 in last 6
of endocarditis months  Suggestion of endocarditis Othe
 New arrhythmia
 New atrial fibrillation  Sp
Aortic Stenosis Patient
Aortic request
Regurgitation Aortic Root Dilatatio
 TIA or stroke  N
Patient
Vmax >4.0 m/s orrequest
EOA < 1.0cm2 every 6 months + consider
 Suggestion of endocarditis  Pa
annual ETT Severe: every 6 months or every 3 months at request of Marfan: annually unless dilated to > 40 mm
 Suggestion ofCalcium
V max 3.5 – 4.0 m/s + AV endocarditis
every 6 months cardiologist if LV significantly dilated (consider ETT annually) months  Su
2
V max 3.0 – 4.0 m/s or EOI 1.0 – 1.5cm every year + ETT at baseline, Moderate: every 1-2 years Non-Marfan: annually
when becomes severe, and
Aortic Stenosis
consider every year after this
Mild: not unless aortic root dilated Bicuspid: annually
if early surgery clinically
2
V max >4.0 m/s or EOA < 1.0cmappropriate Echocardiographic alerts:
every 6 months + consider Echocardiographic alerts:
V max 2.5 – 3.0 m/s every 3 yearsannual ETT  LVSD approachingSevere:50 mm every 6 months
or LVDD 70 mm or every 3 months at request
 Marfan Marfa
45 mmofor change > 3 mm in o
V max 3.5 – 4.0 m/s + AV Calcium every 6 months  LVSD change (>5mm from previous
cardiologist study) or volume
if LV significantly dilated (consider ETTvalve
 Bicuspid annually)
55 mm or changemonth
>3m
Echocardiographic Alerts 2
V max 3.0 – 4.0 m/s or EOI 1.0 – 1.5cm every year + ETT at baseline, increase since last study  Non-Marfan 55 mm or change Non-M
> 3 mm
 Any reduction in LV ejection fraction
Moderate: every 1-2 years
when becomes severe,  LVEFandapproaching 50%  Worsening AR
 EOI <0.6cm 2 Mild: not unless aortic root dilated Bicusp
 V max >5.0m/s consider every year after this
Other alerts:
if early surgery clinically Other alerts:
 Rapid progression of V max > 0.3 m/s per year
 New diastolic dysfunction (pseudonormal orappropriate
restrictive) Echocardiographic alerts:
 Spontaneous symptoms  Chest pain, dysphagia or changeEcho
in voi
 New arrhythmia
Aortic
V max 2.5root dilated
– 3.0 m/sto 45 mm (Marfan s), 55every
mm (other)
3 years  LVSD approaching 50 mm or LVDD 70 New mm arrhythmia  M
 Patient request  Patient request
Other Alerts 
 LVSD
Suggestion of endocarditis
change (>5mm from previous study) or volume  Bi
 Suggestion of endocarditis
Echocardiographic
Spontaneous symptoms Alerts increase since last study  N
Any
 New reduction in LV ejection
arrhythmia fraction  LVEF approaching 50%  W
2
EOI <0.6cm
 Patient request
 Suggestion of endocarditis
V max >5.0m/s
Other alerts: Othe
 Rapid progression of V max > 0.3 m/s per year Tricuspid
Pulmonary Stenosis  / Pulmonary
Spontaneous Regurgitation
symptoms  Ch
 New diastolic dysfunction (pseudonormal or restrictive)
 New arrhythmia Post-Endocarditis (non-op
 N
 Aortic
Severe: root dilated to 45 mm (Marfan s), 55 mm (other)
every year Severe: every 6 months
Moderate: every 1-2 years Moderate: every 1-2 Patient request
 years  Pa
Echocardiogram at 1, 3, and 6
Other
Mild: Alerts
no follow up unless indicated  Suggestion of endocarditis  Su
Echocardiographic alerts: Then according to residual pa
 Spontaneous symptoms
Echocardiographic
 New arrhythmia alerts:  Progressive RV dilatation
 New RV dilation  New RV hypokinesis
 Patient request
 Velocity > 3.5 m/s
 Suggestion of endocarditis Other alerts:
Other alerts:  Spontaneous symptoms Biscuspid Valve (no AS/
 Spontaneous symptoms
Pulmonary Stenosis
 New arrhythmia
Tricuspid / Pulmonary Regurgitation
 New arrhythmia  Suggestion of endocarditis Every 3 years
 Suggestion of endocarditis  Patient request
Severe:
Patient every
requestyear Severe: every 6 months
Moderate: every 1-2 years Moderate: every 1-2 years
Mild: no follow up unless indicated
Echocardiographic alerts:
Echocardiographic alerts:  Progressive RV dilatation
 New RV dilation  New RV hypokinesis
 Velocity > 3.5 m/s
Other alerts:
Other alerts:  Spontaneous symptoms
 Spontaneous symptoms  New arrhythmia
 New arrhythmia  Suggestion of endocarditis
 Suggestion of endocarditis  Patient request
 Patient request
Figure 14.1 Suggested echocardiographic and clinical alerts for

referral from nurse- or physiologist-led clinics to the cardiologist.
156
The Heart
Core Information
Valve Clinic
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Mitral Regurgitation Mitral & Tricuspid Valve Repair Replacement Heart Valves
Mitral & Tricuspid Valve Repair Replacement Heart Valves
y 6 months + annual ETT – Echo at 12 months –
Every valve once postoperatively if not
very 1-2 years – Echo at 12 months – If repair, competent, continue clinical surveillance annually in
lowed nurse-led clinic.
If repair, competent, continue clinical surveillance annually in Every valve once postoperatively
performed before discharge if not
nurse-led clinic. If repair impaired, continue echo surveillance perperformed
native before discharge
Mechanical valves annually only if there is any of
ographic alerts:
dysfunction. the following:
proaching 40 mm
proaching 60%
If repair impaired, continue echo surveillance per native Mechanical
 valves annually
Associated only if(see
root dilatation there is any
specific of
guide)
Echocardiographic alerts:
lic pressure approachingdysfunction.
50mmHg the following:
 LV dilatation
 Worsening regurgitation – see MR/TR sections
 More than mild paraprosthetic regurgitation
 Systolic anterior motion  Associated root dilatation (see specific guide)
ts: Echocardiographic alerts:  More than moderate TR
ms
Other alerts:
 LV dilatation
 Worsening regurgitation – see MR/TR sections
hythmia
  Spontaneous symptoms
Systolic anterior motion
 More than
New mild paraprosthetic
designs regurgitation
of biological aortic valve every
equest
on of endocarditis
 New arrhythmia  More than moderate
year after TR Trifecta)
5 years (e.g.
 Patient request
Other alerts:  Suggestion of endocarditis Established aortic biological designs every year
 Spontaneous symptoms New designsafter of biological aortic valve every
10 years
 New arrhythmia Aortic Root Dilatation year after 5 years (e.g. Trifecta)
 Patient request Biological mitral valves every year after 5 years
y 6 months or every 3 months at request of Marfan: annually unless dilated to > 40 mm, then every 6
Suggestion
f LV significantly dilated(consider of endocarditis
ETT annually) months Established aortic biological designs every year
Ross procedures every year
very 1-2 years
less aortic root dilated
Non-Marfan: annually
after 10 years
Bicuspid: annually
Aortic Root Dilatation AVR native root monitoring (previous bicuspid
ographic alerts: Echocardiographic alerts: BiologicalAV)
mitral valves every year after 5 years
uest of 50 mm or LVDD
proaching Marfan:
70 mm annually unless dilated
 Marfanto 45
> mm
40 mm, then>every
or change 6 one year
3 mm in (Dimensions on post-op echo)
ange
TT (>5mm from previous
annually) study) or volume
months  Bicuspid valve 55 mm or change > 3 mm in one year <40 mm No routine surveillance
since last study
Non-Marfan: annually  Non-Marfan 55 mm or change > 3 mm in one Ross
year procedures
40 – 45 mm every year Echo at 5 yearly then
proaching 50%  Worsening AR
Bicuspid: annually review
AVR native >45 mm monitoringAnnual
root echo bicuspid
(previous
ts: Other alerts:
eous symptoms Echocardiographic alerts:  Chest pain, dysphagia or change in voice AV) AVR with Aortic Root Replacement (Marfans/
hythmia
equest  Marfan 45 mm or change  New arrhythmia
> 3 mm in one year (Dimensions on Danlos)
Ehlers post-op echo)
 Patient request
ron
volume
of endocarditis  Bicuspid valve 55 mm orSuggestion
change >of3endocarditis
mm in one year <40 mm Per valve type aboveNo routine surveillance
 Non-Marfan 55 mm or change > 3 mm in one year 40 – 45 mm 2 yearly CMR or CT scanning
Echo (renal bloods
at 5 yearly then needed
 Worsening AR prior to scan)
review
>45 mm Echocardiographic
Annualalerts:
echo
Other alerts:  New or worsening regurgitation
cuspid / Pulmonary Regurgitation
Chest pain, dysphagia or change in voice AVR with Aortic
Post-Endocarditis (non-operated) Root –Replacement
Obstruction reduction of EOA(Marfans/
by 25%
 New arrhythmia  Change in LV or systolic function (or RV for
y 6 months
very 1-2 years  Patient request
Ehlers Danlos)
right-sided valves)
Per valve type above
Echocardiogram at 1, 3, and 6 months
 Suggestion of endocarditis Then according to residual pathology
ographic alerts: 2 yearly CMR or CT scanning (renal bloods needed
Other alerts:
ive RV dilatation
hypokinesis prior to scan)
 Exertional symptoms
 TIA
 INR > 4.0 or <2.0 during last 6 months
Biscuspid Valve (no AS/AR) Echocardiographic alerts:
ts:
eous symptoms  New arrhythmia
ation
hythmia  New or worsening regurgitation
Patient request
on of endocarditis Every 3 years  Obstruction – reduction
 Suggestion of EOA by 25%
of endocarditis
equest Post-Endocarditis (non-operated)
 Change in LV or systolic function (or RV for
Echocardiogram at 1, 3, and 6 months right-sided valves)
Then according to residual pathology
Other alerts:
 Exertional symptoms
 TIA
 INR > 4.0 or <2.0 during last 6 months
Biscuspid Valve (no AS/AR)  New arrhythmia
 Patient request
Every 3 years  Suggestion of endocarditis
157
Table 14.1 Usual frequency of TTE (clinical) follow-up*6, 7

6–12/12
Aortic regurgitation – 2 y (1 yr)
(6/12)*
Aortic stenosis Young pts 2–3 yr (2–3 yr) 1 yr (1 yr) 6/12 (6/12)*
3–5 yr (3–5 yr) (with
Primary mitral
mitral prolapse; 1–2 yrs (1yr) 6/12 (6/12)*
regurgitation
otherwise, not needed)
Mitral stenosis – 2–3 yr (2–3 yr) 1 yr (1 yr)
Dilated aorta 1 yr (1 yr) (may need MRI or CT)
Bicuspid aortic valve 3–5 yr (with no AR or AS and no aortic dilatation)
Repaired mitral valve Baseline and 1 yr, then according to any residual MR
* More frequently if close to thresholds for surgery.
Box 14.2 Points to cover in the routine

annual follow-up
Includes native and post-repair or replacement surgery.
History
● New symptoms? Change in exercise capacity? Slowing down?
● Psychological or cognitive issues, including understanding of the
condition.
● What to look out for (TIA, bleeding, fever, breathlessness).
● Management of other conditions (e.g. COPD).
● Medication check.
Examination
● New AF? Blood pressure?
● Progression of valve disease?
● Evidence of heart failure?
● Post-surgery scar problems: keloid, pain, wire protruding.
Anticoagulation
● INR control: Stable? Frequency of testing? Diet if INR variable?
Bleeding? Home testing?
158
The Heart
Core Information
Valve Clinic
● Correct INR range?

● Could a NOAC be indicated (valve disease other than mechanical
prosthesis or mitral stenosis)?
● When can warfarin stop after surgery?
● Perioperative anticoagulant bridging.
● Contraception and pregnancy planning advice.
Endocarditis advice
● Dental surveillance and antibiotic prophylaxis.
● Other advice (e.g. tattoo, piercing).
● What symptoms to look out for.
Lifestyle advice
● Smoking cessation.
● Weight loss.
● Exercise.
Table 14.2 Suggested start time for routine annual TTE in normally
functioning prosthetic valves8
Mechanical
Not needed in the absence of another indication (e.g. dilated aorta)
Biological
Onset of routine TTE Risk of early failure Valve types
TAVI
From implantation High or unknown
New designs
Mitral or tricuspid
position
Aortic position
After 5 years from implanted at age
Higher
implantation <50 or with risk
factors: diabetes,
hypertension, renal
failure
Designs with good
After 10 years from
Lower durability data (e.g.
implantation
Hancock II, Perimount)
159
References
1. Lancellotti P, Rosenhek R, Pibarot P, et al. Heart valve clinics: Organisation,
structure and experiences. Eur Heart J 2013;34(21):1597–606.
2. Chambers JB. Valve clinic: Why, who and how? Education in Heart. Heart
2019;105:1913–20.
3. BHVS link to guide to setting up a valve clinic. https://bhvs.org/bhvs-set-up-valve-
clinic/
4. BHVS link to patient information leaflets. https://bhvs.org/patient-information/
5. BHVS link to patient book. https://bhvs.org/product/patient-book/
8. Chambers J, Briffa N, Garbi M & Steed RV. Echocardiography in replacement heart
valves. Echo Research Pract 2019. doi.org/10.1530/ERP-18–0079.
160
The Aorta and
Dissection 15
The Aorta
1. Where to measure
● The diameter of the sinus, sinotubular junction, and ascending thoracic
aorta is measured in the parasternal long-axis view in the minimum
standard study (Chapter 1).
● Upper limits of normal values are given in Figure 15.1.
● Diameters at other levels (arch, descending thoracic, and abdominal aorta)
require multiple views and should be measured if there is a high likelihood
of dilatation:
● Dilatation of the root or ascending aorta on the initial views
● Significant aortic valve disease (stenosis or regurgitation)
● Bicuspid aortic valve
● Congenital and genetic syndromes associated with aortic dilatation, for

example, Marfan syndrome (Table 15.1)
● A short-axis view at the level of the sinus of Valsalva should be recorded since
this may show asymmetric dilatation of the sinuses. Measure from the apex
of the sinus to the aorta between the sinuses diametrically opposite.
● CT or MRI are indicated if the ascending aorta is not well seen on TTE and
there is a high likelihood of dilatation.
2. How to measure
● There is no published consensus on the method for measuring aortic
dimensions, but most echocardiography departments do the following
(Figure 15.2):
● 2D rather than M-mode measured perpendicular to the long-axis.
● ‘Inner edge to inner edge’ rather than ‘leading edge to leading edge’.
● Most guidelines suggest measurement of the annulus in mid-systole but

the rest of the aorta at end-diastole. In practice, the timing of the clearest
image may not be exact, and it is then reasonable to measure in systole3.
● Individual departments should agree on a standard. When comparing serial
data, it is important to assess measurements made in an equivalent manner
and at comparable points in the cardiac cycle. This may require reanalysis of
previous data using the current convention, where required.
161
DOI: 10.1201/9781003242789-15
The Aorta and Dissection
Figure 15.1 Levels and normal values for measuring the diameter of
the aorta. Upper limits are calculated from the NORRE dataset1, 2 as mean +2 standard
deviations.
162
The Aorta
Table 15.1 Causes of aortic dilatation
Atherosclerosis
Congenital/genetic causes: Bicuspid aortic valve, familial thoracic aortic
aneurysm, Marfan syndrome, Ehlers–Danlos type IV, Loeys–Dietz, Turner’s
syndrome, autosomal dominant polycystic kidney disease
Infections: Mycotic aortitis, syphilis, Staphylococcus aureus aortitis
Inflammatory causes: Takayasu arteritis, giant cell arteritis, Behcet’s arteritis,
rheumatoid arthritis, ankylosing spondylitis
Trauma: Cardiac catheterization or deceleration injury or, rarely late, after prior
dissection
Figure 15.2 Method of measuring the aortic diameter. This shows a

representative parasternal long-axis view of the aorta for measuring diameters at the
sinus of Valsalva, sinotubular junction, and ascending aorta in diastole. The annulus is
measured in systole.
163
3. Is the aorta dilated?

