Echo

Facts
Includes over 480 illustrations and more than
180 online video examples

Georg Goliasch & Thomas Binder

Wien 2014

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 First Edition, August 2014
Copyright (c) 2014
123sonography gmbh
Tuchlauben 7/7, A-1010 Vienna Austria
w: www.sonography.com
m: office@123sonography.com

Authors: Thomas Binder, MD, Georg Goliasch, MD, PhD

Layout/Print: Karin Dreher, Inge Vorraber,
Copy and language editing: Sujata Wagner
ISBN: 978-3-903013-01-8

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, recording or any information storage and retrieval sys-
tem, without permission in writing by the publishers/authors.

All illustrations and images are property of 123sonography GmbH, Vienna and copyright protected.

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 Foreword

This book has evolved from a simple companion syllabus for our 123sonography Masterclass to
a textbook that now stands on its own. Our users’ feedback revealed that while learning online
is highly effective, it is equally important to have a hardcopy book in your hands. Having a
compendium version online was very important because it enabled us to collect our users’
feedback. The latter was of paramount importance in writing this book.

As the title of the book implies, we provide relevant facts that you need to know if you are
practicing echocardiography and wish to go beyond. We have included chapters on stress
echo, contrast echo, 3D echo, and deformation imaging.

We used as little text as possible, listing the contents in tabular form so that the book can be
viewed as a study guide and a reference book. We took care to include all relevant reference
values, formulas, and checklists that will help in your daily practice. The book is richly illustrated:
it contains more than 300 figures, most of which have been taken from our online 123sonogra-
phy.com Masterclass course. Importantly, we have included many practical notes on how to
image. These will help to improve your imaging skills and, ultimately, your diagnostic yield.
The book may also be viewed as an atlas of echocardiography. In contrast to our workbook, we
have incorporated more than 180 echo examples. The cine videos are available on the web
(http://123sonography.com/echofacts). After all, how else can you learn echocardiography than
by viewing images of the moving heart?

Our 123sonograpahy echo project has grown tremendously since we launched the website
over three years ago. We have become very attached to our users and friends.
We hope this book will serve as a step forward towards our goal of improving the quality of
echocardiography in all parts of the world and making you a better echocardiographer.

Thomas Binder Georg Goliasch

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 Acknowledgments

Collecting the large number of images for this book was a joint effort on the part of all the
people working at our lab. The book would not have been possible without the assistance of
our sonographers Beatrix Buschenreithner, Ulrike Grojer, Regina Schlossnickel, and Andrea
Schuckert, and many of our residents who were always on the lookout for suitable loops and
cases. We are sure they will recognize many of their contributions.

Bernhard Richter was responsible for the corrections and improvements made while publishing
this version of the book. Bernhard possesses the rare skills needed to edit a book from the
perspective of an expert as well as a student. His efforts had a tremendous impact on its quality.

Thanks to Sujata Wagner for her reliability and hard work. She converted many of our awkward
Germanic phrases into fluent and comprehensible English.

To Oliver Hübler for his support and programming, which permitted us to put up the web-ba-
sed atlas that complements this book. No programming hurdle is insurmountable for him.

Saskia Erbschwendner who collected, sorted, and categorized all the user feedback that was so
valuable to us. And for setting us up so that the work could actually go into print.

Georg Greutter, “the man on the drums”, for paving the way in planning and marketing the
book. He transformed us into a publishing company.

Karin Dreher and Inge Vorraber, who enthused the book with life. They are responsible for its
unique style, layout, and graphics.

Thanks to our mentors and supporters: Helmut Baumgartner, Massoud Zangeneh, Gerald
Maurer, Partho Sengupta and Senta Graf. They taught us much of the knowledge that we now
share with you.

Most of all, our thanks to the many users who provided us with their valuable feedback, and
those who are embarking on this fruitful and rewarding journey of learning echocardiography.