● Upper limits of normal using the large NORRE dataset are given in Figure 15.11, 2.
● Where the measurement is borderline:
● If the patient is at an extreme of body size, index to height (Appendix
Figures A.1 and A.2 for nomograms).
● Repeating the measurement after a delay of six or so months is an
option to confirm stability4.
● The Z score is the number of standard deviations between the observed
measurement and the mean expected using formulae derived from age,
sex, and either height or BSA5. This is useful in growing children.
● Commonly used age-independent thresholds for dilatation are:
● Ascending aorta >41 mm (>21mm/m2)
● Arch >36 mm
● Descending aorta >35 mm (>16 mm/m2)
● Abdominal aorta >30 mm
● A difference in proportion can be used to diagnose dilatation, for example,

an ascending/descending thoracic aortic diameter >1.5. The diameter of the
ascending aorta and sinotubular junction should be similar and both slightly
larger than the annulus.
● The shape may give a guide to the presence of dilatation6 and the cause:
● Marfan syndrome: typically ‘pear-shaped’ annuloaortic ectasia.
● Bicuspid valve: ascending aorta more than sinus.
● Atherosclerosis (degenerative): sinus and ascending aorta.
● A coronary sinus aneurysm can be missed if short-axis views are not

examined (Table 15.3). Use colour flow and spectral Doppler to look for
fenestrations. Coronary sinus rupture is a cause of LV volume overload.
4. Cut points for surgery

● If thresholds for surgery are close, it is usual to confirm dimensions using
orthogonal planes provided by CT or CMR.
● Despite the aortic size being related to body habitus, minimum thresholds for
considering referral for surgery are based on absolute diameters (Table 15.3)
other than for people with height-limiting syndromes. The decision for surgery
Table 15.2 Coronary sinus aneurysm
Sinus involved Site of extension

Right RV outflow tract
Left Left atrium
164
Non-coronary Right atrium
The Aorta
Table 15.3 Guideline thresholds for prophylactic intervention in

thoracic aortic aneurysm7, 8
Guideline diameter for

considering intervention
Ascending aorta or sinus of Valsalva
≥50 mm
No associated conditions Or ≥45 mm with risk factors* or at time of
aortic valve surgery or prior to pregnancy
≥55 mm
Or ≥50 mm with risk factors* or prior to
Bicuspid aortic valve
pregnancy
Or ≥45 mm if aortic valve surgery planned
≥50 mm (root)
≥45 mm (root) with risk factors* or prior
Marfan syndrome
to pregnancy
Cross-sectional root area:height ratio ≥10
Turner syndrome ≥25 mm/m2 prior to pregnancy
Loeys–Dietz syndrome Individualise
(or TGFBR1 or 2 mutation) Or ≥45 mm prior to pregnancy
Ehlers–Danlos syndrome No specific threshold
Familial thoracic aortic aneurysm No specific threshold
Aortic arch
None ≥55 mm
Descending thoracic aorta
Suitable for stent graft ≥55 mm
Needs open surgery ≥60 mm
* Risk factors: High rate of increase (≥5 mm/yr if no associated conditions, otherwise ≥3 mm/yr),
family history of dissection, uncontrolled hypertension, coarctation.
takes account of many clinical factors (e.g. coronary disease, valve disease) and
must be individualised.
5. Other features
● Is the aortic wall thickened (≥5 mm)?
● Is there atherosclerosis? This is usually best seen by TOE. However, on
good-quality TTE, atheroma may be seen in the ascending aorta and arch.
● Is there significant calcification in the aorta? Severe calcification may
affect the feasibility of coronary bypass and valve surgery.
● How much aortic regurgitation (page 94)?
165
● Has the aortic diameter changed from previous studies? A significant

rate of increase is taken as ≥5 mm/year if there are no associated conditions
but otherwise ≥3 mm/year9. Check by comparing the images that the
measurements were taken at the same level and in the same part of the cycle.
● How long is the abnormal part of the aorta? If the ascending aorta is dilated,
check whether the arch and descending thoracic aorta are normal. This may
require imaging using CT or MRI if TTE image quality is not adequate.
● Check for coarctation in all subjects, particularly if there is a bicuspid aortic
valve, unexplained aortic dilatation, or hypertension in a young adult.
● Is there mitral or tricuspid prolapse? This is relevant in patients with
Marfan or Ehlers–Danlos syndromes.
● Is there coexistent pulmonary artery dilatation (Table 10.7)? This may be
seen in Marfan syndrome and, to a lesser degree, with a bicuspid aortic valve.
● Consider measuring the descending thoracic and abdominal aorta. Use
all views. This should be done in:
● Marfan and Ehlers–Danlos syndromes
● Dissection
● Dilatation of the aortic arch
● Dilatation of the descending aorta shown on initial parasternal long-axis views
Dissection and Acute Aortic

Syndromes
Acute aortic syndrome is characterised by instantaneous-onset chest pain.
There is often an underlying predisposition (e.g. Marfan syndrome, known aortic
valve, or aortic disease). There may be suggestive clinical findings (asymmetric
pulses or blood pressure).
● The main cause is dissection, which may involve the ascending aorta (Stanford
type A) or affect the descending aorta alone (Stanford type B) (Figure 15.3).
Figure 15.3 Classification of dissections. Type A dissections involve the

166 ascending aorta. Type B dissections involve only the descending thoracic aorta.
Dissection and Acute Aortic Syndromes
● TTE has 80% sensitivity for type A and 50% for type B dissections,
potentially allowing the initial diagnosis to be made in the emergency room.
● If the initial TTE is non-diagnostic, CT or TOE are indicated to detect a dissection
or the other causes of acute aortic syndrome: intramural haematoma (20%),
penetrating atherosclerotic ulcer (5%), aortic pseudoaneurysms, and contained
or free rupture (usually after trauma or surgery).
1. Is there a dissection flap?
● An intraluminal flap is the hallmark of dissection. Blooming from
calcium deposits or reverberation artefact can sometimes cause
confusion. Factors suggesting artefact:
● Fixed relationship with a heavy reflector, for example, anterior aortic
wall.
● No movement at a phase different from the aorta.
● Only apparent in certain views.
● ‘Pseudoflap’ extends outside the aorta.
● The ‘pseudoflap’ has no effect on colour Doppler (a real flap

would divide colour onto true and false lumens, or there would be
increased velocities through entry tears).
● Echocardiography has several goals in the assessment of aortic
dissection (Table 15.4).
● Echocardiographic findings can aid the differentiation between true and
false lumens (Table 15.5).
● If there is a high clinical suspicion for aortic dissection but the TTE appears
normal:
● Check all views, including suprasternal and right intercostal.
● Consider intramural haematoma. Check for thickening of the aortic

wall (>5 mm).
● Consider CT or, occasionally, TOE according to availability.
2. What is the maximum aortic diameter?

Dissection is unlikely in an aorta of normal diameter.
3. How much aortic regurgitation?
If present, determine its severity (Chapter 8). Possible mechanisms are
given in Table 15.6, but the decision for aortic valve replacement is made at
surgery guided by TOE.
4. Is there pericardial fluid?
This suggests rupture into the pericardial sac, which is a common cause
of death in acute dissection. It may suggest the diagnosis even if a flap
cannot be imaged.
167
Table 15.4 Role of echocardiography in diagnosing aortic dissection

and assessing its complications*
Diagnostic goal Echocardiographic definition

Identify presence of a dissection flap. A flap that divides two lumens.
Define extension of the aortic Proximal and distal extent of the flap,
dissection. true and false lumens (Table 15.5).
Disruption of the flap with flow through
Localise entry tear.
the site of the tear.
Thrombosis of the false lumen. Mass inside the false lumen.
Presence, severity, and mechanism See Table 15.6 for mechanisms and
of aortic regurgitation. Chapter 8 for grading severity.
New regional wall motion abnormality
in RCA territory occasionally with
Coronary involvement. involvement of the flap with the RCA
ostium. Dissection does not cause new
anterior infarcts.
Aortic branch involvement. Flap invagination into aortic branches.
Detect pericardial and/or pleural Echo-free pericardial/pleural space
effusions. (Chapter 17).
* All features are better seen by TOE than TTE, but TTE is better at showing the distal extent of
the dissection in the abdominal aorta, LV wall motion, and assessing valve regurgitation.
Table 15.5 Differentiating between the true and false lumen10
True lumen False lumen

Size Usually false larger than true
Pulsation Systolic expansion Systolic compression
Normal systolic Reduced systolic antegrade flow or
Flow direction
antegrade flow delayed, absent, or reversed flow
Communication flow From true to false lumen in systole
Table 15.6 Mechanisms of aortic regurgitation seen in aortic dissection10
Dilatation of the sinus of Valsalva, sinotubular junction, or aortic annulus

Rupture of the annular support and a tear at the insertion point of a valve leaflet
Intramural haematoma distorting the valve
Prolapse of the intima into the LV outflow tract
Previous aortic valve disease
168
Dissection and Acute Aortic Syndromes
5. LV function
● Severe impairment of LV function on TTE can guide the decision
towards conservative management, especially in dissections involving
only the descending thoracic aorta.
● An inferior wall motion abnormality may occur as a result of ascending
aortic dissection involving the right coronary artery.
MISTAKES TO AVOID
● Making oblique measurements of the aortic diameter, particularly in

off-axis views.
● Overdiagnosis of dissection from a reverberation artefact.
● Exclusion of dissection with TTE alone. TTE is a good screening
procedure, but a negative result is not definitive and should be
supplemented with CT or TOE.
● Failing to image the ascending aorta when clinically necessary.
● Monitoring aortic size using TTE alone if image quality is not adequate.
CHECKLIST REPORT FOR THE AORTA

1. Diameter at each level. Re-measure and compare serial studies. Have any
measurements changed?
2. Check for abnormalities associated with a dilated aorta, for example,
coarctation, bicuspid aortic valve.
3. Is there associated AR? Grade?
4. If there is suspected dissection: Is there a flap? Is there abnormal LV wall
motion? Is there a pericardial effusion?
References
1. Kou S, Caballero L, Dulgheru R, et al. Echocardiographic reference ranges
for normal cardiac chamber size: Results from the NORRE study. Eur Heart J
Cardiovasc Imaging 2014;15(6):680–90.
2. Saura D, Dulgheru R, Caballero L, et al. Two-dimensional transthoracic
echocardiographic normal reference ranges for proximal aorta dimensions: Results
from the EACVI NORRE study. Eur Heart J CVI 2017;18(2):167–79.
3. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber
169

J Am Soc Echocardiogr 2015;28(1):1–39.
4. Zafar MA, Li Y, Rizzo JA, et al. Height alone, rather than body surface area,
suffices for risk estimation in ascending aortic aneurysm. J Thorac Cardiovasc
Surg 2018;155(5):1938–50.
5. Devereux RB, de Simone G, Arnett DK, et al. Normal limits in relation to age, body
size and gender of two-dimensional echocardiographic aortic root dimensions in
persons ≥15 years of age. Am J Cardiol 2012;110(8):1189–94.
6. Detaint D, Michelena HI, Nkomo VVT, et al. Aortic dilatation patterns and rates in
adults with bicuspid aortic valves. Heart 2014;100(2):126–34.
7. Isselbacher EM, Preventza O, Black JH, et al. ACC/AHA Guideline for the diagnosis
and management of aortic disease. J Am Coll Cardiol 2022;80(24):e223–e393.
8. Erbel R, Aboyans V, Boileau C, et al. 2014 ESC Guidelines on the diagnosis and
treatment of aortic diseases: Document covering acute and chronic aortic diseases
of the thoracic and abdominal aorta of the adult. Eur Heart J 2014;35(41):2873–926.
9. Evangelista A, Flachskampf FA, Erbel R, et al. Echocardiography in aortic diseases:
EAE Recommendations for clinical practice. Eur J Echocardiogr. 2010;11(8):645–58.
10. Goldstein SA, Evangelista A, Abbara S, et al. Multimodality imaging of diseases of
the thoracic aorta in adults. J Am Soc Echocardiogr 2015;28(2):119–82.
170
Adult Congenital
Heart Disease 16
● Patients with congenital disease should be cared for at specialist centres,
but they may still present as an emergency or be followed at a non-
specialist centre with uncorrected simple lesions, or after intervention1.
● Examples of echocardiographic abnormalities found in congenital
syndromes are given in Table 16.1.
● A first diagnosis of a simple, or occasionally, a more complex, lesion may still
be made in a general echocardiography laboratory. This chapter describes:
● Simple defects.
● A sequential segmental approach to an unexpected complex case.
● The appearances after intervention.
● Patients with congenital disease may be admitted acutely because of

cardiac or other disease. Advice should be sought from a regional centre,
but findings of immediate concern include:
● Poorly functioning LV or RV.
● Severe valve obstruction or regurgitation.
● Evidence of endocarditis (the risk is 20 times higher than for the general
population, except for those with isolated pulmonary stenosis or ASD)2.
● Atrial arrhythmia, because of the risk of decompensation, especially in a
Fontan circulation or with a single ventricle.
Simple Defects
1. Atrial septal defect (ASD)
● This is the most common congenital defect found in adult practice
(Table 16.2).
● Suspect an ASD if the RV is dilated. Another cause of RV dilatation is
partial anomalous pulmonary veins.
● Describe the position (Figure 16.1):
● Secundum (80%)—approximately in the centre of the septum. May
be elliptical or round and can contain multiple fenestrations.
● Primum (15%)—next to the atrioventricular valves (Table 16.3).
● Superior sinus venosus (5%)—may be difficult to image

transthoracically; CMR or TOE usually needed.
171
DOI: 10.1201/9781003242789-16
Adult Congenital Disease
Table 16.1 Echocardiographic abnormalities in congenital syndromes
Typical Less common

Dysplastic valvar pulmonary ASD, VSD, branch PS,
Noonan
stenosis, HCM tetralogy of Fallot
Bic AV, aortic stenosis,
Turner coarctation, dilated aorta with Hypoplastic left heart
risk of aortic dissection
Williams Supravalvar AS, coarctation PA and branch stenosis
LEOPARD Valvar PS, HCM
Tetralogy of Fallot, VSD, Interrupted arch, aortic
DiGeorge
truncus arteriosus arch abnormalities
Klinefelter PDA, ASD, MV prolapse
Allagile Branch PS, tetralogy of Fallot VSD, ASD, AS, coarctation
Keutel Branch PS
Persistent duct, branch PS,
Congenital rubella
coarctation
Fetal alcohol VSD, ASD
Neurofibromatosis Coarctation
Bicuspid aortic valve,
Loeys–Dietz Aortic dilatation
persistent duct, ASD
● Inferior sinus venosus (<1%).

● Coronary sinus defect (unroofed coronary sinus) is not a true ASD but
permits a left-to-right shunt from the LA via the coronary sinus to the RA.
● TTE has limited use in the assessment of anomalous pulmonary
venous connections in adults with ASD3, 4. CMR is usually necessary.
● Shunt direction? In adult practice, this will be predominantly left to right,
but if pulmonary vascular resistance is increased, flow may be bidirectional
or right to left. Optimise the colour scale settings to 25–40 cm/s. For the
detection of bidirectional shunting, use PW in addition to colour Doppler.
● Estimate the anatomical and physiological size of the defect:
● RV dilatation (RV larger than LV in an apical 4-chamber view) implies a
haemodynamically significant shunt and is an indication for closure.
● The size can be measured approximately by callipers on 2D or 3D
TTE without colour. Use 3D for an en-face view of the ASD.
● ASD defects ≥10 mm in diameter, or defects that occupy >1/3 of the
length of the total interatrial septum are usually significant and may
require closure.
172
Simple Defects
Figure 16.1 Position of ASD. 1º is a primum defect, and 2º is a secundum defect.
● The number of defects in the atrial septum should be quantified if

multiple (fenestrated ASD defect).
● The estimated shunt (Qp/Qs) (see page 242) may aid the initial
diagnosis and help determine whether closure is still indicated if
there is pulmonary hypertension.
● 3D TTE refines assessment of the size, shape, and rims of the ASD
and its proximity to the surrounding cardiac structures.
● Describe RV size and function (Chapter 4).
● Estimate pulmonary artery pressure (Chapter 5).
● The systolic pressure may be elevated because of high right-sided flow.
● If pulmonary resistance is not significantly raised, the diastolic
pressure is normal or low.
● Usually, if the PA systolic pressure is >50% systemic pressure, it is
advisable to measure PA pressures and resistance invasively before
considering closure.
● Describe LV size and function (Chapter 2). LV function may
decompensate after ASD closure.
173
Table 16.2 Checklist in ASD
Position (secundum, primum, sinus venosus)

Anatomical characteristics—size, shape, rims (including 3D TTE when available)
Aneurysmal atrial septum +/– prominent Eustachian valve or Chiari network
Number of defects
Direction of shunt (left to right, bidirectional, right to left)
Shunt size (Qp/Qs >1.5 indicates significant shunting)
RV size and function
PA pressure
LV size and function (may decompensate after ASD closure)
Other congenital or acquired defects?
Table 16.3 Features of a ‘primum’ ASD (part of the spectrum of

atrioventricular septal defect)
Defect adjacent to the atrioventricular valves

Common atrioventricular valve rather than separate tricuspid and mitral valves
Lack of offset between left- and right-sided atrioventricular valve
Left atrioventricular valve appears ‘cleft’ or trileaflet
Long LV outflow tract caused by an offset between aortic valve and ‘mitral
valve’ (normally the non-coronary aortic cusp is continuous with the base of
the anterior mitral leaflet)
May be associated with a VSD
● If there is a primum defect (Table 16.3), look for a ventricular inlet

defect and assess the atrioventricular valves.
● TOE is usually indicated before device closure (Table 16.4) and TTE
afterwards.
● It is possible to mistake flow from the superior vena cava for flow
across an ASD. Take multiple views. If there is still doubt, consider:
● Saline contrast injection, which may make the ASD obvious as a void.
● Pulsed Doppler on the right atrial side of the septum. ASD flow has
a peak in late diastole and systole. For the superior vena cava, the
peaks are earlier.
● Shunt calculation (Appendix, page 242).
● CMR or TOE, occasionally CT, or Intracardiac Echocardiography, if

available.
2. Ventricular septal defect (Table 16.5)
● In adults, a VSD may be newly diagnosed or unoperated as a child
174
(either because it was too small or there was Eisenmenger syndrome).
Simple Defects
Table 16.4 TOE assessment before secundum ASD device closure
How many defects or fenestrations?

Total septal length
Aneurysmal atrial septum?
Prominent Eustachian valve?
Diameters of defect (2D and 3D + colour flow Doppler)
Aorta (a margin is not necessary when a
septal occluder device is used)
Rim distances to:
IVC and SVC
Atrioventricular valves
Check correct drainage of pulmonary veins
Other defects, especially cleft mitral valve
LA appendage: Check no clot that could be dislodged
Presence of pericardial effusion pre-procedure
Table 16.5 Checklist in VSD
Position, size (anatomical and physiological), and direction of shunt and margins
LV size and evidence of overload
PA pressure
Other congenital or acquired defects.
Distance from aortic valve—suitable for device closure?
Aneurysmal tissue associated with septal leaflet of tricuspid valve?
● The possible late complications of a small VSD are:

● Increase in flow across the VSD because of increased LV pressures.
● Jet lesion causing hypertrophy of the RV, leading to a double-

chambered RV.
● Progressive aortic regurgitation caused by prolapse of the right or
non-coronary aortic cusp.
● Discrete subaortic stenosis.
● Endocarditis (see Chapter 13).
● Localise the site of the defect (Figure 16.2):

● Perimembranous (80%). In a parasternal short-axis view, it is
adjacent to the tricuspid valve. It could involve the RV inlet or outlet.
● Muscular (15–20%). These may be multiple.
● Doubly committed subarterial or juxta arterial (5%). This may

175
be associated with prolapse of the right or non-coronary cusp of
Figure 16.2 Position of ventricular septal defects. (a) Parasternal short-axis at

aortic level; (b) parasternal long-axis view; (c) apical 5-chamber.
the aortic valve. In a parasternal short-axis view, it is inferior to the

pulmonary valve in a 12–3 o’clock position.
● Atrioventricular septal defect (Table 16.3).
● Gerbode defect, which is a shunt between the LVOT and right
atrium. This is rare. The jet may be confused with TR.
● Shunt direction? In adult practice, this will usually be left to right, but
if the pulmonary vascular resistance is high, flow may be right to left or
bidirectional.
● Estimate the size:
● A restrictive defect (LV pressure is significantly higher than RV
pressure) is shown by a Vmax > 4.0 m/s.
● The shunt size can be estimated (Appendix, page 242) as a guide,
but the LV size and activity are usually used as an indication for
surgery in asymptomatic patients.
● In the presence of pulmonary hypertension, a left-to-right shunt >1.5
and a PA systolic pressure (or pulmonary vascular resistance) <2/3
systemic levels suggest that surgery may still be considered5.
● Assess the LV. LV volume load and systolic dilatation suggest a large
shunt and are criteria for closure.
● Assess the RV. Hypertrophy of muscular bands may be associated
176 with a perimembranous defect, causing a double-chambered RV.
Simple Defects
● Estimate pulmonary artery pressures (Chapter 5).