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 Free Access to the Videos at
123sonography.com/echofacts

Echo Atlas

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 Content
001 // PRINCIPLES OF ECHOCARDIOGRAPHY
10 Physics of Ultrasound
11 2D Images
13 Artefacts
15 Optimizing 2D Images
15 MMode
16 Spectral Doppler
17 Flow Dynamics
18 Color Doppler

002 // HOW TO IMAGE

22 How to Move the Transducer
22 Imaging Windows
28 Image View

003 // HEART CHAMBERS AND WALLS

30 The Left Ventricle
32 LV Function
34 The Right Ventricle
37 The Left Atrium
40 The Right Atrium
41 Left Ventricular Hypertrophy

004 // DIASTOLIC FUNCTION

46 Basics of Diastolic Dysfunction
51 Specific Situations

005 // DILATED CARDIOMYOPATHY

54 Background
54 Echo Features
55 Specific Forms

006 // HYPERTROPHIC CARDIOMYOPATHY

60 Basics
61 Echocardiographic Evaluation

007 // RESTRICTIVE CARDIOMYOPATHY

66 Basics
67 Specific Forms

008 // CORONARY ARTERY DISEASE

70 Segmental Approach
72 Wall Motion Abnormalities
76 Patterns of Myocardial Infarction
77 Complications

009 // AORTIC STENOSIS

82 Basics
85 Quantification of Aortic Stenosis
88 Special Circumstances
89 Sub- and Supravalvular Aortic Stenosis
90 Indication for Aortic Stenosis Surgery/Intervention

010 // AORTIC REGURGITATION

94 Basics
97 Hemodynamic Calculation of Regurgitant Volume and Fraction
97 Proximal Isovelocity Surface Area (PISA) Method
98 Acute Aortic Regurgitation
98 Indications for Surgery in Severe AR (ESC 2012)

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 Content
011 // MITRAL STENOSIS
100 Introduction
102 Quantification
103 Mitral Valve Pressure Half-Time
104 Valvuloplasty

012 // MITRAL REGURGITATION

108 Basics
108 Quantification of Mitral Regurgitation
111 Mechanisms of Mitral Regurgitation
116 Mitral Valve Prolapse
117 Flail Leaflet
117 Other Causes of Mitral Regurgitation
118 Indication for Surgery

013 // TRICUSPID VALVE DISEASE

122 Basics
122 Causes of Tricuspid Regurgitation
124 Quantification of Tricuspid Regurgitation
125 Tricuspid Stenosis

014 // PROSTHETIC VALVE

128 Types of Valves
129 Echo Assessment of Prosthetic Valves
133 Complications
137 Mitral Valve Repair

015 // ENDOCARDITIS
140 Principles of Endocarditis
141 Native Valve Endocarditis
143 Complications of Native Valve Endocarditis
145 Right Heart Endocarditis
145 Prosthetic Valve Endocarditis
146 Pacemaker/Polymer-Associated Endocarditis
147 Non-Infective/Abacterial Endocarditis
148 Indications for Surgery

016 // RIGHT HEART DISEASE

150 Basics of Pulmonary Hypertension
152 Echo Assessment of Pulmonary Hypertension
155 Disease of the Right Ventricle
155 Right Ventricular Infarction
156 Right Ventricular Hypertrophy
156 Arrhythmogenic Right Ventricular Dysplasia

017 // AORTIC DISEASE

160 Imaging of the Aorta
161 Basics
161 Aortic Aneuryms
164 Aortic Dissection
167 Aortic Coarctation (CoA)

018 // PERICARDIAL DISEASE

170 The Pericardium
170 Pericardial Effusion
173 Pericardial Tamponade
175 Pericardial Constriction
176 Other Diseases of the Pericardium

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 Content
019 // TUMORS AND MASSES
180 Pseudotumours
181 Masses

020 // CONGENITAL HEART DISEASE

188 Basics
188 Atrial Septal Defect (ASD)
191 Patent Foramen Ovale (PFO)
192 Ventricular Septal Defects (VSD)
194 Patent Ductus Arteriosus (PDA)
195 Coronary Fistulas
196 Tetralogy of Fallot
197 Transposition of the Great Arteries

021 // STRESS ECHOCARDIOGRAPHY

202 Indications and Echocardiographic Features
203 Clinical Targets of Stress Echocardiography and Stress of Choice)
204 Stress Echocardiography – an Easy Approach
206 Stress Echo and “Other Echo Modalities”
207 Ischemia Testing
208 Viability Testing
209 Stress Echo in Low-Flow Low-Gradient Severe Aortic Stenosis

022 // CONTRAST ECHOCARDIOGRAPHY

212 Principles
213 Contrast Agents
215 Applications of Echo Contrast
216 Right Heart Contrast
219 Quantification of Left Ventricular Function
221 Myocardial Perfusion Imaging

023 // 3D ECHOCARDIOGRAPHY
224 Basics of Three-Dimensional Echocardiography
224 Forms of 3D Echocardiography
227 3D Image Acquisition
227 Clinical Applications of 3D Echocardiography

024 // MYOCARDIAL DEFORMATION IMAGING

236 Principles of Myocardial Mechanics
236 Measures of Myocardial Deformation
238 Tissue Doppler Imaging
241 Speckle Tracking Echocardiography
247 Clinical Applications of Myocardial Deforming Imaging

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 001 //
Principles of Echocardiography

CONTENTS
10 Physics of Ultrasound

11 2D Images

13 Artefacts

15 Optimizing 2D Images

15 MMode

16 Spectral Doppler

17 Flow Dynamics

18 Color Doppler
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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES PHYSICS OF ULTRASOUND

The higher the ultrasound Ultrasound Wave

frequency, the better the
resolution. However, you lose
penetration.

Wave propagation occurs through The velocity of ultrasound is 1540 m/s in

compression and decompression of tissue and 1570 m/s in blood.
tissue.

Medical Ultrasound

Frequencies between 2 – 10 MHz are used.

SEND RECEIVE

Alternating current applied to piezoelec- Received ultrasound waves (echoes)

tric crystals generates ultrasound waves.. cause the piezoelectric crystals to
generate an electric signal which is
transformed into an image..

Diagnostic ultrasound Safety of Ultrasound

has no adverse effects.
Physical effects of ultrasound:
• Thermal effect (depends on US intensity)
• Cavitations

The higher the pulse Ultrasound Pulse

repetition frequency, the
higher the frame rate and
image resolution.

Pulse Pulse repetition period

The higher the US frequency, the higher the pulse repetition frequency.

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

2D IMAGE NOTES

2D Image Ultrasound is a cut-plane

technique. Several elements
are used to generate a 2D
image.

Types of Probes In echocardiography we use

curvilinear probes. The
advantage of such probes is
their small ”footprint”. Thus,
it is easier to image from
small intercostal spaces.

Image quality increases with

higher scan line densities.

Image Quality

What determines overall resolution?

• Spatial resolution – lateral • Contrast resolution

• Spatial resolution – axial • Temporal resolution

Determinants of Spatial Resolution

Lateral resolution Axial resolution

Beam width/line density Ultrasound frequency

Ultrasound frequency Pulse repitition frequency

Gain Gray

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES 2D IMAGE

Harmonic imaging Harmonic Imaging

uses the resonance
characteristics of
tissue. The advantage
is less artefacts,
improved spatial and
contrast resolution, SEND
” RECEIVE
leading to better
image quality. Legend: The signal returned by tissue includes the transmitted
”fundamental” frequency as well as signals of other frequencies. In harmonic ima-
ging one uses those frequencies that are a multiple (harmonic) of the fundamental
(sending) frequency.

Aim for high frame Frame Rate – Influence

rates. They allow the
study of rapid motion The frame rate describes the number of frames/sec that are displayed.
when using the image Frame rate depends on:
review function.
• Sector width • Frequency
• Scan lines • Depth

Limitations of 2D Imaging

• Attenuation • Limited penetration (obesity, narrow

• Tissue properties (fibrosis, calcification) imaging window)
• Artefacts

Attenuation

Definition: Decrease in amplitude and intensity as the ultrasound wave travels

through a medium

Attenuation may be caused by:

• Absorption (proportional to frequency) • Reflection
• Refraction • Shadowing
• Transfer of energy from the • Pseudoenhancement
beam to tissue

Enemies of Ultrasound
Air (reflection of ultrasound) and bone (absorption of ultrasound)
In both conditions you cannot see what is behind.