● Be careful to position the cursor away from VSD flow when
recording TR Vmax.
● Usually, if the PA systolic pressure is >50% systemic pressure, it is
advisable to measure PA pressures and resistance invasively before
considering closure.
MISTAKES TO AVOID
● Forgetting to look for an ASD in a volume-loaded RV. Consider other

imaging modalities (CT, CMR, TOE) to exclude sinus venosus defects and
abnormal pulmonary venous drainage if no ASD was detected on TTE.
● Failing to recognise LV volume load with a VSD as an indication for surgery.
● Mistaking VSD flow on continuous wave Doppler for tricuspid
regurgitation when calculating PA pressures.
● Missing a restrictive muscular defect towards the apex. This may be first
detected using a continuous wave probe placed at the apex.
● Mistaking SVC flow for an ASD.
3. Persistent duct (PDA) (Table 16.6)

This is a channel between the proximal descending thoracic aorta and the
origin of the left pulmonary branch. It is usually at or beyond the level of left
subclavian artery.
● Look for reversed flow in the main pulmonary artery using parasternal
short- and long-axis views and for the duct in the suprasternal view
(Figure 16.3a).
● Estimate pulmonary artery pressure. When normal, flow is continuous
throughout the cardiac cycle (Figure 16.3b). When raised, flow through
the duct may diminish, cease, or reverse during systole.
● The shunt size can be estimated (Appendix, page 242) as a guide, but
LV volume load suggests a large shunt.
Table 16.6 Checklist in persistent duct
Size and direction of flow

LV size and function (volume load in moderate or large persistent duct)
PA size (commonly dilated)
RV function (pressure load with Eisenmenger physiology) and pulmonary
artery pressure
Other congenital or acquired defects?
Coarctation or tapering of the descending aorta?
177
Figure 16.3 Persistent ductus. A large duct with normal pulmonary pressures
imaged from a parasternal short-axis view with and without colour Doppler
(a) and on continuous wave Doppler (b).
4. Coarctation (Table 16.7)

● This is a narrowing of the aorta, usually just beyond the left subclavian
artery at the site of the ductus arteriosus.
● Always check for coarctation in patients with:
● Bicuspid aortic valve
● Early-onset systemic hypertension
● Murmur
● Syndromes associated with coarctation (Turner, Williams, congenital

rubella, neurofibromatosis)
178
Simple Defects
● Appearance
● Describe the site and appearance (membrane, tunnel, S-shape)
using imaging and colour flow assessment.
● Measure aortic dimensions above and below the coarctation.
● Look for associated aortic root dilatation and bicuspid aortic valve.
● Check for LV hypertrophy and assess LV systolic and diastolic function.
● Continuous wave Doppler

● The most reliable feature on continuous wave recording is forward
flow during diastole (Figure 16.4).
● Elevated flow velocities are usually seen in systole but may
occasionally be absent or difficult to record if there is a severe or
complete coarctation with extensive collaterals.
Table 16.7 Checklist in coarctation
Site and morphology (membrane, tunnel, S-shape).

Systolic and diastolic flow.
Presence of bicuspid valve?
Diameter of aorta at all levels, ascending and descending thoracic and
abdominal.
LV adaptation, especially hypertrophy, systolic, and diastolic function.
Other congenital or acquired defects.
Figure 16.4 Coarctation. Continuous wave recording from the suprasternal notch.
179
● Intervention is not decided by the velocities or gradients across the

coarctation but by the presence of systemic hypertension and:
● A pressure difference >20 mmHg between upper and lower limbs, or
● Narrowing ≥50% relative to aortic diameter at diaphragm level on

CT or CMR.
5. Ebstein’s anomaly (Table 16.8)
● This is characterised by:
● Apical displacement of the septal/posterior leaflets of the tricuspid
valve towards the apex. The distance between the mitral annulus and
the base of the displaced leaflet indexed to BSA (displacement index)
must be >8 mm/m2.
● An elongated anterior leaflet meeting the septal leaflet.
● Division of the RV into an atrialised portion and a residual functional RV.
● Associated tricuspid regurgitation.
● The diagnosis is often suspected from a combination of:

● Right-sided dilatation in the parasternal views.
● Tricuspid regurgitation originating more apically than normal on the

apical 4-chamber view.
● The haemodynamic effect of the anomaly is related to:
● The size and function of the residual functional RV
● The degree of tricuspid regurgitation.
● The presence of other congenital defects, especially ASD, which

occurs in about 1/3 of cases.
● Surgery is indicated1, 6 for:
● Symptoms and more than moderate TR.
● Progressive right-sided dilatation or reduction in RV function.
Table 16.8 Checklist in Ebstein’s anomaly
Degree of apical displacement of the septal and posterior leaflets.

Degree of tethering of the anterior leaflet to the free wall, which affects the
ability to repair the valve.
Grade of tricuspid regurgitation?
Size of the residual functional RV—if >1/3 total, makes repair more likely.
Function of the residual RV.
Are there associated congenital defects? 1/3 have ASD, 10% have left-sided
abnormalities, for example, cor triatriatum, cleft mitral valve, parachute mitral
valve, bicuspid aortic valve. Other defects include congenitally corrected
180 transposition, and pulmonary outflow stenosis.
Table 16.9 Echo features of congenitally corrected transposition
Pulmonary artery and aorta in parallel on parasternal long-axis view

Both valves seen en face in a parasternal short-axis view
Ventricles reversed (morphological RV connected to the LA)
Dilated and hypertrophied morphological RV invariable
Left AV valve (tricuspid) regurgitation
Associated congenital defects (VSD, PS, malformations of the tricuspid valve,
complete heart block)
● Isolated closure of ASD or PFO may be performed in systemic

embolization, depending on RV function.
6. Congenitally corrected transposition of the great arteries (Table 16.9)
● Just the ventricles are transposed:
● The RA connects to a morphological LV and thence to the
pulmonary artery.
● The LA connects to a morphological RV and thence to the aorta.
● This may present in adulthood. The key is that the systemic circulation
is supplied by the morphological RV.
● The morphological RV is always dilated and hypertrophied in response
to the systemic pressure. Regurgitation of the left atrioventricular valve
(tricuspid) may worsen ventricular function and require intervention.
Sequential Segmental Approach to

Assessment of Congenital Heart
Disease
● Congenital disease should be suspected if specific abnormalities are found
(Table 16.10).
● You may have little or no background information (e.g. new diagnosis,
emergency admission, details of corrective surgery not available).
● Defining terms:
● ‘Situs’ is the term used to define whether the heart and organs are
correctly positioned. More specifically, it refers to the position of the atria
relative to the great veins.
● ‘Atrioventricular valve’ refers to the tricuspid and mitral valves. The ‘left
atrioventricular valve’ makes no assumptions that this is truly the mitral valve.
● ‘Semilunar valve’ refers to the pulmonary and aortic valves.
181
Table 16.10 Findings suspicious of congenital disease
Dilated or hypertrophied right ventricle

Lack of AV valve offsetting in the 4-chamber view (endocardial cushion defect)
Abnormal AV valves offsetting (congenitally corrected transposition)
Pulmonary artery and aorta seen in parallel or pulmonary and aortic valves
seen in the same parasternal short-axis view (congenitally corrected
transposition)
Hyperdynamic LV without aortic or mitral regurgitation
Dilated coronary sinus (usually persistent left-sided SVC)
● ‘Morphological left ventricle’ means the ventricle attached to the mitral

valve.
● ‘Systemic ventricle’ means the ventricle supplying the systemic circulation.
● ‘Discordant’ means incorrect connections, for example, left atrium
attached to morphological right ventricle or aorta leading from
morphological right ventricle.
Perform a systematic study using a sequential segmental approach

1. Define situs (are the atria correctly positioned?)
● The morphological left and right atria are distinguished by the relative
position of the inferior vena cava (IVC) and abdominal aorta.
● What is the position of the IVC and abdominal aorta in the subcostal
short-axis view? The aorta normally lies posterior and to the left of the
spine. The IVC lies anterior and to the right.
● Follow the IVC (and SVC if visible) to the right atrium using
subcostal views and check that this is on the correct side of the
heart.
● With situs anomalies or a right-sided aortic arch, the aorta may lie to
the right of the spine and the IVC to the left.
2. Is the heart correctly positioned?

● Position is defined by both:
● Position of the heart: in the left chest, midline, right chest.
● Position of the apex: apex to the left, apex to midline, apex to the
right (apex to right: dextrocardia; heart in right chest but apex to left:
dextroposition; apex in midline: mesocardiac).
● Keep the probe marker in the normal orientation to allow for correct
imaging interpretation on retrospective review.
182
3. Are the atria attached to the correct ventricles?

● This is usually appreciated best from the apical 4-chamber view.
● Atrioventricular connections can be7:
● Concordant (e.g. right atrium to morphological RV).
● Discordant (e.g. right atrium to morphological LV).
● Absent (e.g. absent right atrioventricular connection).
● Double-inlet connection (e.g. both atria open to a single dominant

ventricle).
● The morphological RV is recognised because:
● Its atrioventricular valve inserts more towards the apex and has
three leaflets (3D may be very helpful).
● There is no continuity between the atrioventricular valve and the
semilunar valve.
Other helpful features are:
● There are more trabeculations than in the morphological LV.
● There is usually a moderator band (LV occasionally has a false tendon).
● Chords attached to the septum.
4. Are the ventricles attached to the correct great arteries?

● Ventriculoarterial connections can be7:
● Concordant (e.g. morphological RV to pulmonary artery).
● Discordant (e.g. morphological RV to aorta).
● Absent (e.g. pulmonary atresia or aortic atresia).
● Double outlet—both vessels arise from the same ventricle.
● Common arterial trunk—a single vessel that gives rise to the coronary
arteries and head and neck vessels but also the pulmonary arteries.
● The pulmonary artery is recognised by its early bifurcation into left and
right branches.
● The aorta is recognised by giving off the coronary arteries and the head
and neck branch arteries.
5. Assess the size and systolic function of both ventricles (Chapters 2 and 4)
● It is usual for a morphological RV connected to the systemic circulation
to be dilated and hypertrophied.
● Make sure to assess the atrioventricular valve jet from the ventricle
connected to the pulmonary circulation.
● If there is outflow obstruction from valve stenosis or a band, the calculated
pressures will reflect ventricular and not pulmonary artery systolic pressure. 183
Figure 16.5 Atrioventricular septal defect. (a) A normal 4-chamber view

showing that the tricuspid valve is offset or closer to the apex than the mitral valve. In (b),
there is lack of offsetting, implying that there is a common AV valve. In addition, there is a
large atrial septal defect (arrow).
7. Are there any shunts at atrial or ventricular level?

● Measure size anatomically and estimate the shunt (page 242).
8. Are the cardiac valves normal in appearance?

● Assess stenosis and regurgitation as for acquired valve disease.
● If there is no offsetting of the atrioventricular valves, the diagnosis is
likely to be atrioventricular septal defect (Figure 16.5). Check for a cleft
in the left atrioventricular valve (anterior bridging leaflet).
9. Is there aortic coarctation or a persistent duct (pages 177 and 178)?
10. Are the origins of the coronary arteries correctly positioned?
● In the parasternal short-axis view, the left coronary artery is usually
seen at about 4 o’clock and the right at about 11 o’clock.
11. Is the coronary sinus dilated?
● This is usually caused by a persistent left-sided SVC (image from the
medial edge of the left supraclavicular fossa). A bubble study from the
left arm will identify this.
Post-Procedure Studies
1. Device closure for an ASD or patent foramen ovale (Table 16.11)
● Patients with residual shunts, raised PA pressure, or who have been
repaired late should be followed at a specialist centre1, 6.
2. Closure of a VSD (Table 16.12)
● After device closure, follow-up every two to four years is recommended1, 6.
184
3. Closure of a persistent ductus (Table 16.13)

● Patients with no residual shunt, a normal LV, and normal PA pressure
do not need follow-up beyond six months.
● Patients with LV dysfunction or residual PA hypertension need follow-
up at a specialist centre.
4. Coarctation (Table 16.14)
● Long-term follow-up is recommended1, 6.
5. Tetralogy of Fallot (Table 16.15)

Table 16.11 TTE Checklist after device closure of an ASD
(Figure 16.6) or PFO
Device position
Is there any residual atrial shunt? Minor flow between the disks of the device is
normal and will disappear with time.
Does the device obstruct the IVC or SVC or the pulmonary veins?
Is the device close to the mitral valve, and is there new or worse mitral
regurgitation? Is there worse tricuspid regurgitation?
RV size and function (size may start to decrease soon after closure).
Pericardial effusion (as a sign of perforation during the procedure or early erosion).
PA pressure.
LV size and systolic function.
Figure 16.6 ASD closed using an Amplatzer device.

185
Table 16.12 TTE after closure of a VSD
Is there a residual shunt?

LV size and function.
Aortic regurgitation if closure of perimembranous VSD.
Pulmonary artery pressure.
Tricuspid regurgitation (septal leaflet most commonly damaged).
Table 16.13 TTE after closure of a persistent duct
Is there a residual shunt?

LV size and function.
Pulmonary artery pressure.
Associated lesions.
Table 16.14 TTE after coarctation repair or stenting
Is there a residual, new, or in-stent stenosis on imaging?

On continuous wave Doppler, an elevated systolic velocity is normal, but there
should be no diastolic forward flow.
Assess the aorta beyond the repair, looking for aneurysmal dilatation.*
Assess the ascending aorta (which may be dilated) and aortic valve (may be
bicuspid).
Assess LV size, function, and hypertrophy.
* Better performed with CMR.
Table 16.15 TTE after repair of tetralogy of Fallot7
RV size and function, including RV pressure.

Assess the RV outflow tract for muscular hypertrophy and/or aneurysm.
TR degree and mechanism:
● Patch disrupting septal-anterior commissure
● Annular dilatation
● Organic abnormality of the valve
● Pacing electrode
RA size.
LV size (is there evidence of systolic dysfunction?).
Is the VSD patch competent, or is there a residual VSD?
Assess pulmonary valve for stenosis and regurgitation (especially if trans-
annular PV patch was used).
186
Assess branch pulmonary artery flow on colour and pulsed Doppler if possible.
There may be a residual branch stenosis.
Size of aortic root and ascending aorta and ‘sidedness’ of aortic arch.
Degree of aortic regurgitation secondary to aortic dilatation.
Origin of coronary arteries.
Presence of systemic-to-pulmonary collateral vessels.
Presence of associated anomalies.
● The main diagnostic morphological features are:

(a) Non-restrictive VSD with (b) overriding aorta
(c) RV outflow obstruction (valvar or infundibular or both) with (d) RV
hypertrophy
● The possible complications shown on TTE after repair are given in
Table 16.15.
References
1. Baumgartner H, De Backer J, Babu-Narayan SV, et al. ESC 2020 Guidelines for the
management of adult congenital heart disease. Europ Heart J 2021;42(6):563–645.
2. Verheugt CL, Uiterwaal CSPM, van der Velde ET, et al. Turning 18 with congenital
heart disease: Prediction of infective endocarditis based on a very large population.
Eur Heart J 2011;32(15):1926–34.
3. Valente AM, Cook S, Festa P, et al. Multimodality imaging guidelines for patients
with repaired tetralogy of Fallot. J Am Soc Echo 2014;27(2):111–41.
4. Silvestry FE, Cohen MS, Laurie B. Armsby, et al. Guidelines for the
echocardiographic assessment of atrial septal defect and patent foramen
ovale: From the American Society of Echocardiography and Society for Cardiac
Angiography and Interventions. J Am Soc Echo 2015;28(8):910–58.
5. Naqvi N, McCarthy KP & Ho SY. Anatomy of the atrial septum and interatrial
communications. J Thoracic Dis 2018;10(Suppl 24):S2837–47.
6. Stout KK, Daniels CJ, Aboulhosn JA, Aboulhosn JA, et al. AHA/ACC 2018 Guideline
for the management of adults with congenital heart disease: A report of the
American College of Cardiology/American Heart Association Task Force on Clinical
Practice Guidelines. J Am Coll Cardiol 2019;73(12):e81–192.
7. Bellsham-Revell H & Navroz Masani N. Educational series in congenital heart
disease: The sequential segmental approach to assessment. Echo Research and
Practice 2019;6(1):R1–8.
187
Pericardial Disease
17
● Echocardiography is indicated for:
● Pericardial effusion (Table 17.1).
● Pericardial constriction.
● Pericarditis (although this is diagnosed clinically, not on

echocardiography).
● It may be used to guide percutaneous pericardiocentesis.
Pericardial Effusion
1. Pericardial or pleural?
● The differentiation is usually obvious. The key is where the effusion ends
in relation to the descending thoracic aorta (Table 17.2 and Figure 17.1).
● The differentiation may be hard after cardiac surgery with a localised
posterior effusion, particularly around the right atrium.
● Pleural and pericardial effusions may coexist.
2. Size, distribution and characteristics

● Pericardial fluid is always present, so a trivial effusion (Table 17.3) can
be seen even in normal people, especially around the right atrium.
● Size (Table 17.3) is graded semi-quantitatively, but whether there is
evidence of tamponade (Table 17.4) is more important.
● Small effusions may cause tamponade if acute (e.g. after
instrumentation of the heart—pacing, ablation, coronary dissection) or
if there is LV hypertrophy.
● Is the effusion generalised or localised, for example, posterior, apical,
or anterior?
● Is there enough fluid in the subcostal view for safe pericardiocentesis
(usually >20 mm)?
● What is the consistency of the fluid?
● Echolucent.
● Localised strands which are common if the protein content is high,

particularly in TB.
189
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Pericardial Disease
Table 17.1 Cause of pericardial effusion1
Common
Viral (Coxsackievirus, echovirus, HIV), TB,
Infection
Coxiella
Cancer Angiosarcoma, metastases
Metabolic Low albumin, hypothyroidism, renal failure
Reactive Chest infections, especially pneumococcal
SLE, rheumatoid arthritis, Sjögren’s
Systemic inflammatory diseases
syndrome, systemic sclerosis
Heart failure
Idiopathic
Uncommon
Post-radiation
Autoimmune pericarditis, typically two to
Post-pericardiotomy (Dressler)
six weeks after cardiac surgery, myocardial
syndrome
infarction, or trauma
Direct injury Blunt or sharp chest injury, ablation
Drugs Isoniazid, minoxidil, hydralazine, phenytoin
Aortic dissection
Table 17.2 Differential diagnosis of pericardial and pleural effusions
Pericardial Pleural
Ends anterior to the descending aorta Ends posterior to the descending aorta
Almost never overlaps left atrium May overlap left atrium
Fluid between heart and diaphragm No fluid between heart and diaphragm
on subcostal view on subcostal view
Tamponade may be present No signs of tamponade
Rarely >40 mm in depth May often be >40 mm in depth
If large, swinging of the heart Heart not mobile
Table 17.3 Grading pericardial effusions by size
Parietal and visceral pericardium only

Trivial
separated in systole
Small <10 mm at end-diastole
Moderate 10–20 mm at end-diastole
190 Large >20 mm at end-diastole