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

ARTEFACTS NOTES

Types of Artefacts Imaging is difficult in patients

with small intercostal spaces
• Near field clutter • Side lobe artefact (bone) and in patients
• Reverberation • Beam width artefacts with COPD (air).
• Acoustic shadowing • Attenuation artefacts
• Mirror imaging/double images (caused by refraction)

REVERBERATION –
apical four-chamber view/2D

Highly echogenic pericardium

leading to reverbations

Specific Forms

Side lobes Reverberation

Side
Main lobe lobe

Side lobes usually occur at strong Reverberation occurs when the echo
reflectors (e.g. prosthetic material). Power bounces back and forth several times
density is higher in the central beam than – sometimes between a structure and
in side lobes. This may lead to the edge the surface of the transducer.
effect, which makes structures appear
wider than they actually are.

Beam width artefact

US beam

Beam width artefacts occur

when the beam width is wide
Image and unfocused.
Wide Narrow

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES ARTEFACTS
GAIN SETTINGS – PSAX/2D

Different gain settings in the

same patient. Structures are
missed when gain settings are
too low (upper left). Delineation
of different gray scales (tissue
characteristics) is impaired when
the gain is set to high
(lower right).

Artefacts are When Do Artefacts Occur?

inconsistent.
• Good image quality (e.g. mirror artefacts) • Strong reflectors (e.g. calcification,
• Poor image quality prosthetic material)
• More frequent in fundamental imaging

ARTEFACT IN PROSTHETIC VALVE

– apical four-chamber view/2D

Shadowing and reverberations of

the left atrium caused by a me-
chanical mitral valve prosthesis.

Tips to Avoid Artefacts

• Know the pitfalls • Be cautious of strong reflections

• Know the anatomy • Use multiple views

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

OPTIMIZING THE 2D IMAGE NOTES

Important Settings Know your echo
• Gain • Depth machine!
• Time gain compensation (TGC) • Imaging frequency
• Sector width • Focus

Post-Processing Use predefined settings for

specific situations (i.e. patients
• Gray scale • Compression who are difficult to examine)
• Contrast • Color maps and for specific modalities (i.e.
standard echo, contrast).

COLOR MAPS – PSAX/2D

Different 2D color maps for

individualized 2D display.

MMODE

MMode MMode has lost much of its

importance, but is still
Advantage Where is it used? valuable in certain situations.
• High temporal resolution • Aorta/left atrium (measurements,
• Good for certain measurements opening of the aortic valve)
• Allows measurement of time intervals • Left/right ventricle (measurements,
• Timing of events LV function)
• Mitral/prosthetic valve (type of valve)
• Endocarditis (motion of suspected
vegetation)
• Tricuspid annular plane systolic
excursion (TAPSE) for RV function
RV
• Mitral valve (mitral stenosis)
IVS
• Mitral valve annular excursion (MAPSE)
for longitudinal LV function
Post. • Display of mid-systolic notching
wall
(flying W) of the posterior pulmonary

Diastole Systole valve cusp

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES MMODE

Other Forms of MMode

Anatomical MMode Freedom of axis

Anatomical MMode

Color Doppler MMode Timing of flow (i.e. flow

propagation)

Tissue Doppler MMode Myocardial function,
timing of events

Curved MMode Functional information along Conventional MMode

a variable MMode line

SPECTRAL DOPPLER

The measured velocity

Doppler Formula
greatly depends on the angle
between blood flow and the
v cos
d = 2f
ultrasound beam. Always try c 0
to be as parallel to blood
flow as possible. Use color d = frequency alteration between The Doppler formula allows us
Doppler to visualize the S and E (=Doppler shift)(Hz) to calculate velocities (i.e.
direction of flow. f0 =  transmitting frequency (Hz) blood and tissue), based on
v = blood flow (m/s) the Doppler shift between the
c =  sound propagation send and the receive signal.
velocity (1550 m/s)
 = Doppler irradiation angle

Doppler

Pulsed wave (PW) – Doppler Low velocity (< approx. 1.5 m/s) (site specific)

Continous wave (CW) – Doppler High velocity (> approx. 1.5 m/s) (site unspecific)

Tissue Doppler Lower velocity, higher amplitdue

Aliasing will occur when blood Doppler Aliasing

flow velocity exceeds the
Nyquist limit. The Nyquist limit Depends on
is equal to a half of the pulse • Depth • Width of sample volume
repetition frequency. Use the • Velocity • Doppler frequency
baseline shift to ”stretch” the
Nyquist limit.