Figure 17.1 Pericardial vs pleural fluid. A pericardial effusion ends anterior to

the descending thoracic aorta; a pleural effusion ends posterior to the aorta. A pleural
effusion may extend over the left atrium, a pericardial effusion never does to any
significant degree.
● Echodense—haematomas occur after cardiac surgery, chest trauma

and aortic dissection.
● Are there reasons that drainage with a needle might not be feasible?
● Too small.
● Position (e.g. too posterior to reach percutaneously).
● Loculated.
● Echodense.
3. Is tamponade present?
● Ultimately, this is a clinical diagnosis, but it is aided by the TTE (Table 17.4)2.
● In mechanical ventilation, the signs will be modified. Respiratory
variation of echocardiographic measures is minimal or reversed with
positive-pressure ventilation.
191
Pericardial Disease
Table 17.4 Echocardiographic evidence of tamponade
Key signs
Fall in transmitral E wave (and aortic) velocity during inspiration >25%
(Figure 17.2)3
Prolonged and widespread diastolic RV collapse
Dilated IVC (>20 mm) with inspiratory collapse <50% (Figure 17.3)
Other signs
Decrease in LV size on inspiration
Increase in trans-tricuspid velocities on inspiration >40%
Note: NB collapse of the right atrium and right ventricular outflow tract occurs before RV free
wall collapse and is a nonspecific sign.
Figure 17.2 Increased paradox. This signal was recorded in a patient with
tamponade. The subaortic peak velocity falls by >25% during inspiration.
● Tamponade may be caused by a regional pericardial effusion,

particularly after cardiac surgery.
● The decision to drain an effusion may be based on:
● Haemodynamic deterioration without another obvious cause
● Presence of sufficient fluid on the TTE to drain safely
192
Figure 17.3 Engorged inferior vena cava. There is little change in diameter
throughout the respiratory cycle or after a sniff.
● After cardiac surgery, there may be tamponade because of haematoma

compressing the atria. TTE can be challenging, and diagnosis may
require TOE.
● If there is tamponade despite a small effusion, especially if chronic
(>3 months), consider effusive-constrictive pericarditis. This requires
investigation as for pericardial constriction.
4. Differential diagnoses
● The main differential diagnoses of pericardial fluid are:
● Pleural fluid.
● Fat, which most commonly occurs anteriorly or between the RV

and diaphragm. It often has a brighter signal than the myocardium
and fascial planes sliding across each other during the cardiac cycle.
There may also be a little echolucent fluid.
● Pericardial cyst (see page 210).
● Increased left-sided respiratory variation may also be caused by:

● Asthma.
● Right heart failure.
● Circulatory underfilling.
193
Pericardial Disease
5. LV function
● Is LV function poor?
● Pericardial effusions can complicate myocarditis.
● Rapid total pericardiocentesis may cause circulatory collapse.
● Wall motion abnormalities may complicate tamponade even with

normal coronary anatomy.
6. Pericardiocentesis
TTE can help with:
● Checking if there is sufficient fluid for safe pericardiocentesis.
● Measuring the depth of the effusion below the skin.
● Confirming the needle tip is in the fluid (reinject a little fluid to create
bubble contrast).
● Confirming resolution of effusion.
Pericardial Constriction
● This needs to be considered in patients with clinical evidence of heart
failure but normal LV ejection fraction.
● Causes of pericardial constriction are tuberculosis, radiation, post-viral,
rheumatoid arthritis, idiopathic, and rarely, after cardiac surgery.
● The key to the physiology is that the ventricles are normal but surrounded
by a rigid ‘box’, causing:
● Increased ventricular interdependence (i.e. as the RV gets bigger on
inspiration, the LV must get smaller).
● On inspiration, the fall in intrathoracic pressure is not transmitted inside
the pericardium, so pulmonary venous flow and, therefore, left-sided
velocities drop.
● Visual assessment in suspected pericardial constriction is given in Table 17.5
and Doppler assessment in Table 17.6.
Table 17.5 Visual assessment in pericardial constriction
Septal bounce (Figure 17.4). Often the first clue. Caused by an early diastolic
pressure rise in the RV4.
Inspiratory septal shift. The interventricular septum deviates towards the LV
during inspiration.
Pericardial thickening. Not reliably detected or excluded on TTE, but extensive
thickening may still alert to the diagnosis. Thickness is better measured on CT.
Atrial size. Mild or moderate biatrial enlargement.
194 IVC. Dilated with reduced contraction on inspiration.
Pericardial Constriction
Table 17.6 Doppler assessment in pericardial constriction
Key signs
LV filling pattern. Characteristically restrictive (E/A ratio >2 and E deceleration
time <150 ms) (Figure 17.5a).
Respiratory variability (in spontaneous respiration). Record the transmitral E
wave or the peak transaortic velocities. Subtract the lowest (inspiratory) from
the highest (expiratory) velocity and express as a percentage of the highest
velocity. This is characteristically increased by >25% (Figure 17.5a).
Tissue Doppler. Normal S’ and normal or raised E’ velocities are characteristic.
The peak E’ velocity may be higher at the septal than the lateral annulus (which
may become tethered to the pericardium).
Estimated PA pressure. This is moderately increased (usually to <50 mmHg).
Other signs
Hepatic vein flow. Flow reversal is maximal on the first beat after expiration.
Pulmonary vein flow. A systolic-to-diastolic (S/D) velocity ratio >0.65 on
inspiration and a D velocity fall by >40% on inspiration are characteristic.
Figure 17.4 Septal bounce. This is an M-mode recording showing inward motion
of the septum in systole but also diastole (the bounce).

http://goo.gl/Iw5YNB

http://goo.gl/Qo7JIz 195
Pericardial Disease
Figure 17.5 Differentiating pericardial constriction and constrictive

cardiomyopathy. (a) This was recorded in a patient with pericardial constriction.
The transmitral E deceleration time was 137 ms, and the peak E velocity fell by around
50% on inspiration. (b) This was recorded in a patient with amyloid secondary to
multiple myeloma. The E wave varies little throughout the respiratory cycle.
1. Pericardial constriction or restrictive cardiomyopathy?

● The distinction is important because the treatments are different.
Constriction is potentially curable with surgery.
● Many of the causes of pericardial constriction also affect the
myocardium, so constriction and restrictive cardiomyopathy may
coexist, and it is necessary to determine which is dominant.
● The key is that the ventricles are normal in constrictive pericarditis but
abnormal in restrictive cardiomyopathy (Table 17.7).
2. Other imaging modalities: 5–7
● CMR or CT are needed if a definitive diagnosis cannot be made on
TTE. Where uncertainty remains, a left and right heart catheter study is
indicated. Uncertainty is particularly likely if the RR interval is variable
(e.g. AF or atrial ectopics).
Acute Pericarditis
● Acute pericarditis is a clinical diagnosis8, but a basic TTE is usually
recommended7 to:
● Detect pericardial effusion and tamponade.
● Exclude regional or global LV dysfunction (myocarditis or acute coronary

syndrome).
● Occasionally, the TTE may provide diagnostic clues, for example, valve
involvement in SLE.
196
Acute Pericarditis
Table 17.7 Differentiating pericardial constriction and restrictive

cardiomyopathy
Common to both
Normal LV size and usually normal ejection fraction
Restrictive transmitral physiology (E/A >2 and E dec <150 ms) (Figure 17.5)
Dilated unreactive IVC (Figure 17.3)
Points differentiating constriction and restrictive
cardiomyopathy
Restrictive
Constriction
cardiomyopathy
LV ± RV hypertrophy or
Myocardial appearance Normal
unusual echotexture
Thickened pericardium
Pericardial thickness Normal
or hyperechogenicity
Fall in transmitral E velocity
or aortic velocity on >25% <15%
inspiration (Figure 17.5)3,5
Tissue Doppler septal E’5 ≥8 cm/s <6 cm/s
LA and RA dilatation Mild or moderate Severe
Septal bounce (Figure 17.4) Present Absent
Septal shift toward LV in
Present Absent
inspiration
Hepatic flow reversal Expiration Inspiration
GLS Normal Reduced
PA systolic pressure <50 mmHg May be >50 mmHg
Table 17.8 Other imaging modalities
Cardiac magnetic resonance

Less accurate than CT for pericardial thickness but can identify pericardial
inflammation
Better tissue characterisation than echocardiography for pericardial masses
and for contents of the effusion (blood vs fluid)
CT
Measures pericardial thickness (abnormal if >4 mm), although a normal
thickness does not exclude constriction
Detects calcification and masses
Evaluates the rest of the chest for evidence of malignancy and other lung pathology 197
Pericardial Disease
MISTAKES TO AVOID
● Failing to image subcostally to check that there is sufficient depth of

pericardial effusion to allow safe pericardiocentesis.
● Forgetting to check for a septal ‘bounce’, dilated IVC, and short
transmitral E deceleration time in a patient with clinical heart failure but
normal LV size and ejection fraction.
● Diagnosing epicardial fat as a pericardial effusion.
CHECKLIST REPORT IN PERICARDIAL DISEASE

1. Pericardial effusion.
a. Size and site.
b. Consistency.
c. Is there fluid in the subcostal approach?
2. RV collapse.
3. LV size and function, including septal ‘bounce’, transmitral filling pattern,
and respiratory variability.
4. Tissue Doppler at the septal mitral annulus.
5. PA pressure.
6. IVC size and response to inspiration.
7. Atrial size.
References
1. Imazio M & Adler Y. Management of pericardial effusion. Eur Heart J.
2013;34(16):1186–97.
2. Fowler N. Cardiac tamponade—A clinical or an echocardiographic diagnosis?
Circulation 1993;87(5):1738–41.
3. Goldstein JA. Cardiac tamponade, constrictive pericarditis, and restrictive
cardiomyopathy. Curr Probl Cardiol 2004;29(9):503–67.
4. Coylewright M, Welch TD & Nishimura RA. Mechanism of septal bounce
in constrictive pericarditis: A simultaneous cardiac catheterisation and
echocardiographic study. Heart 2013;99(18):1376.
5. Habib G, Bucciarelli-Ducci C, Caforio ALP, et al. Multimodality imaging in restrictive
cardiomyopathies: An EACVI expert consensus document in collaboration with the
‘Working Group on Myocardial and Pericardial Diseases’ of the European Society
198
Acute Pericarditis
of Cardiology endorsed by the Indian Academy of Echocardiography. Eur Heart J

CVI 2017;18(10):1090–1.
6. Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography
Clinical Recommendations for Multimodality Cardiovascular Imaging of Patients
with Pericardial Disease: Endorsed by the Society for Cardiovascular Magnetic
Resonance and Society of Cardiovascular Computed Tomography. J Am Soc
Echocardiogr 2013;26(9):965–1012.
7. Cosyns B, Plein S, Nihoyanopoulos P, et al. European Association of Cardiovascular
Imaging (EACVI) position paper: Multimodality imaging in pericardial disease. Eur
Heart J Cardiovasc Imaging 2015;16(1):12–31.
8. Chiabrando JG, Bonaventura A, Vecchié A, et al. Management of acute
and recurrent pericarditis: JACC State-of-the-art review. J Am Coll Cardiol
2020;75(1):76–92.
199
Masses
18
● The aim is to differentiate between thrombus, vegetation, tumour, and
normal findings.
● Secondary tumours are at least 20 times more common than primary
tumours of the heart1, 2.
● The most common benign primary tumours are atrial myxoma (70%),
papillary fibroelastoma (10%), fibroma, and mainly in infants and children,
rhabdomyoma1, 2.
● The most common primary malignancies are the sarcomas, especially
angiosarcomas, which usually arise in the RA. Lymphomas are less
common.
Describe the Basic Characteristics of the Mass (Table 18.1)

The site of attachment and shape may be more easily appreciated using 3D echo.
Table 18.1 Characteristics of the mass
Site of attachment
Size, shape
Density (low intensity, dense, mixed)
Mobility (fixed, mobile, free)
Evidence of invasiveness, including pericardial involvement
Mass Attached to a Valve

● This can be solid or thin (Table 18.2).
● It is not possible to differentiate reliably a vegetation from a myxomatous
mitral valve with ruptured chords. The TTE has to be interpreted within the
clinical context.
● Echogenicity related to a valve annulus:
● Mitral annular calcification: occasionally large and mistaken for an
abnormal mass.
● Fat in the tricuspid annulus: this is normal.
201
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Masses
Figure 18.1 Fibroelastoma. An apical 4-chamber view showing a small

pedunculated mass of mixed echogenicity is attached to the posterior leaflet of the
mitral valve.

http://goo.gl/X6G9Lf
Left or Right Atrial Mass

● Many apparent masses are normal (Table 18.3). Pathological masses are
listed in Table 18.4.
● For an RA mass:
● An associated pericardial effusion suggests an angiosarcoma (Figure 18.2).
● Check the IVC for tumour extension from a primary tumour in the
kidneys, liver, uterus, or ovaries.
● Thrombus from a DVT may also appear in the IVC. Typically, a tumour will
cause IVC dilatation (Figure 18.3), while a thrombus will not.
● For an LA mass:
● If immobile and attached to the wall, check the pulmonary veins and look
for a tumour mass outside the heart.
● Thrombus is unlikely without a substrate (dilated LA, mitral stenosis,
atrial fibrillation).
202
Left or Right Atrial Mass
Table 18.2 Masses attached to valves
Native valves
Solid mass
Infective: Occurs on any valve, usually moving independently
Vegetation
of the valve and associated with valve destruction.
Libman–Sacks in SLE or isolated antiphospholipid syndrome:
Usually broad-based, <10 mm in diameter, attached to aortic
or mitral valves and associated with generalised thickening.
May be calcified when chronic.
Malignant: Indistinguishable from infective vegetations, but
valve destruction less common.
Other: rheumatoid arthritis.
Small (usually <10 mm), with a short stalk, rounded with
Fibroelastoma fronds, often with mixed echogenicity. Attached to the aortic
> mitral valve > pulmonary or tricuspid valves (Figure 18.1).
Usually generalised mild ‘fleshiness’ associated with
Myxomatous
prolapse but may be florid in Barlow’s syndrome. Mainly
tissue
affects the mitral valve, less commonly the tricuspid valve.
The edges of atherosclerotic degeneration may be ‘furry’.
Calcific deposit
Atheroma may occasionally be pedunculated
Thin mass
Single This produces a whip-like appearance most often seen in the
ruptured chord LA and moving between LA and LV.
Also called Lambl’s excrescences. These are attached to the
Fibrin strand
closure line of the aortic valve.
Replacement valves
Solid mass
This is more common in mechanical valves and requires TOE
Thrombus
for full delineation.
These may be attached to the cusps of a biological valve or
Vegetation
the sewing ring of any design.
In old valves, disruption of the fabric covering the sewing
Other ring or endothelial tags can rarely cause noninfected masses
attached to the sewing ring.
Thin mass
These may be obvious around the sewing ring on TOE,
Stitch
occasionally on TTE.
These are seen mainly in mechanical valves and consist of
Fibrin strand
10–20 mm strands attached to the leaflets and wriggling.
203
Masses
Table 18.3 Non-pathological atrial ‘masses’
Attached at the opening of the IVC, this can be

Eustachian valve fixed or mobile, thin or thick, and up to 20 mm
in length.
Attached between the Eustachian valve and the
Chiari membrane or network
atrial septum. Thin and may move gently.
May look like a mass if the RA is scanned
Crista terminalis
obliquely in the 4-chamber view.
The apex may initially be seen as an apparent
Atrial septal aneurysm mass in the LA in parasternal long-axis views,
although the diagnosis is obvious in other views.
This is deposited in a dumb-bell shape at either
Atrial septal fat
end of the septum and sparing the centre.
Sections of the electrode will lie outside the
Pacemaker electrode plane of the ultrasound so requires multiple
views.
Usually, the ‘railway track’ appearance of the
Long central line
cannula is obvious.
Table 18.4 Pathological atrial masses
Location Characteristics
Fixed band across LA in cor triatriatum.
Mobile mass in RA: Thrombus or tumour entering via IVC or
Intracavitary thrombus wedged in PFO.
Free-floating ball thrombus in the LA (associated AF and
mitral stenosis).
Myxoma: Attached at the centre on the left much more
commonly than the right. Mixed echogenicity. When large,
may prolapse through the mitral valve in diastole or prevent
Septum full closure in systole.
Thrombus: A vein cast may become embedded in a PFO and
may be seen in both RA and LA.
95% of LA thrombus starts here and may be seen in a 2-chamber
LA appendage
apical view on TTE but usually requires TOE for detection.
Thrombus: Commonly around the LA appendage or at the
most basal part of the LA between the pulmonary veins or of
LA or RA Wall the RA between the IVC and SVC in a 4-chamber view.
Tumour: A sessile immobile mass attached to the free wall of
the RA is often an angiosarcoma (Figure 18.2).
204
Left or Right Ventricular Mass
Figure 18.2 Angiosarcoma. An off-axis 4-chamber view showing a mass attached

to the free wall of the right atrium. This is the most common malignant cardiac tumour
and may often be associated with a pericardial effusion.

http://goo.gl/5YB8z6

● See Table 18.5.
● An associated pericardial effusion suggests that the mass is malignant.
● LV thrombus is rare without an underlying structural abnormality (e.g. dilated LV,
hypertrabeculation, regional wall motion abnormality) but may occur in a normal
LV if there is thrombophilia (e.g. primary biliary cirrhosis, Behçet’s disease).
● RV thrombus may complicate deep vein thrombosis or occur as a
complication of an RV cardiomyopathy.
● If the presence of a thrombus is uncertain, use different views and consider
transpulmonary contrast.
● Could the mass be normal (Table 18.7)?
205
Masses
Table 18.5 Causes of LV or RV masses
Intracavitary
Thrombus Table 18.6
Causes thrombus at the apex of RV and LV (Figure 7.2,
Endomyocardial
page 73) which may extend to the base of the heart and
fibrosis
involve the AV valves.
Occurs predominantly in non-compaction (Figure 7.3,
Hypertrabeculation
page 74).
Fibroelastomas and myxomas may occasionally occur in
Benign tumours
the LV or RV.
Solely or predominantly intramyocardial
Occur anywhere in LV or RV wall and may then extend
inwards or outwards. Most commonly from breast,
Metastasis
lung, stomach, and colonic carcinoma. Also occur with
melanoma, germ cell carcinoma, thymoma.
Lymphomas or sarcomas extend outwards and may be
Primary malignancy
associated with a pericardial effusion.
Usually in the septum or LV free wall. May be up to 100 mm
Fibroma
in diameter. Characteristic central calcification (Figure 18.4).
Multiple bright intramural masses often extending into
Rhabdomyoma
the cavity. Usually resolve in childhood.
Myocardial nodules can occur in sarcoid, TB, or
Systemic disease
rheumatoid arthritis.
Cystic, semisolid, or solid. Single or multiple. Also seen
Hydatid disease3
in the pericardium.
Table 18.6 Features of thrombus
Underlying wall motion abnormality

Cleavage plane between thrombus and LV wall
Higher density than myocardium
Present in more than one view
Causes a void on colour mapping or contrast echocardiography
206
Figure 18.3 Tumour in the inferior vena cava. Subcostal view showing a large
tumour mass stretching the inferior vena cava and entering the right atrium.

http://goo.gl/lyfK0e
Figure 18.4 Fibroma. Parasternal short-axis view showing a large intramyocardial mass
which is distinct from the surrounding myocardium.

http://goo.gl/iW0932
207
Masses
Table 18.7 Normal LV or RV ‘masses’
Trabeculation is a feature of the RV, and minor trabeculation

Trabeculation is also common in the LV and increases with athletic training,
especially in Afro-Caribbean people.
Prominent
Normal feature of the RV.
moderator band
LV false tendon Runs parallel with the septal endocardium.
Prominent An occasional cause of confusion resolved by following back the
papillary muscle apparent mass to show continuity with LV wall and chords.
Aberrant papillary Ectopic extra papillary tissue is sometimes seen (e.g. in the
muscles LVOT).
Near-field effects Not seen in every view. Resolves with changes in focus and
at the apex gain. Occasionally need contrast to resolve.
Pericardial Mass
● Apparent pericardial masses associated with a pericardial effusion are often
proteinaceous deposits over the pericardium rather than true masses. These
are especially common with TB or bleeding (e.g. pericarditis on heparin).
● True masses caused by tumour deposits within the pericardium may cause:
● Generalised thickening of the pericardium (metastatic disease).
● Localised tumour mass (primary tumours or less commonly, solitary metastasis).
● An associated pericardial effusion.
● Look for:
● Invasion of the underlying myocardium.
● Constrictive physiology.
Extrinsic Mass
Table 18.8 Masses outside the heart
Diagnosis Note
Abnormal findings
Mediastinal tumour Commonly lymphoma (Figure 18.5).
Lymph node Most common adjacent to the pulmonary artery.
Haematoma Tissue characterisation on CT and CMR.
Pericardial cyst Table 18.9.
208
Extrinsic Mass
Diagnosis Note
Rare (far more common in LV or RV).
May be single or multiloculated or solid.
Pericardial
Suspect according to background disease
hydatid3
prevalence.
Needs CT or MRI.
Not usually a diagnostic problem with an associated
Pseudoaneurysm
myocardial infarct.
Polycystic disease affecting the kidney or individual
Subdiaphragmatic
cysts of the liver should be reported as incidental
masses
findings.
Normal findings confused with masses
Descending thoracic aorta Continuity of structure in all views. Contains blood flow.
Mixed echogenicity. Can be enhanced by the patient
Hiatus hernia
drinking a fizzy drink.
May be especially prominent in a patient with pectus
Back bone
excavatum.
Seen most commonly anteriorly in a parasternal
Pericardial fat long-axis view and between the diaphragm and RV
subcostally.
Figure 18.5 Lymphoma. This is a parasternal short-axis view showing a mediastinal

mass (a) that extends down the anterior aorta in a long-axis view (b).

http://goo.gl/vt0xV4
209
Masses
Table 18.9 Differentiating a pericardial cyst from a localised effusion
Pericardial cyst Localised effusion

May be after cardiac
Circumstance Incidental finding
surgery or pericarditis
Commonly right (50–70%)
Position > left costophrenic angle Cardiac border
(30–40%)
Well-circumscribed and More diffuse and
Shape
ovoid crescentic
Effect of respiration Shape may change Fixed
Mass in the Great Vessels

1. Haemodynamic effect
● Assess the presence and degree of valve regurgitation or obstruction
to inflow, depending on the site of the mass.
2. Other features
Diagnosis of the mass may also be aided by:
● Presence of a pericardial effusion, suggesting malignancy.
● Substrate for thrombus formation: atrial fibrillation; enlarged LA; mitral
stenosis; dilated hypokinetic LV; regional wall motion abnormality.
Table 18.10 Masses in the great arteries
Pulmonary artery
Associated with deep vein thrombosis and
Thrombus
pulmonary embolism
Sarcoma Rare
Myxoma Very rare
Aortic
Serpiginous motion of a flap in a dilated aorta is
Dissection usually obvious, but a localised dissection after
instrumentation may produce a small focal thickening.
Pedunculated atheroma Most commonly seen on TOE.
Rare complication of cardiac surgery. Classical
Fungal aortitis appearance of large vegetation attached to the aortic
wall at the site of the aortotomy.
210
Mass in the Great Vessels
● Medical history, for example, cancer, pulmonary embolism, evidence

of infective endocarditis.
3. Other imaging modalities (Table 18.11)
If characterisation is difficult, consider other techniques.
Table 18.11 Other techniques for characterising cardiac masses4
Technique Value
Confirms presence and site
Contrast Echo
Demonstrates vascularity
TOE Improves characterisation of all atrial masses
Improves tissue characterisation
May differentiate thrombus from myxoma
CMR
Can confirm presence of cardiac lipomas
Perfusion (vascularity of masses)
Demonstrates metabolic activity in malignancy and
PET
involvement of other organs
Mediastinal extent and involvement of other organs;
CT
demonstrates local invasion
MISTAKES TO AVOID
● Overdiagnosing normal variants as abnormal.

● Failing to check the IVC if there is a right atrial mass.
● Ignoring the clinical background when suggesting the nature of a mass,
for example, the presence of atrial fibrillation, especially with atrial or LV
dilatation, makes thrombus more likely than tumour.
CHECKLIST REPORT FOR A MASS

1. Location and site of attachment.
2. Size, density, and mobility.
3. Involvement of adjacent veins and evidence of invasion.
4. Haemodynamic effect.
5. Is there a pericardial effusion?
6. Is there a substrate for thrombus?
211
Masses
References
1. Lam KY, Dickens P & Chan AC. Tumors of the heart. A 20-year experience with a
review of 12,485 consecutive autopsies. Arch Pathol Lab Med 1993;117(10):1027–31.
2. Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: Diagnosis and
management. Lancet Oncol 2005;6(4):219–28.
3. Dursun M, Terzibasioglu E, Yilmaz R, et al. Pictorial essay. Cardiac hydatid disease:
CT and MRI findings. Am J Roentgenology 2008;190:226–32.
4. Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography
Clinical Recommendations for Multimodality Cardiovascular Imaging of Patients
with Pericardial Disease: Endorsed by the Society for Cardiovascular Magnetic
Resonance and Society of Cardiovascular Computed Tomography. J Am Soc
Echocardiogr 2013;26(9):965–1012.
212
Echocardiography
in Acute and Critical
Care Medicine
19
The Critically Ill Patient
● A cardiac ultrasound scan is used by the resuscitation team to detect:
● Reversible causes (e.g. tamponade, pulmonary embolism, severe
hypovolaemia).
● The presence of myocardial contraction during cardiac arrest (10–35% of
patients in asystole), which is associated with higher survival rates.
● Pathology suggesting that prolonged resuscitation is likely to be futile
(e.g. cardiac rupture).
● If time allows in critically ill medical patients, a basic echocardiogram (which
includes colour) extends the diagnostic range to include shunts and valve
disease (Table 19.1).
● All basic scans can be extended according to the clinical and
echocardiographic findings, for example, the addition of TR Vmax further
improves the detection of pulmonary embolism (Table 19.2).
The Acutely Ill Patient

● Haemodynamic instability after myocardial infarction (Table 19.1)
● Possible pulmonary embolism (Table 19.2)
● Unexplained severe hypotension (Table 19.3)
● Pulmonary oedema (Table 19.4)
● Chest pain where aortic dissection is suspected (Table 19.5)
● Trauma (Table 19.6)
● Acute exacerbation of COPD. While not usually a critical emergency,
20% may have LV failure1 so that early TTE may lead to an important
change in management.
213
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Echocardiography in Acute and Critical Care Medicine
Table 19.1 Checklist for basic echocardiography in critically ill patients
Pericardial tamponade
Acute complications of infarction
● Ventricular septal rupture*
● Free wall rupture*
LV hypertrophy suggesting HCM
RV dilatation and dysfunction (e.g. secondary to pulmonary embolism; see Table 19.2)
Critical valve disease, especially aortic stenosis
Obstructed prosthetic valve*
Aortic dissection rupturing into pleural space or abdominal cavity*
Gross hypovolaemia
* Likely to require a more detailed echocardiogram.
Table 19.2 Echocardiographic signs of pulmonary embolism with

haemodynamic instability2–4
RV dilatation and free wall hypokinesis often with preserved contraction at the apex
(McConnell’s sign). Basal RV/LV ratio >1.0 in apical 4-chamber view.
D-shaped LV in parasternal short-axis view.
TR Vmax usually <4.0 m/s*.
IVC dilated and unreactive.
Diminished RV longitudinal function: TAPSE <17 mm.
Pulmonary acceleration time <80 ms*.
Right heart thrombus.
* Requires a more detailed echocardiogram.
Table 19.3 Checklist in hypotension
Signs of underfilling
IVC <10 mm in diameter collapsing completely on inspiration
Small and active RV and LV (‘kissing papillary muscles’) on parasternal short-axis
view
Low E and A waves on transmitral pulsed Doppler*
Respiratory variability in VTIsubaortic > 20% (in the absence of other pathology,
particularly pericardial effusion, RV dilatation, or asthma)*
Cardiogenic causes
LV global or regional systolic dysfunction*
Dynamic LVOT obstruction*
RV systolic dysfunction (see also Table 19.2)
Severe valve lesions*
IVC diameter >21 mm with <50% contraction on sniff
214
The Acutely Ill Patient
Sepsis5
LV typically normal in size or mildly dilated with global hypokinesis, but all forms of
impairment can occur
Fluid-loading and inotropes may lead to hyperkinesis
RV mildly dilated and hypokinetic (in the presence of ARDS)
Hypotension after cardiac surgery
HCM-like physiology following:
● Aortic valve replacement for aortic stenosis with small LV cavity, systolic anterior
mitral valve motion, and LVOT acceleration
● Systolic anterior mitral motion after mitral valve repair
Prosthetic valve regurgitation or obstruction (TOE)
Native valve dysfunction
Localised haematoma over atria (TOE) or small effusion elsewhere, causing acute
tamponade
RV stunning post-bypass and/or ischaemia
Table 19.4 Pulmonary oedema
Impaired LV systolic or diastolic function

Complications of a myocardial infarction:
● Ventricular septal rupture*
● Contained free wall rupture
Severe native valve disease
Severe dysfunction of a prosthetic heart valve* (may need TOE)
Table 19.5 Chest pain
Signs suggestive of or compatible with dissection:*

● Dissection flap
● Dilated ascending aorta
● Severe aortic regurgitation
● Pericardial fluid
Wall motion abnormalities suggesting acute coronary syndrome
Signs of pulmonary embolism (Table 19.2)
* If TTE normal but a high suspicion for dissection remains, consider TOE or CT.
215
Table 19.6 Checklist for echocardiography after blunt or penetrating

trauma
Blunt
Contusion:
● RV dilatation and hypokinesis
● Localised LV thickening and wall motion abnormality, especially
antero-apically
Ventricular septal rupture
Regional wall motion abnormality (from coronary artery dissection)
Deceleration
Valve rupture causing acute mitral or tricuspid regurgitation, occasionally
aortic regurgitation
Aortic dilatation and dissection flap or intramural haematoma
(CT or TOE)
Aortic transection (TOE)
Penetrating
RV wall hypokinesis
Ventricular septal defect
Pericardial effusion or haematoma (which may be localised)
Pleural fluid
Mitral regurgitation from valve laceration or damage to papillary muscle or
chords
Aortic regurgitation from laceration of aortic valve
Hyperdynamic LV (from offloading)
Further Indications for Echocardiography

on Critical Care Units
● The haemodynamic assessment of the heart is altered by mechanical
ventilation (Table 19.7), so the diagnosis of tamponade is based more on
clinical features than in a spontaneously breathing patient.
216
Further Indications for Echocardiography on Critical Care Units
● In the presence of a pericardial effusion, a fall in blood pressure or cardiac

output and/or the development of acute renal failure with no other
reasonable cause should prompt consideration of drainage.
The following situations require focused TTE, sometimes with additional TOE:
● Hypotension after cardiac surgery (Table 19.3).
● Estimation of filling pressures, low in Table 19.3 and high in Table 19.8.
● Assessment of likely cardiac output response to increased filling.
● The response of the VTIsubaortic to passive leg raising aids the decision for
fluid resuscitation. A rise by ≥15% suggests that cardiac output will rise
after fluid administration6. The role of measuring variation in IVC diameter
with respiration is less clear.
Table 19.7 Effects of mechanical ventilation7
The timing of paradox is reversed: a fall in left-sided cardiac output during

expiration and a decrease in right-sided venous return during inspiration.
Respiratory variation may be greater than normal, depending on the
inspiratory pressure, but if >25%:
● Check ventilation settings.
● Exclude a pericardial effusion.
● Check LV and RV size and function.
● Check for hypovolaemia.
High positive end-expiratory pressure (PEEP) reduces venous return and
afterload to cause:
● Reduced stroke volume.
● Reduced E’.
● Lengthening of E deceleration time.
● RV dilatation and dysfunction if PEEP very high (>15 mmHg).
Table 19.8 Signs of high filling pressures
High RA pressure
IVC >21 mm in diameter and unresponsive or unreactive SVC on TOE
Dilated right atrium
Atrial septum bulges to the left throughout the cardiac cycle
High LA pressure
E/E’ ratio >14
E dec time <150 ms
Atrial septum bulges to the right throughout the cardiac cycle
Dilated left atrium if filling pressure chronically high
217
Table 19.9 Other common indications for echocardiography on critical

care units
Indication Checklist*
LV systolic and diastolic dysfunction? A high
LVEDP is the most common cause.
Inability to wean from
RV size and dysfunction?
ventilator
Severe valve disease?
Pericardial effusion?
Evidence of pulmonary embolism
(Table 19.2).
Unexplained hypoxaemia
Shunt: This requires a bubble study if an ASD
is not obvious (pages 56, 57).
ARDS not responding to RV size and function.
first-line measures PA pressures.
Pre- and peri-administration
RV function and PA pressures.
of nitric oxide
Pre- and post-inotrope LV and RV function.
Possible endocarditis Chapter 13.
Embolic event Table 20.3.
* A full study looking for abnormalities in all parts of the heart is needed.
● Other common indications for critical care echocardiography are given in

Table 19.8.
● The Appendix gives guides to the echocardiographic assessment on ECMO
(Table s A.1–A.3), LV assist devices (Table A.4), and intra-aortic balloon
pumps (Table A.5).
Echocardiography in COVID-19
● Cardiac involvement confers a high risk of mortality.
● The role of TTE is to:
● Identify acute cardiac injury or hitherto-unknown but pre-existing cardiac
dysfunction (Table 19.10).
● Aid triage of patients.
● A focused TTE should suffice acutely (Chapter 1).

● Consult local and societal guidance for advice on protection of patient and
sonographer and decontamination of ultrasound equipment.
218
Echocardiography in COVID-19
Table 19.10 Indications for echocardiography in COVID-19 (Figure 19.1)
Acute
Critically unwell (hypotension, pulmonary oedema, high oxygen requirements)
Evidence of cardiac involvement (elevated biomarkers, e.g. troponin, D-dimer,
ferritin, BNP; ECG changes; cardiac symptoms)
Known cardiac disease
Follow-up: Inpatient
Monitor RV and LV function and pulmonary pressure if:
● The baseline study is abnormal
● When the patient is either not improving or deteriorating
● When moving to rescue strategies (e.g. airway pressure release ventilation)
Follow-up: Outpatient
● Document resolution of acute abnormalities
● New heart failure suspected
Figure 19.1 Changes in COVID-19. Right ventricular dilatation ± systolic

dysfunction is the most common cardiac finding during acute, severe COVID-19 and may
reverse with recovery. (Reproduced with permission from [9].)
CHECKLIST FOR REPORT IN COVID-19

1. LV dimensions, volume, and systolic function.
2. RV—dilatation and/or dysfunction and evidence of pulmonary hypertension.
3. Subclinical RV and/or LV dysfunction (e.g. longitudinal strain for outpatient
cases with continuing exercise limitation).
4. Presence of incidental abnormalities (e.g. valve disease).
5. Pericardial and pleural effusions.
219
References
1. Rutten FH, Cramer MJM, Grobbee DE, et al. Unrecognized heart failure in
elderly patients with stable chronic obstructive pulmonary disease. Eur Heart J.
2005;26(18):1887–94.
2. Kasper W, Geibel A, Tiede N, et al. Distinguishing between acute and subacute
massive pulmonary embolism by conventional and Doppler echocardiography. Br
Heart J 1993;70(4):352–6.
3. Kjaergaard J, Schaadt BK, Lund JO, et al. Quantitative measures of right
ventricular dysfunction by echocardiography in the diagnosis of acute nonmassive
pulmonary embolism. J Am Soc Echocardiogr 2006;19(10):1264–71.
4. McConnell M V, Solomon SD, Rayan ME, et al. Regional right ventricular
dysfunction detected by echocardiography in acute pulmonary embolism. Am J
Cardiol 1996;78(4):469–73.
5. Etchecopar-Chevreuil C, François B, Clavel M, et al. Cardiac morphological and
functional changes during early septic shock: A transesophageal echocardiographic
study. Intensive Care Med 2008;34(2):250–6.
6. Blanco P. Rationale for using the velocity-time integral and the minute distance
for assessing the stroke volume and cardiac output in point-of-care settings.
Ultrasound J 2020;12:21. doi.org/10.1186/s13089–020–00170-x.
7. Luecke T & Pelosi P. Clinical review: Positive end-expiratory pressure and cardiac
output. Crit Care 2005;9(6):607–21.
8. Hothi SS, Jiang J, Steeds RP, et al. Utility of non-invasive cardiac imaging
assessment in coronavirus disease 2019. Front Cardiovasc Med 2021;8:1–16.
9. Moody WE, Liu B, Mahmoud-Elsayed HM, et al. Persisting adverse ventricular
remodeling in COVID-19 survivors: A longitudinal echocardiographic study. J Am
Soc Echocardiogr 2021;34(5):562–6.
220
General Clinical
Requests 20
These tables give guidance on what to assess in various common indications
for echocardiography:
● Murmur (Table 20.1)
● Suspected heart failure (Table 20.2)
● Stroke, TIA, and peripheral embolism (Table 20.3)
● Hypertension (Table 20.4)
● Cardiac arrhythmia (Table 20.5)
● Cocaine (Table 20.6)
● HIV (Table 20.7)
● Neuromuscular diseases (Table 20.8)
● Inflammatory diseases (Table 20.9)
● Hypereosinophilia (Table 20.10)
● Drugs causing valvopathy: ergot alkaloids (cabergoline, pergolide), ergot
dopamine agonists (pergolide and cabergoline), appetite suppressants
(fenfluramine and dexfenfluramine), and the weight loss agent benfluorex
(Table 20.11)
● Radiation (Table 20.12), mainly after treatment for non-Hodgkin’s lymphoma
or left-sided breast cancer more than 20 years ago
Table 20.1 Checklist in murmur
Valve thickening or regurgitation.

Subaortic septal bulge.
ASD: Clue is dilated active RV.
VSD: parasternal long- and short-axis views with colour box on the
membranous septum detects most.
Colour box over the septum in parasternal long- and short-axis and apical
4-chamber views.
Apical septal defects may be missed (put CW probe over the site of the
maximum murmur).
Aortic coarctation (suprasternal view).
Pulmonary valve/artery and branch stenosis (steerable continuous wave in
pulmonary artery).
PDA (parasternal short and suprasternal views).
221
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General Clinical Requests
Table 20.2 Checklist in suspected heart failure
LV cavity size and wall thickness and systolic and diastolic function
RV size and function and evidence of pulmonary hypertension (TR Vmax, RV
outflow acceleration time).
LA volume (as a sign of chronically high LV filling pressures).
IVC size and response to respiration.
Valve appearance and function.
Constriction checklist (Tables 17.5 and 17.6 on pages 196, 197) if restrictive LV
filling with normal LV ejection fraction.
Table 20.3 Checklist in stroke, TIA or peripheral embolism1
LV global hypokinesis, aneurysm, or large regional wall motion abnormality.