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

SPECTRAL DOPPLER NOTES

PW DOPPLER ALIASING – apical
four-chamber view/PW MV

Pulsed-wave Doppler in a patient

with mitral stenosis. The maxi-
mum velocity exceeds 2.5 m/s
and exceeds the aliasing limit.
Velocity profiles are noted both
above and below the zero line.

Tissue Doppler Imaging Tissue Doppler is

angle dependent.
Information
• Myocardial velocity • Strain PW spectral tissue Doppler
• Displacement • Strain rate measures deformation and
velocities at a specific site
(within the sample volume).

TISSUE DOPPLER – apical

four-chamber view

Tissue Doppler color display of

the heart during early systole.
Red indicates myocardial motion
towards the transducer.

FLOW DYNAMICS

Bernoulli Equation
The simplified Bernoulli equation permits
easy estimation of pressure gradients P(mmHg)
from velocities.
V(m/s) P = 4xV2

P(mmHg)

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES FLOW DYNAMICS

Where Can You Apply the Bernoulli

Equation in the Heart?

Direct applications (gradients) Indirect applications (pressure decay)

Valvular stenosis Aortic regurgitation quantification

Defects (i.e. VSD, coarctation, PDA) Diastolic function (deceleration time)

Tricuspid regurgitation signal (sPAP) dP/dt (contractility)

Prosthetic valves Mitral stenosis (pressure half-time method)

Sites where Gradients can be measured.

COLOR DOPPLER

The manner of displaying Color Encoding

flow, flow velocities or
turbulant flow is determined Flow towards the transducer is coded in red, and flow away
by the color map. Most from the transducer in blue.
scanners allow you to
change the color map.
Check your machine setings.

towards + 62 m/s

away - 62 m/s

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

COLOR DOPPLER NOTES

Color Doppler and Aliasing The phenomenon of

aliasing provides good
Once the Nyquist limit is reached, the color changes abruptly delineation of jets
(red to blue, or blue to red). The color Doppler display will show (e.g. PISA).
a mosaic pattern. Some color maps also display variants of velocity
in green (high variants in velocities indicate turbulent flow).

COLOR DOPPLER ALIASING–

apical four-chamber view/
Flow towards the transducer Color Doppler
turbulant/high velocity
lower velocity flow– green Patient with mitral stenosis. The
color Doppler of mitral valve
inflow shows the typical pattern
of a high velocity jet. Red color
Aliasing border
denotes the direction of flow
(from orange to blue) towards the transducer. The sud-
den change from yellow to blue
depicts the region where aliasing
Flow towards occurs.
the transducer higher
velocity (orange)

Flow towards the

transducer
low velocity (red)

Color Doppler Frame Rate Always aim for a high color

Doppler frame rate.
• Scan line density
• Emphasis (2D vs. color) Try to use the same settings for
• Sector width (2D) quantification of regurgitation in
• Sector width (color) all patients (maps, aliasing limits,
• Pulse repetition frequency color gain).
• Depth

19

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 001 // PRINCIPLES OF ECHOCARDIOGRAPHY

NOTES

20

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 002 // How to Image

CONTENTS
22 How to Move the Transducer
22 Imaging Windows
22 Image View
28 Abbreviations
21

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 002 // HOW TO IMAGE

NOTES HOW TO MOVE THE TRANSDUCER

Use enough
ultrasound gel.

Displacement Rotation Angulation

IMAGING WINDOWS

Suprasternal
Use as many views as Parasternal 2nd–4th intercostal space R L

possible, including left sternal border

atypical views. Always
image so that the Apical 4th – 5th intercostal space,
pathology of interest lateral Right parasternal Left parasternal
is seen best.
Subcostal Below xiphoid

Right parasternal 2nd–4th intercostal space,

right sternal border Apical

Suprasternal Suprasternal notch Subcostal

IMAGE VIEW

Parasternal Long-Axis Views

RV

AV
Ao
LV
MV
AMVL
LA

Parasternal
long-axis view

RV
Anterior

Posterior TV

Right
parasternal long axis

22

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 002 // HOW TO IMAGE

IMAGE VIEW NOTES

Parasternal Short-Axis Aiews

RV

RA RC
AC
LC
PA
LA

l-PA
r-PA
Parasternal short
axis – base

Move down one intercostal

space to obtain good image
quality and a “more“ spherical
RV (round) configuration of the

MV distal parts of the left

ventricle.