LV cardiomyopathy (DCM, HCM, non-compaction).
Signs of hypertension (see Table 20.4) as the underlying cause.
Mitral valve disease: stenosis > regurgitation.
Evidence of endocarditis.
Masses intracardiac tumours (e.g. LA myxoma, sarcoma), LV thrombus, LA or
LAA thrombus,* fibroelastoma.
ASD or patent foramen ovale (bubble study according to clinical indications
usually in patients aged < 50).
Aortic arch and ascending aortic atheroma.
Evidence of aortic dissection: dilated aorta, dissection flap (rarely presents
without chest pain).
Atrial fibrillation or flutter (may occasionally be first diagnosed on TTE,
especially if paroxysmal).
* Will usually require TOE, CT, or CMR.
Table 20.4 Checklist in hypertension
LV size and thickness (subaortic septal bulge may be an early sign but is also
seen in normotensive elderly people).
LV systolic and diastolic function.
LA volume.
Aortic dimensions (sinus, sinotubular junction, and ascending aorta).
Coarctation in the young.
Aortic valve thickening and competence.
222
Table 20.5 Checklist after arrhythmia
After ventricular tachycardia2

LV size, wall thickness, and systolic function (especially evidence of aneurysm
or any other wall motion abnormality).
RV size and systolic function (evidence of ARVC/D [see page 75]).
Severe valve disease.
Mitral annular dysjunction.
Atrial fibrillation or flutter
LA volume and RA area. LA thrombus?
Interatrial septum (check for ASD).
LV size and systolic and diastolic function.
RV size and function and PA pressure.
Mitral valve appearance and function.
Table 20.6 Checklist in cocaine3
Acute
Wall motion abnormality (myocardial infarction)
Generalised LV hypokinesis (myocarditis)
Aortic dissection
Long-term use
Dilated LV
LV hypertrophy
Evidence of endocarditis
Table 20.7 Checklist in HIV4
Dilated LV
LV systolic dysfunction (commonly mild, less commonly severe)
LV diastolic dysfunction
Evidence of endocarditis (increased susceptibility to infection)
Pericardial thickening and malignancy (e.g. Kaposi’s sarcoma, non-Hodgkin’s
lymphoma)
223
Table 20.8 TTE abnormalities in neuromuscular disorders5–8
Regional wall motion abnormalities, usually

inferolateral, from age 10 yr (mid-wall
fibrosis may show on CMR even with
normal TTE).
Duchenne muscular dystrophy By 18 yr, nearly all have cardiomyopathies,
usually dilated. Some have LV hypertrophy.
Pulmonary hypertension and RV dysfunction
(secondary to respiratory failure) almost
universal.
Dilated cardiomyopathy; usually begins in the
inferolateral wall.
Becker muscular dystrophy ~40% have DCM on TTE by age 30 yr.
CMR may show inferolateral mid-wall fibrosis,
even with normal TTE.
Facioscapulohumeral
Cardiomyopathy rare.
muscular dystrophy
LV hypertrophy in ~20%.
LV dilatation and systolic dysfunction in ~14%.
Myotonic dystrophy
CMR: Dilatation, hypertrophy, and reduced LV
ejection fraction detected earlier than TTE.
DCM moderately common.
Emery-Dreifuss muscular
Unlike Duchenne and Becker, early disease
dystrophy
not associated with fibrosis on CMR.
Cardiac involvement is disease- and genetics-
specific and can result in DCM with RV and
Limb girdle dystrophy LV fatty infiltration:
(genetically and clinically ● Type 2A and 2B most common: DCM rare.
heterogenous disorders with ● Types 2C–2F: DCM common.
proximal muscular weakness) ● The lamin mutation subgroup can have
diastolic dysfunction and mid-wall fibrosis
of the basal infero-septum on CMR.
LV hypertrophy: Concentric > asymmetric.
Reduced LV ejection fraction in more severe
Friedrich’s ataxia
cases.
CMR may show inferolateral mid-wall fibrosis.
Mitochondrial cardiomyopathies
HCM in 50%, DCM, and non-compaction also
MELAS/MERRF
seen. Restrictive cardiomyopathy rare.
DCM uncommon. May have mitral and
Kearns–Sayre
tricuspid prolapse.
Abbreviations: CMR, cardiac magnetic resonance scan; DCM, dilated cardiomyopathy; HCM,
hypertrophic cardiomyopathy.
224
Table 20.9 Checklist in systemic inflammatory diseases9
LV dysfunction secondary to myocarditis.

Generalised valve thickening and vegetations
Systemic lupus (mitral and aortic most commonly affected)
erythematosus (SLE) with regurgitation (stenosis very rare).
Pulmonary hypertension.
Pericardial effusion (tamponade uncommon).
Generalised valve thickening and vegetations
(mitral and aortic most commonly affected)
with regurgitation (stenosis very rare).
Primary antiphospholipid
Right-sided thrombus.
syndrome
LV dysfunction (secondary to systemic
hypertension or coronary disease).
Nodules typically at base of leaflets.
Rheumatoid arthritis Valve thickening commonly mild and focal but
may be diffuse.
Aortic root dilatation with thickening and
Ankylosing spondylitis fibrosis of the base of the aortic cusps and
anterior mitral leaflet.
Aortic valve vegetations with regurgitation.
Granulomatosis with Pericarditis.
polyangiitis LV systolic dysfunction.
Aortic aneurysms.
Eosinophilic granulomatosis Myocarditis common.
with polyangiitis Pericardial effusion.
Myocardial fibrosis leading to diastolic >
systolic LV dysfunction.
Systemic sclerosis Pulmonary hypertension and RV failure
(scleroderma) (secondary to lung fibrosis).
Pericardial effusion (c40%).
Aortic or mitral valve thickening (c10%).
LV diastolic dysfunction (40%).
Polymyositis/dermatomyositis Pulmonary hypertension (interstitial lung
disease).
Mixed connective tissue
disease
Cardiac involvement uncommon.
Sjögren’s syndrome Pulmonary hypertension (secondary to lung
involvement).
Myocarditis.
Behçet’s disease RA and RV thrombus.
Pulmonary artery aneurysms.
225
(Continued)
Table 20.9 Checklist in systemic inflammatory diseases (Continued)
Cogan’s disease Aortic dilatation and aortic regurgitation.

Sarcoidosis See Table 7.4, page 64.
Aortic dilatation with secondary aortic
regurgitation.
Pulmonary artery dilatation.
Takayasu’s arteritis Pulmonary stenosis.
Fistulae between pulmonary artery and
coronary or bronchial arteries or aorta.
Subclinical myocardial involvement.
Giant cell arteritis Thoracic aortic aneurysm.
Polyarteritis nodosa DCM.
Heart failure.
Microscopic polyangiitis
Pericarditis.
Myocardial infarction.
Kawasaki disease
Myocarditis and pericarditis acutely.
Table 20.10 Checklist in hypereosinophilia, Loeffler’s endocarditis,

endomyocardial fibrosis10
LV or RV apical cavity obliteration by thrombus and fibrosis (Figure 7.2)

Hyperdense endocardium
Restrictive cardiomyopathy
Fibrous attachment of tricuspid and mitral valves with mitral and tricuspid
regurgitation
Table 20.11 Checklist in drug treatment with dopamine agonists

(pergolide and cabergoline), appetite suppressants (fenfluramine and
dexfenfluramine), and the weight loss agent benfluorex11
More commonly affecting mitral and aortic valves:

● Leaflet thickening, restriction, and regurgitation (stenosis uncommon).
● Chordal thickening and shortening.
● First sign may be increased tenting height of the mitral valve.
● Thickening affects the whole leaflet.
Note: Abnormalities almost never seen with low-dose use in microprolactinoma.
226
Table 20.12 Checklist in radiation12
Aortic and mitral valve thickening,

fibrosis, shortening, and calcification
Regurgitation more common than
Valve disease
stenosis
Incidence 6% at 20 years after
irradiation
Diffuse myocardial fibrosis
LV dysfunction Initially systolic dysfunction, later
restrictive cardiomyopathy
Accelerated coronary disease
Coronary disease
Regional wall motion abnormalities
Chronic pericarditis: pericardial
thickening, adhesions, effusion
Pericardial disease Pericardial constriction: Incidence
4–20%, depending on dose and
concomitant use of chemotherapy
References
1. Cohen A, Donal E, Delgado V, et al. EACVI Recommendations on cardiovascular
imaging for the detection of embolic sources: Endorsed by the Canadian Society
of Echocardiography. Eur Heart J Cardiovasc Imaging 2021;22(6):E24–57.
2. Dejgaard LA, Skjølsvik ET, Lie ØH, et al. The mitral annulus disjunction arrhythmic
syndrome. J Am Coll Cardiol 2018;72(14):1600–9.
3. Missouris CG, Swift PA & Singer DR. Cocaine use and acute left ventricular
dysfunction. Lancet 2001;357(9268):1586.
4. Reinsch N, Kahlert P, Esser S, et al. Echocardiographic findings and abnormalities
in HIV-infected patients: Results from a large, prospective, multicenter HIV-heart
study. Am J Cardiovasc Dis 2011;1(2):176–84.
5. Verhaert D, Richards K, Rafael-Fortney JA, et al. Cardiac involvement in patients
with muscular dystrophies: Magnetic resonance imaging phenotype and genotypic
considerations. Circ Cardiovasc Imaging 2011;4(1):67–76.
6. Beynon RP & Ray SG. Cardiac involvement in muscular dystrophies. Q J Med
2008;101(5):337–44.
7. Weidemann F, Rummey C, Bijnens B, et al. The heart in Friedreich ataxia: Definition
of cardiomyopathy, disease severity, and correlation with neurological symptoms.
Circulation 2012;125(13):1626–34.
8. El-Hattab AW & Scaglia F. Mitochondrial cardiomyopathies. Front Cardiovasc Med
2016;3(25):1–9.
9. Roldan CA. Valvular and coronary heart disease in systemic inflammatory diseases.
Heart 2008;94(8):1089–1.
227
General
GeneralClinical
Clinical
Requests
RequestsGeneral Clinical RequestsEchocardiography
10. Mankad R, Bonnichsen C & Mankad S. Hypereosinophilic syndrome: Cardiac

diagnosis and management. Heart 2016;102(2):100–6.
11. Andrejak M & Tribouilloy C. Drug-induced valvular heart disease: An update. Arch
Cardiovasc Dis 2013;106(5):333–9.
12. Lancellotti P, Nkomo VT, Badano LP, et al. Expert consensus for multi-modality
imaging evaluation of cardiovascular complications of radiotherapy in adults:
A report from the European Association of Cardiovascular Imaging and the
American Society of Echocardiography. Eur Hear J 2013;14(8):721–40.
228
Appendices
Left Ventricle
Cardiac Resynchronisation
1. Patient selection
● The decision for CRT1:
● NYHA class III and IV unresponsive to maximal heart failure therapy
● LVEF ≤35%
● ECG QRS >120 ms and ideally >150 ms2
● Use contrast agents to enhance endocardial delineation if the image

quality is suboptimal.
● Use 3D when image quality is good and staff have expertise in 3D data
acquisition and processing. Ideally, use vendor-neutral analysis software.
2. Cardiac resynchronisation optimisation
● Echocardiographic optimisation is not routine but should be used for
patients with refractory symptoms. There is no consensus, but a guide is:
2.1 Perform a baseline TTE to assess LV remodelling.
● LV dimensions, volumes, and global and regional systolic function.
● Assess MR, TR severity, and PA systolic pressure.
● Compare measurements with the pre-CRT values and report

changes.
● Check that Bi-V pacing >90%. If not, do not continue optimisation.
The pacing physiologist will optimise pacemaker settings.
2.2 Start with AV delay optimisation (cannot perform if patient in AF).
Mitral valve filling time and aortic valve VTI method:
● Annotate pacemaker baseline settings on the screen (mode, base rate, AV
delay). Set up VV delay at 0–4 ms (both ventricles activate at the same time).
● Record PW Doppler of mitral valve inflow and optimise trace for best
visualisation of A wave and opening and closing artefacts.
● Measure diastolic filling ratio (LV filling time/RR interval) at baseline.
Significant atrioventricular dyssynchrony is assumed if this ratio is <40%.
● Record aortic valve CW Doppler and optimise trace for best
visualisation of opening and closing artefacts. Measure baseline VTIaortic
(or VTIsubaortic if there is aortic stenosis). 229
Appendices
Ask a pacing physiologist to change the AV delay in incremental steps of

●
10–20 ms within the range from 80 to 180 ms. Annotate AV delay on the
screen and measure diastolic filling ratio and VTI aortic at multiple settings.
● With longer AV delays, check you have not lost Bi-V pacing. If so, come
down to the longest AV delay that still enables Bi-V pacing.
● Compare measurements and select the AV delay with the highest
diastolic filling ratio and VTIaortic values.
Alternative proposed method—truncation of A wave method:
● Assess mitral valve pulsed Doppler inflow A wave3:
● When A wave is blunted, the AV delay is too short.
● When E and A partially overlap or diastolic MR appears, the AV delay

is too long.
● Choose the AV delay with the best developed A wave without shortening
the A deceleration time, and with the least mitral regurgitation.
2.3 Optimise interventricular delay:
● Set to the optimal AV delay.
● Select different VV delays and annotate them on the screen:
● Both ventricles activated at the same time—baseline.
● The RV activated earlier than the left (e.g. 30 ms and 50 ms).
● The LV activated earlier than the right (e.g. 30 ms and 50 ms).
● Measure VTIaortic (VTIsubaortic if there is aortic stenosis) at different

settings and choose the sequence with the highest value.
CHECKLIST FOR REPORTING CRT

OPTIMISATION:
1. Device implantation date.
2. Changes in symptoms after device implantation.
3. Optimal AV delay (ms).
4. Optimal VV delay (ms).
5. Parameters of LV remodelling and changes when compared to pre-implantation
data.
6. MR severity.
7. TR severity and PA systolic pressure.
Critical Care Monitoring

● Suitability for ECMO (Table A.1)
230 ● Monitoring ECMO (Table A.2)
● Weaning from ECMO (Table A.3)

● Checklist for ventricular assist device (Table A.4)
● Intra-aortic balloon pump (Table A.5)
Table A.1 Suitability for ECMO (extracorporeal membrane oxygenation)
Reversible pathology avoiding ECMO

Surgically correctible valve disease
Indications for venovenous ECMO
Respiratory failure
Needs venoarterial rather than venovenous ECMO
Severe PA hypertension (mean PA pressure >50 mmHg)
Severe LV impairment
Severe valve disease
Absolute contraindication for venoarterial ECMO
Severe aortic regurgitation
Unrepaired aortic dissection
Widespread LV scarring
Use peripheral rather than central lines
Aortic atheroma
ASD, large PFO, atrial septal aneurysm
Table A.2 Echocardiographic monitoring for ECMO5–7
Confirm correct position of cannulae.

Access cannula near mouth of IVC.
Return cannula in mid-RA clear of interatrial septum and tricuspid valve.
Incorrect positions include the coronary sinus or RV or LA via a PFO.
General
LV and RV function.
Grade of any mitral regurgitation.
Aortic valve opening.
Pericardial fluid.
(Continued )
231
Appendices
Table A.2 Echocardiographic monitoring for ECMO5–7 (Continued)
Complications
Cannula displacement.
Cannula thrombosis.
Obstruction of veins or arteries.
LV thrombus.
Tamponade.
Pulmonary embolism.
Hypoxia from recirculation.
Table A.3 Echocardiographic features supporting weaning from VA

ECMO with flow reduction to <1.5 L/min5–7
LVEF >20–25% and ideally >35%

VTIlvot ≥10 cm
Tissue Doppler peak systolic velocity ≥6 cm/s
Non-dilated LV
No cardiac tamponade
Table A.4 Checklist for temporary ventricular assist device8, 9
Before insertion
LV size and function (diastolic volume <120 mL may limit effectiveness)
RV size and function
Grade of mitral and tricuspid regurgitation
Contraindications
Aortic pathology (dissection, abdominal or thoracic aortic aneurysm)
LV apical thrombus
Aortic stenosis or regurgitation
Small LV cavity (e.g. HCM)
ASD
Severe RV dysfunction (RV area change <20% may develop RV failure)
Severe pulmonary hypertension (systolic pressure >50 mmHg)
232
At insertion
Correct position (parasternal or apical long-axis view):
● Inlet area 40–45 mm below aortic valve.
● Catheter angled towards the LV apex.
● Catheter not curled up or obstructing the mitral valve or with the tip in the
papillary muscle area.
Colour Doppler mosaic flow pattern of the exit stream above the sinus
of Valsalva.
Optimise LV filling:
● Maximise E wave velocity and VTImitral.
● Septal shift to right means pump flow too low.
● Septal shift to left means pump flow too high.
Exclude right-to-left atrial shunting.
Monitoring
Verify position of catheter.
Verify outflow mosaic pattern above the sinus of Valsalva.
Confirm permanently closed aortic and pulmonary valves.
LV and RV systolic function:
● Echo-guided increase in pump speed for LV failure.
● Echo-guided decrease in pump speed for RV failure.
Ventricular unloading (transmitral E wave).
PA pressure.
Grade of mitral regurgitation.
Check for pericardial effusion.
Exclude LV thrombus.
Table A.5 Checklist for intra-aortic balloon pump
Contraindications
Moderate or severe aortic regurgitation
Aortic pathology (severe atheroma, dissection, abdominal aneurysm)
Monitoring
Correct position (tip at junction of arch and descending thoracic aorta)
Change in VTIsubaortic with augmentation
Leakage (bubbles in aorta)
Exclude pericardial effusion
233
Appendices
Valve Disease
● Wilkins score (Table A.6)
● Duke criteria for diagnosing endocarditis (Table A.7)
● Normal ranges for prosthetic heart valves (Tables A.8–A.10)
Table A.6 Wilkins score10
Morphology Score
Mobility
Highly mobile, only tips restricted 1
Normal mobility of base and mid-leaflet 2
Valve moves forward in diastole mainly from the base 3
No or minimal movement 4
Leaflet thickening
Near normal 1
Thickening mainly at tips 2
Thickening (5–8 mm) over the whole leaflet 3
Severe thickening (>8 mm) of whole leaflet 4
Subvalvar thickening
Minimal, just below leaflets 1
Over one-third of the chords 2
Extending to the distal third of the chords 3
Extensive thickening and shortening of the whole chord 4
Calcification
A single area of echogenicity 1
Scattered areas at leaflet margin 2
Echogenicity extending to midportion of leaflets 3
Extensive echogenicity over whole leaflet 4
Note: A total score ≤8 suggests a successful result, but the score has not been validated in a
large population and does not assess some key points (Table 9.4, page 106).
234
Valve Disease
Table A.7 Modified Duke clinical criteria for infective endocarditis11
Major— Major—
Minor
Microbiological Echocardiographic
1. Typical microorganisms 1. Vegetations 1. At risk heart condition,
consistent with IE from IVDU
or
two separate sets of 2. Fever > 38ºC
blood cultures: for 2. Abscess 3. Vascular phenomena
example, oral streptococci, ● Emboli
or
Streptococcus bovis group, ● Septic pulmonary
HACEK group, S. aureus 3. Dehiscence of a infarcts
or community-acquired prosthetic valve ● Intracranial
enterococci (in the absence haemorrhage
or
of a primary focus) ● Mycotic aneurysm
4. Perforation of a 4. Immunologic
or
valve phenomena
2. Microorganisms consistent ● Glomerulonephritis
or
with IE from persistently ● Rheumatoid factor
positive blood cultures: 5. Fistula formation ● Roth spots, etc.
at least 2 positive blood 5. Microbiology other
or PET positive for
cultures taken 12 h apart than major criteria
prosthetic valve or
or all 3 or a majority of 4
abscess on CT
separate blood cultures
(1 hr between 1st and last
samples)
or
3. Single positive blood
culture for Coxiella
burnetti or phase 1 IgG
antibody titre >1:800
Normal values for prosthetic heart valves: mean (standard deviation)

(Table A.8–Table A.10)12–14
● The Hatle formula for mitral orifice area (220/pressure half-time) is not
valid in normally functioning mitral prostheses.
● Doppler results are broadly similar for valves sharing a similar design.
For simplicity, results for one design in each category is given with a
list of other valve designs for which data exist.
● Sizing conventions vary, so it is possible that a given label size for a
valve not on the list may not be equivalent to those that are. A change
on serial studies is more revealing than a single measurement, and the
TTE must be interpreted in the clinical context.
235
Appendices
Table A.8 Aortic position—biological valves, mean (SD) values
Stented Porcine—Carpentier-Edwards standard as

example (values similar for Carpentier-Edwards
supra-annular, Intact, Hancock I and II and Mosaic,
Biocor, Epic)
Vmax Peak ΔP Mean ΔP EOA
m/s mmHg mmHg cm2
19 mm 43.5 (12.7) 25.6 (8.0) 0.9 (0.2)
21 mm 2.8 (0.5) 27.2 (7.6) 17.3 (6.2) 1.5 (0.3)
23 mm 2.8 (0.7) 28.9 (7.5) 16.1 (6.2) 1.7 (0.5)
25 mm 2.6 (0.6) 24.0 (7.1) 12.9 (4.6) 1.9 (0.5)
27 mm 2.5 (0.5) 22.1 (8.2) 12.1 (5.5) 2.3 (0.6)
29 mm 2.4 (0.4) 9.9 (2.9) 2.8 (0.5)
Stented Bovine Pericardial—Edwards Perimount as example
(similar for Mitroflow, Edwards Pericardial, Labcor-Santiago,
Mitroflow)
19 mm 2.8 (0.1) 32.5 (8.5) 19.5 (5.5) 1.3 (0.2)
21 mm 2.6 (0.4) 24.9 (7.7) 13.8 (4.0) 1.3 (0.3)
23 mm 2.3 (0.5) 19.9 (7.4) 11.5 (3.9) 1.6 (0.3)
25 mm 2.0 (0.3) 16.5 (7.8) 10.7 (3.8) 1.6 (0.4)
27 mm 12.8 (5.4) 4.8 (2.2) 2.0 (0.4)
Homograft
22 mm 1.7 (0.3) 5.8 (3.2) 2.0 (0.6)
26 mm 1.4 (0.6) 6.8 (2.9) 2.4 (0.7)
Stentless—St Jude Toronto (similar to Prima)
21 mm 22.6 (14.5) 10.7 (7.2) 1.3 (0.6)
23 mm 16.2 (9.0) 8.2 (4.7) 1.6 (0.6)
25 mm 12.7 (8.2) 6.3 (4.1) 1.8 (0.5)
27 mm 10.1 (5.8) 5.0 (2.9) 2.0 (0.3)
29 mm 7.7 (4.4) 4.1 (2.4) 2.4 (0.6)
236
Valve Disease
Table A.9 Aortic position—mechanical, mean (SD) values
Single tilting disk

Medtronic-Hall (similar values Bjork-Shiley monostrut and CC,
Omnicarbon, and Omniscience)
m/s mmHg mmHg cm2
20 mm 2.9 (0.4) 34.4 (13.1) 17.1 (5.3) 1.2 (0.5)
21 mm 2.4 (0.4) 26.9 (10.5) 14.1 (5.9) 1.1 (0.2)
23 mm 2.4 (0.6) 26.9 (8.9) 13.5 (4.8) 1.4 (0.4)
25 mm 2.3 (0.5) 17.1 (7.0) 9.5 (4.3) 1.5 (0.5)
27 mm 2.1 (0.5) 18.9 (9.7) 8.7 (5.6) 1.9 (0.2)
Bileaflet mechanical
Intrannular—St Jude standard (similar Carbomedics standard,
Edwards Mira, ATS, Sorin Bicarbon)
m/s mmHg mmHg cm2
19 mm 2.9 (0.5) 35.2 (11.2) 19.0 (6.3) 1.0 (0.2)
21 mm 2.6 (0.5) 28.3 (10.0) 15.8 (5.7) 1.3 (0.3)
23 mm 2.6 (0.4) 25.3 (7.9) 13.8 (5.3) 1.6 (0.4)
25 mm 2.4 (0.5) 22.6 (7.7) 12.7 (5.1) 1.9 (0.5)
27 mm 2.2 (0.4) 19.9 (7.6) 11.2 (4.8) 2.4 (0.6)
29 mm 2.0 (0.1) 17.7 (6.4) 9.9 (2.9) 2.8 (0.6)
Intra-annular modified cuff or partially supra-annular—On-X
(similar St Jude Regent, St Jude HP, Carbomedics Reduced
cuff, Medtronic Advantage)
19 mm 21.3 (10.8) 11.8 (3.4) 1.5 (0.2)
21 mm 16.4 (5.9) 9.9 (3.6) 1.7 (0.4)
23 mm 15.9 (6.4) 8.6 (3.4) 1.9 (0.6)
25 mm 16.5 (10.2) 6.9 (4.3) 2.4 (0.6)
Supra-annular—Carbomedics TopHat
21mm 2.6 (0.4) 30.2 (10.9) 14.9 (5.4) 1.2 (0.3)
23mm 2.4 (0.6) 24.2 (7.6) 12.5 (4.4) 1.4 (0.4)
25mm 9.5 (2.9) 1.6 (0.3)
(Continued)
237
Appendices
Table A.9 Aortic position—mechanical, mean (SD) values (Continued)
Ball and cage—Starr-Edwards

m/s mmHg mmHg cm2
23 mm 3.4 (0.6) 32.6 (12.8) 22.0 (9.0) 1.1 (0.2)
24 mm 3.6 (0.5) 34.1 (10.3) 22.1 (7.5) 1.1 (0.3)
26 mm 3.0 (0.2) 31.8 (9.0) 19.7 (6.1)
27 mm 30.8 (6.3) 18.5 (3.7)
29 mm 29.3 (9.3) 16.3 (5.5)
Table A.10 Mitral position, mean (SD) values
Stented Porcine—Carpentier-Edwards (similar Intact, Hancock)

Vmax Mean ΔP EOA
m/s mmHg cm2
25 mm 1.5 (0.4)
27 mm 6.0 (2.0) 1.8 (0.5)
29 mm 1.5 (0.3) 4.7 (2.0) 1.9 (0.5)
31 mm 1.5 (0.3) 4.5 (2.0) 2.6 (0.5)
33 mm 1.4 (0.2) 5.4 (4.0) 2.6 (0.5)
Pericardial—Edwards Perimount (similar Labcor-Santiago,
Hancock pericardial)
25 mm 1.4 (0.2) 4.9 (1.1) 1.6 (0.4)
27 mm 1.3 (0.2) 3.2 (0.8) 1.8 (0.4)
29 mm 1.4 (0.2) 3.2 (0.6) 2.1 (0.5)
31 mm 1.3 (0.1) 2.7 (0.4)
Single tilting disc—Bjork-Shiley monostrut (similar Omnicarbon)
25 mm 1.8 (0.3) 5.6 (2.3)
27 mm 1.7 (0.4) 4.5 (2.2)
29 mm 1.6 (0.3) 4.3 (1.6)
31 mm 1.7 (0.3) 4.9 (1.6)
33 mm 1.3 (0.3)
238
Aorta
Bileaflet—Carbomedics (similar St Jude)

25 mm 1.6 (0.2) 4.3 (0.7) 1.5 (0.3)
27 mm 1.6 (0.3) 3.7 (1.5) 1.7 (0.4)
29 mm 1.8 (0.3) 3.7 (1.3) 1.8 (0.4)
31 mm 1.6 (0.4) 3.3 (1.1) 2.0 (0.5)
33 mm 1.4 (0.3) 3.4 (1.5) 2.0 (0.5)
OnX
All sizes 2.2 (0.9)
Caged ball—Starr-Edwards
28 mm 1.8 (0.2) 7.0 (2.8)
30 mm 1.8 (0.2) 7.0 (2.5)
32 mm 1.9 (0.4) 5.1 (2.5)
Aorta
Figure A.1 Nomograms for sinus of Valsalva diameter against height in

men and women aged above and below 50. (Redrawn from data in [15], with
permission of Oxford University Press.)
239
Appendices
Figure A.2 Nomograms for ascending aortic diameter against height in

men and women aged above and below 50. (Redrawn from data in [15], with
permission of Oxford University Press.)
Summary of Formulae
1. Bernoulli equation
his equates potential and kinetic energy up- and downstream from a stenosis.
T
The modified formula is used in two forms:
Short modified Bernoulli equation ∆P (mmHg) = 4 v22
Long modified Bernoulli equation ∆P (mmHg) = 4 (v22−v12)
where ΔP is transvalvar pressure difference, v1 is subvalvar velocity, and v2 is
transvalvar velocity.
The short form can be used when subvalvar is much less than transvalvar
velocity, for example, mitral stenosis, moderate or severe aortic stenosis (V2
> 3.0 m/s), but not mild aortic stenosis or normally functioning replacement
valves.
240
Summary of Formulae
2. Continuity equation
EOA (cm2) = CSA × VTIsubaortic / VTIao
where EOA is effective orifice area, CSA is cross-sectional area of the LV
outflow tract, VTIsubaortic and VTIao are subaortic and transaortic systolic veloc-
ity time integral. For prosthetic mitral valves, the velocity time integral of the
transmitral signal can be substituted for VTIao.
3. Pressure half-time estimation of mitral orifice area
MOA (cm2) = 220/T1/2

where MOA is effective mitral orifice area and T1/2 is pressure half-time in ms.
This formula should only be used in moderate or severe stenosis. It is not valid
in normally functioning replacement valves. The pressure half-time is short-
ened in mitral stenosis if there is significant MR or AR.
4. Stroke volume and cardiac output
SV (mL) = CSA × VTIsubaortic

where CSA is cross-sectional area of the left ventricular outflow tract (in cm2)
and VTIsubaortic is subaortic velocity integral (in cm).
Cardiac output (mL/min) = SV × heart rate
5. Flow
Flow (mL/s) = CSA × VTIsubaortic × 1,000/SET
where CSA is cross-sectional area of the LV outflow tract (in cm2), VTIsubaortic is
subaortic velocity integral (in cm), and SET is systolic ejection time (from opening
to closing artefact of the aortic signal) (in ms).
A number of formulae, 6–10, are sometimes used in research.
6. Energy Loss Index (ELI)
ELI (cm2/m2) = [(EOA.ASTJ)/(ASTJ–EOA)]/BSA

where EOA is effective orifice area in cm2 using the continuity equation (equa-
tion 2), ASTJ is cross-sectional area of the aorta at the level of the sinotubular
junction, and BSA is body surface area in m2.
ELI <0.6 cm2/m2 is a common cut point for severe AS.
241
Appendices
7. Total VA (ventriculo-aortic) impedance

∑va (mmHg/mL/m2) = (mean ΔP + SBP)/SVI
where mean ∆P is recovered pressure (equation 8) in mmHg, SBP is systolic
blood pressure in mmHg, and SVI is stroke volume indexed to BSA in mL/m2.
8. Recovered mean pressure gradient in aortic stenosis

Recovered ΔP (mmHg) = 4v22.2(EOA/ASTJ)(1–EOA/ASTJ)
where v is the transaortic Vmax in m/s, EOA is the effective orifice area in cm2,
and ASTJ is the area of the aorta at the sinotubular junction in cm2.
9. Stroke work loss

SWL(%) = 100.mean ΔP/(mean ΔP + SBP)
where ∆P is mean gradient from the transaortic continuous wave signal in
mmHg and SBP is systolic blood pressure in mmHg.
10. Systemic vascular resistance
Systemic vascular resistance (dyne.sec/cm5) = (mean arterial

pressure × 80)/cardiac output
where mean arterial pressure is in mmHg and cardiac output is in L/min. Nor-
mal is 800–1,200 dyne.sec/cm5.
Shunt Calculation
Table A.11 Chamber volume load and levels for shunt calculation
Level for shunt calculation

Loaded chamber Downstream Upstream
ASD RV Pulmonary artery LV outflow
VSD LV Pulmonary artery LV outflow
PDA LV LV outflow Pulmonary valve
● The stroke volume is calculated for the aortic valve (equation 4) and then for
the pulmonary valve using the diameter at the pulmonary annulus and the
VTI calculated with the pulsed sample at the level of the annulus.
● If the annulus cannot be imaged reliably, the diameter of the pulmonary
artery and the level for velocity recording should be taken at a downstream
point, where imaging is possible.
● The shunt is then the ratio of the downstream to the upstream stroke
242
volume (Table A.11).
Summary of Formulae
Figure A.3 Body surface nomogram. Put a straight edge against the patient’s
height and weight and read off the body surface area on the middle column.
243
Appendices
References
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response to CRT (PROSPECT) trial. Circulation 2008;117:2608–16.
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resynchronisation therapy. Hjerteforum 2015;1(28):34–42.
3. EACVI 3D. Echocardiography Box: Echo parameters in CRT patients’ selection.
https://www.escardio.org/Education/Practice-Tools/EACVI-toolboxes/3D-Echo/echo-
parameters-in-crt-patients-selection.
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markers of dyssynchrony as predictors of super-response to cardiac
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Anaesth 2017;20(Suppl 1):S1–3
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membrane oxygenation. Echo Res Pract 2015;2:D1–1.
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heart pumps. J Am Coll Cardiol CVI 2009;2:1332–3.
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receiving a new left ventricular assist device: The Impella Recover 100. Eur J Echo
2004;5:430–7.
10. Wilkins GT, Weyman AE, Abascal VM, Block PC & Palacios IF. Percutaneous balloon
dilatation of the mitral valve: An analysis of echocardiographic variables related to
outcome and the mechanism of dilatation. Brit Heart J 1988;60:299–308.
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management of infective endocarditis. Europ Heart J 2015;36:3075–128.
12. Rajani R, Mukherjee D & Chambers J. Doppler echocardiography in normally
functioning replacement aortic valves: A literature review. J Heart Valve Dis
2007;16:519–35.
13. Rosenhek R, Binder T, Maurer G & Baumgartner H. Normal values for Doppler
echocardiographic assessment of heart valve prostheses. J Am Soc Echo
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prosthesis and long-term management. Circulation 2009;119:1034–48.
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244
Index
Note: Page numbers in bold indicate a table and page numbers in italics indicate a figure on the
corresponding page.
A global systolic function Doppler measurements, 82

active RV, 37, 37 and, 29 general steps, 87 – 88
acute and critical mitral valve and, 30 low-gradient, low-flow,
care medicine myocardial infarction and, 87, 88
echocardiography 30 – 31 recovered mean pressure
acutely ill patient, 213 right ventricle and, 30 gradient in, 242
after blunt or penetrating stress echocardiography severity assessment,
trauma, 216 and, 32 83 – 86, 84, 85
basic echocardiography true and false aneurysms surgery indicated on TTE,
in critically ill patients, and, 32, 33 89, 89
214, 214 acute pericarditis, 196 – 197 transcatheter valve (TAVI)
checklist in aneurysm workup, 89, 89
hypotension, 214 apical, 33, 68 unclear diagnosis of, 87, 87
chest pain, 215 atrial septal, 55, 56 aortic valve disease
COVID-19, 218, 219, 219 coronary sinus, 164, 164 acute aortic regurgitation,
critical care monitoring, thoracic aortic, 165 96, 97
230, 231 – 233 true and false, 32, 33 aortic regurgitation, 90 – 96,
echocardiographic signs aorta 91 – 94, 92, 94 – 95
of pulmonary embolism cut points for surgery, 164 aortic stenosis, 81, 81 – 89,
with haemodynamic how to measure, 161 84, 85, 87, 88, 89
instability, 214 nomograms, 240 mixed mitral and, 134
effects of mechanical other features, 165 mixed moderate, 133
ventilation, 217 where to measure, 161 apical aneurysm, 33, 68
further indications, aortic dilatation, 163, 164 appetite suppressants, 226
216 – 218, 218, 219 aortic regurgitation (AR) arrhythmia, 223
pulmonary oedema, 215 appearance of valve and arrhythmogenic RV
signs of high filling aorta, 81 – 82, 81 cardiomyopathy/dysplasia
pressures, 217 assessing other valves and (ARVC/ARVD), 75 – 76,
acute aortic regurgitation, right heart, ’95 76, 76
96, 97 colour flow mapping, 91, 91 ASE/EACVI values, 35, 36
acute aortic syndrome, continuous wave signal, 92 atrial enlargement, 55, 55
166 – 167 echocardiographic criteria atrial septal aneurysm, 55, 56
aortic regurgitation present for surgery, 95, 95 atrial septal defect (ASD), 55,
in, 168 flow reversal at the arch, 56, 171–174, 172, 173, 174
dissection flap, 167, 168 92, 92 – 93 device closure, 184,
LV function in, 169 grading severity of, 94, 94 185, 187
maximum aortic left ventricle, 95 atrial septum, 53 – 59,
diameter, 167 present in acute aortic 56 – 57, 57
pericardial fluid in, 167 syndrome, 166 atrial thrombus, 106
acute coronary syndrome aortic stenosis (AS)
assessing regional LV appearance of valve and B
systolic function in, 29 aorta, 81 – 82, 81, 82 balloon valvotomy, 106,
complications, 29, 31, clinical correlates, 87 106, 130
31 – 32, 32 CT calcium scoring, 87 basic scan, 2, 3 – 4
245
Index
benfluorex, 226 sequential segmental in COVID-19, 218, 219, 219

Bernoulli equation, 240 approach to assessment deciding on level of, 1–3, 2, 3
blunt or penetrating of, 181 – 184, 182, 184 escalation for urgent clinical
trauma, 216 tetralogy of Fallot, 185, 186 advice based on, 9, 9
body surface nomogram, 243 ventricular septal defect focused study, 4
bubble contrast study, 57, 57 (VSD), 174, 174 – 177, low-dose dobutamine
176, 184, 186 stress, 87
C congenitally corrected minimum standard study,
cardiac output, 241 transposition of great 5, 5 – 8
cardiac resynchronisation, arteries, 181, 182 report organisation, 8 – 9
192 – 193 continuity equation, 241 stress, 32
cardiac ultrasound, 1 continuous wave (CW) signal summary of formulae,
cardiomyopathies mitral regurgitation, 113 240 – 243, 243
arrhythmogenic right mitral stenosis, 104 transoesophageal
ventricle/dysplasia, coronary sinus aneurysm, 164 echocardiogram/
75 – 77, 76, 76 COVID-19, 218, 219, 219 echocardiography, 141,
cardio-oncology, 77 – 79, critical findings, 10, 10 141 – 142
78, 78 ejection fraction, LV, 21, 21
dilated LV, 61 – 65, 64, 65 D endocarditis
hypertrophied LV, 65 – 71, diastolic dysfunction, 11 assessing LV in, 150, 151
67, 70 – 71 heart failure (HFpEF), checking other valves, 151
non-compaction, 74 – 75, 24 – 25, 24, 24 detecting a predisposing
74, 75 diastolic function, LV, 23 – 25, abnormality and,
restrictive, 72, 73, 73, 24, 24 151, 152
72 – 73 dilated cardiomyopathy grading regurgitation,
cardio-oncology, 76, 77–79, 78 (DCM) 151, 152
chemotherapy, 77 – 79, 78, 78 complications, 64, 65 local complication, 149, 150
coarctation, 178, 179, general appearance, 61, 63 Loeffler’s, 226
179, 185 LV size and systolic other imaging
cocaine, 223 function, 61, 62 – 64 modalities, 153
colour flow mapping LV systolic and diastolic transoesophageal
aortic regurgitation, function, 64 echocardiogram/
90 – 95, 91 other imaging modalities, echocardiography,
mitral regurgitation, 110, 64 – 65 152, 152
113 – 114 dilated RV, 35 – 40, 36, 37 – 38 TTE normal despite clinical
comprehensive study, 7 left sided disease and, 40 suspicion of, 152 – 153
congenital heart disease, dissection, aortic. See acute valve destruction, 150, 151
adult, 172, 171 – 172 aortic syndrome vegetations, 149, 150
atrial septal defect (ASD), dP/dt, LV, 22 endomyocardial
171 – 175, 172, 173, drug treatment with cardiomyopathy, 73, 73
174 – 175, 184, 185, 187 dopamine agonists, 226 endomyocardial fibrosis, 73,
coarctation, 177, 178, 179, 73, 226
179, 185 E Energy Loss Index (ELI), 241
congenitally corrected Ebstein’s anomaly, extracorporeal membrane
transposition of great 180 – 181, 180 oxygenation (ECMO),
arteries, 181, 182 echocardiography 230, 231 – 232
Ebstein’s anomaly, after mitral valve repair,
180 – 181, 180 118, 118 F
persistent ductus arteriosus basic scan, 3 – 4, 4 false aneurysms, 31, 32, 32
(PDA), 177 – 178, 177, common requests flow, 241
178, 184, 186 (see general clinical focused study, 4
post-procedure studies, checklists) formulae, summary of,
184 – 187, 185 – 187 comprehensive study, 7 – 8 240 – 243, 243
246
Index
G apical aneurysm, 68 global systolic function,

general clinical checklists vs athletic heart, 70 29 – 30, 29 – 30, 31
arrhythmia, 223 differential diagnosis of hypertrophied,
cocaine, 223 LVOT obstruction, 68 cardiomyopathies and,
drug treatment with vs hypertension, 69, 70 65 – 71, 66, 67, 70 – 71
dopamine agonists, intra-LV or LVOT flow linear cavity dimensions,
appetite suppressants, acceleration, 68 15, 16, 16
and weight loss agent LA size, 68 masses, 205 – 208, 206,
benfluorex, 226 LV systolic and diastolic 206, 208
HIV, 223 function, 67 regional wall motion, 20,
hypereosinophilia, other imaging 20, 21
Loeffler’s endocarditis, modalities, 71 RV dilation and disease of,
endomyocardial pattern of hypertrophy, 66, 67 35 – 37
fibrosis, 226 vs phenocopies, 70, 71 systolic function, 20 – 23,
hypertension, 222 valve assessment, 21 – 23, 22, 23, 26
murmur, 221 70 – 71, 71 volumes, 18 – 20, 19, 19
radiation, 227 wall thickness, 67 wall thickness, 16 – 18,
stroke, TIA, or peripheral hypertrophy, LV, 61, 65 – 66, 17 – 18, 17
embolism, 222 67, 70 – 71 linear cavity dimensions, LV,
suspected heart failure, 222 hypertrophy, RV, 39 15 – 16, 16, 16
systemic inflammatory hypokinetic RV, 37, 37 localised effusion, 210
diseases, 225 hypotension, 215 Loeffler’s endocarditis, 226
TTE abnormalities low-dose dobutamine stress
in neuromuscular I echocardiography, 87, 87
disorders, 224 infective endocarditis, 235 LVOT obstruction, 68, 69
global longitudinal strain infiltrative diseases, 39 lymphoma, 209
(GLS), 22, 23 cardiomyopathy, 73, 73
global systolic function, 29 intra-aortic balloon pump, M
great vessels, masses in, 231, 233 masses
210, 210, 211 attached to valve, 202, 203
L basic characteristics of,
H left atrium (LA), 53 – 54, 53 201, 201
heart failure, suspected, 222 enlargement, 55, 55 extrinsic, 208 – 210,
heart valve clinic high filling pressure, 217 209 – 210
echocardiographic and masses, 208, 208 – 209, 209 in great vessels, 210,
clinical alerts for referral left-sided disease and RV 210 – 211
from, 156 dilation, 40 left or right atrial, 202 – 205,
organisational requirements left ventricle (LV) 203 – 204, 205
for, 155 in acute aortic left or right ventricular,
points to cover in routine syndrome, 167 205 – 208, 206, 207, 208
annual follow-up includes aortic regurgitation, 90 – 96 outside the heart, 208
native and post-repair or cardiac resynchronisation, pericardial, 208
replacement surgery, 158 229 – 230 pericardial cyst, 208 – 209
transthoracic diastolic function, 23 – 24, mechanical ventilation
echocardiography (TTE), 24, 24 effects, 217
155, 158 diastolic heart failure minimum standard study, 5, 5
high filling pressures, 217 (HFpEF), 24, 26, 26 mitral leaflet, 30, 31
human immunodeficiency endocarditis and, 151, 152 mitral regurgitation (MR),
virus (HIV), 223 in focused study, 2 30, 30
hypereosinophilia, 226 function in mitral acute, 115
hypertension, 222 regurgitation, 113 appearance and movement
hypertrophic cardiomyopathy function in pericardial of valve, 106 – 110, 107,
(HCM), 39 effusion, 194 108 – 110, 110
247
Index
assessing, 104 mixed moderate mitral pericardial masses, 208

colour flow mapping, valve disease, 134 pericardiocentesis, 194
111 – 113, 111 – 112 modified Duke clinical criteria peripheral embolism, 222
continuous wave for infective endocarditis, persistent ductus arteriosus
signal, 113 235, 235 (PDA), 177, 177, 178
general steps, 113 murmur, 221 closure of, 185, 186
grading, 114, 115 myocardial infarction, 30 – 31 pleural effusions, 189,
LV function, 113 190, 191
pulsed Doppler, 113 N PR early-diastolic signal, 49
mitral stenosis (MS) neuromuscular disorders, 224 pressure half-time estimation
appearance of valve, non-compaction of mitral orifice area, 241
annulus, and chords, 101, cardiomyopathy, 74 – 75, PR late-diastolic signal, 45
102 – 103 74, 75 prosthetic heart valves
assessing mitral non-infiltrative appearance of valve, 135
regurgitation, 104 cardiomyopathy, 73 colour Doppler, 137,
assessing other valves, 105 Noonan’s syndrome, 39 139, 139
continuous wave signal, 104 complications, 140
examining the right heart, dysfunction of, 140 – 147
P
104 – 105 patent fossa ovalis (PFO), 56, high Vmax:
grading, 104, 104 57, 58 patient-prosthesis
patient has symptoms but pericardial constriction mismatch vs obstruction,
orifice area is greater differentiated from 141 – 142, 142 – 144,
than 1.5 cm2, 105, 105 constrictive 143, 145
planimeter the orifice area, cardiomyopathy, 194, normal values for, 141,
103, 103 194, 196 141 – 142
risk of atrial thrombus, 106 Doppler assessment, 195 other disease, 146
valve suitable for balloon other techniques, 196, 197 paraprosthetic
valvotomy, 104, 104 septal bounce, 195 regurgitation, 144
mitral valve, 30 visual assessment, 194 patterns of normal
in cardiomyopathies, 61 pericardial cyst, 208 regurgitation, 139
echocardiography after pericardial disease regurgitation detected in,
repair of, 118, 119 acute pericarditis, 196 143 – 144, 146
mitral valve disease pericardial constriction, signs of early failure,
mitral regurgitation, 194 – 196, 194 – 195, 141, 141
106 – 114, 107, 108 – 112, 195 – 196, 197 spectral Doppler, 139 – 140
110, 115 pericardial effusion, transoesophageal
mitral stenosis, 101 – 106, 189 – 194, 190, 191, 192, echocardiogram/
101, 102 – 103, 105 192 – 193 echocardiography,
mixed aortic and, 133 pericardial effusion 146, 146
mixed moderate, 133 cause of, 190 types of, 136 – 137, 138
specialist pre- and differential diagnoses, 193 pulmonary artery (PA)
post-operative differentiation between pressure, 40
assessment, 116 – 119, pleural and, 189, confirming and grading, 50
116 – 117, 118, 119 190, 191 estimating, 43 – 45
mixed moderate aortic valve LV function, 194 estimating probability of
disease, 133 pericardiocentesis, 194 pulmonary hypertension
mixed moderate mitral valve size, distribution, and from, 45 – 50, 45, 46 – 48,
disease, 133 characteristics, 49 – 50
mixed valve disease 189 – 191, 190 estimating systolic, 43 – 45,
mixed mitral and aortic tamponade present in, 43 – 44
valve disease, 134 191 – 193, 192, 192, 193 pulmonary embolism, 214
mixed moderate aortic pericardial fluid in acute aortic pulmonary hypertension (PH),
valve disease, 134 syndrome, 167 10, 42
248
Index
assessing probability of, enlargement, 54, 55 stroke volume, 241

45 – 50, 45, 46 – 48, 49 – 50 high filling pressure, 217 stroke work loss, 242
causes of, 49, 49 – 50 masses, 202, 204 – 205, surgery
pulmonary oedema, 215 205, 207 aortic stenosis, indicated on
pulmonary regurgitation, 47, right-sided valve disease TTE, 95 – 96, 95
127, 127, 128 – 129 pulmonary stenosis and appearance of repairs
pulmonary stenosis regurgitation, 126 – 130, after, 119
and regurgitation, 127, 128, 129, 130 balloon valvotomy,
126 – 127, 127 tricuspid regurgitation (TR), 105 – 116, 105 – 106, 130
appearance of valve, 127 121 – 125, 122, 122 – 123, cut points for aortic,
assessing pulmonary 124, 125 164 – 165
artery, 130, 130 tricuspid stenosis (TS), Ebstein’s anomaly,
assessing RV size and 125, 126 180 – 181, 180
function, 130 right ventricle (RV) points to cover in heart
checking level of active or hypokinetic, valve clinic after,
obstruction, 128 37 – 38, 37 158 – 159
factors suggesting, acute coronary syndrome post-procedure studies of
127, 127 and, 30 congenital heart disease,
grading, 127, 130 difference between right 184 – 187, 185, 185 – 187
indications for invasive atrial (RA) and, 43 – 44, in primary mitral
intervention, 130 43 – 44 regurgitation, 116, 116
other techniques, 130 dilated, 35 – 37, 36, 36 – 37 in secondary mitral
pulmonary artery hypertrophy, 39 regurgitation, 116 – 118,
pressure, 128 left-sided disease and, 40 117, 118
pulsed tissue Doppler systolic masses, 205 – 208, 206, tricuspid regurgitation (TR)
velocity, 21, 22, 22 207, 208 and, 124, 125
pulmonary artery pressure valve replacement, 130
R and, 40 suspected heart failure, 222
radiation, 227 shunt, 40 systemic inflammatory
recovered mean pressure size and function in diseases, 225 – 226
gradient in aortic tricuspid regurgitation systemic vascular
stenosis, 242 (TR), 124 resistance, 242
reports size and systolic systolic function, LV, 20 – 23,
escalation for urgent clinical function in pulmonary 20, 21 – 23, 22 – 23
advice based on, 10, 10 hypertension, 49 acute coronary syndrome
non-echocardiographer systolic function and, 29
understanding of, 10 – 11, quantification, 38, 38, 38 cardio-oncology, 77 – 78
11 – 12 tricuspid and pulmonary systolic function, RV, 38 – 39,
organisation of, 8 – 9 regurgitation, 40 38 – 40, 38
restrictive cardiomyopathy, cardio-oncology, 77 – 78
72 – 74, 73, 73 S in pulmonary
differentiated from sequential segmental hypertension, 49
pericardial constriction, approach to congenital systolic pressure, pulmonary
194, 194, 196 heart disease, 181 – 184, artery (PA), 45
right atrial (RA) pressure 182, 184
difference between right shunt, RV, 40 T
ventricular (RV) and, shunt calculation, 242, 242 Takotsubo cardiomyopathy,
43 – 44, 43 – 44 storage diseases, 39, 66 29, 30
estimating, 44 stress echocardiography, tamponade, 191 – 193, 192,
size and systolic 32 – 33 192, 193
function in pulmonary low-dose dobutamine, 87, 87 tetralogy of Fallot, 185,
hypertension, 49 stroke, 222 186 – 187
right atrium (RA), 54, 54 stroke distance, 21 – 22 thoracic aortic aneurysm, 165
249
Index
tissue Doppler imaging (TDI), cardio-oncology, 77 tricuspid stenosis (TS), 125, 126
38, 38 complications after true aneurysms, 31, 32,
total VA (ventriculo-aortic) myocardial infarction 32, 34
impedance, 242 after, 31
transcatheter valve (TAVI) endocarditis and, 152, 153 V
workup, 89, 90 minimum standard study, valve disease, 234 – 239,
transient ischemic attack 5–7 234 – 239
(TIA), 222 pericardiocentesis, 194
vegetations, endocarditis,
transoesophageal trauma, blunt or
149, 150
echocardiogram/ penetrating, 216
velocity time integral, 21 – 22
echocardiography (TOE) tricuspid annular plane
ventricular assist device
endocarditis, 152 – 153, 153 systolic excursion
(VAD), 231, 232 – 233
prosthetic heart valves, (TAPSE), 38, 38
ventricular septal defect
140, 140 tricuspid regurgitation
(VSD), 174, 174 – 176, 176
transthoracic (TR), 40
closure, 184, 186
echocardiography (TTE), appearance and movement
volumes, LV, 18 – 20, 19, 19
1 – 2, 2 of valve, 121, 122, 122
abnormalities in echocardiography and
neuromuscular surgery, 124 – 125, 125 W
disorders, 224 estimating pulmonary wall thickness, LV, 16 – 18,
aortic valve surgery artery pressure, 124 17 – 18, 17
indicated on, 89, 89 grading, 121, 123 weight loss agents, 226
cardiomyopathies and, 61 RV size and function in, 124 Wilkins score, 234, 234
250

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Echocardiography

This book sets echocardiography within a routine clinical context. It aims

Camelia Demetrescu BSc, MSc, HSSE

Sandeep S Hothi MA, PhD, FRCP, FACC, FBSE, FESC

John Chambers MD, FESC, FACC

and by CRC Press

CRC Press is an imprint of Taylor & Francis Group, LLC

© 2024 Camelia Demetrescu, Sandeep S Hothi and John Chambers

ISBN: 978-1-032-15160-1 (hbk)

1 Defining the Study 1

2 Left Ventricular Dimensions

3 Acute Coronary Syndrome 29

4 The Right Ventricle 35

5 Pulmonary Pressure and Pulmonary

6 The Atria and Atrial Septum 53

8 Aortic Valve Disease 81

9 Mitral Valve Disease 101

10 Right-Sided Valve Disease 121

11 Mixed Valve Disease 133

12 Prosthetic Heart Valves 135

14 The Heart Valve Clinic 155

15 The Aorta and Dissection 161

16 Adult Congenital Heart Disease 171

17 Pericardial Disease 189

20 General Clinical Requests 221

This book sets echocardiography within a routine clinical context. It aims

How We Handled Guidelines and Data

Camelia Demetrescu, BSc, MSc, HSSE, is Consultant Clinical

Sandeep S Hothi, MA, PhD, FACC, FBSE, FESC, FRCP, is

John Chambers, MD, FRCP, FESC, is Emeritus Professor of Clinical

The information in this book is based on a synthesis of data and guidelines

The ALERT icon flags up points to be particularly aware of or mistakes to

A point requiring discussion in an individual patient with integration into the

AF atrial fibrillation LV left ventricle/ventricular

RVEDV RV end-diastolic volume TS tricuspid stenosis

Basic scan—can be performed with a handheld device with colour by an

a comprehensive study is more appropriate for a patient with a family

Figure 1.1 Choosing the level of echocardiogram.

The Basic Scan

● The result is classified as:

● Requiring higher-level TTE (which can often be done immediately if

Figure 1.2 A template showing views for the basic echocardiogram.

● A suggested aide-memoire is given in Figure 1.2, but individual laboratories

The Focused Study

● RV tissue Doppler S′ velocity, TAPSE, and TR Vmax in sickle cell disease, in

● LV measurements to estimate LV mass in hypertension10.

The Minimum Standard Study

● Reduce the risk of missing significant abnormalities.

● Minimise inter- and intra-observer variability and enable accurate

● Clinically important measurements should be included in the text of the report.

Table 1.2 Minimum standard adult transthoracic echocardiogram (TTE)

View Essential imaging modalities**

Table 1.2 Minimum standard adult transthoracic echocardiogram (TTE)

View Essential imaging modalities**

Table 1.3 Minimum measurements for standard adult TTE protocol

The Comprehensive Study

Table 1.4 Views and measurements or descriptions as add-ons to the

Table 1.4 Views and measurements or descriptions as add-ons to the

● Information regarding echocardiographic machine, type of image

● A good-quality ECG trace for heart rate and rhythm.

1 Defining the Study 1

2 Left Ventricular Dimensions

3 Acute Coronary Syndrome 29

4 The Right Ventricle 35

5 Pulmonary Pressure and Pulmonary

6 The Atria and Atrial Septum 53

8 Aortic Valve Disease 81

9 Mitral Valve Disease 101

10 Right-Sided Valve Disease 121

11 Mixed Valve Disease 133

12 Prosthetic Heart Valves 135

14 The Heart Valve Clinic 155

15 The Aorta and Dissection 161

16 Adult Congenital Heart Disease 171

17 Pericardial Disease 189

20 General Clinical Requests 221