Parasternal short axis –

mitral valve

PM
PMPM AL
PM

Parasternal short axis

– mid-ventricle

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 002 // HOW TO IMAGE

NOTES IMAGE VIEW

Use a medial position (A) to Apical Views Rotate counterclockwise

visualize the lateral wall of the
LV and a lateral position (B) to
visualize the RV. RV LV LV LV
RV
TV MV MV AV
MV
LA Ao
LA
RA LA

4-chamber view 2-chamber view 3-chamber view

The orientation of the

septum indicates
whether you are in
lateral or medial
position relative to the
true apex. Use all views
to fully examine all Parasternal Parasternal Parasternal
approach approach approach
aspects of the left and
right ventricle. A B

Four-chamber view Two-chamber view Three-chamber view

Orientation of the Apical Views

Four-chamber view

Three-chamber view
Two-chamber view

24

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 002 // HOW TO IMAGE

IMAGE VIEW NOTES

Five-chamber view The five-chamber view shows

the anterior portions of the
LV interventricular septum.

RV LVOT

Ao
RA LA

Avoid foreshortening; place

Coronary sinus view the transducer as lateral and
caudal as possible.

RV LV

RA CS
RL – PV
LL – PV
RU – PV
LA LU – PV

Subcostal Views
Abdominal gas may
Subcostal four-chamber view obscure the apex on
the subcostal view.

LIVER

RV
RA LV

LA

In some patients it
Inferior vena cava view (rotate counterclockwise) may be possible to see
the superior vena cava
on this view.
LIVER
IVC

RV
RA

LA

SVC

25

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 002 // HOW TO IMAGE

NOTES IMAGE VIEW

Obtain subcostal Subcostal short-axis view (rotate clockwise)

views in all patients.

RV
RA
Ao PA

ry
ry

te
te

ar
ar
The suprasternal view allows Suprasternal View

tid
y

lic
er

ro
t

ha
ar

ca
you to detect coarctation, a

ep
an

on
oc
persistent Botalli‘s duct, or vi

m
a

hi
cl

m
ac
b

co
aortic dissection, as well as su

Br

ft
t
ef

Le
quantify retrograde flow in L
the aorta (aortic
regurgitation). r-PA
Asc Ao

Desc Ao
Suprasternal view

MMode – LA is measured in MMode MMode aorta/left atrium

its largest extension at end
systole. The dimensions of
the aorta are measured at
end diastole, shortly before AO

the aortic valve opens.

LA

MMode left ventricle

Measure the end-diastolic

diameter where the LV is RV
IVS
largest, shortly before
LV
contraction starts (beginning Posterior Wall
of the QRS complex).

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 002 // HOW TO IMAGE

IMAGE VIEW NOTES

Reference Values – MMode

Aorta (mm) < 40 LVEDD (mm) 42 – 59

Left atrium (mm) 30 – 40 Posterior wall (mm) 6 – 10

IVS (mm) 6 – 10 Fractional shortening (%) > 25

Tricuspid Annular Plane MAPSE (longitudinal

Systolic Excursion (TAPSE) > 16 mm LV function) > 12 mm

Reference Values – Doppler

Aortic valve velocity (m/sec) CW 0.9 – 1.7

LVOT velocity (m/sec) PW < 1.3

Pulmonary valve velocity (m/sec) CW 0.5 – 1.0

Tricuspid valve PW 0.3 – 0.7

Tricuspid regurgitation (m/sec) CW 1.7– 2.3

E wave (m/sec) PW < 1.3

Mitral annulus e‘ (cm/sec) TDI PW 0.8 – 1.3

Right ventricular lateral wall (cm/sec) TDI PW 12.2 (41 – 60a)/

10.4 (>60a)

Color Doppler Optimize the 2D image

before using color
• Optimize the 2D image before you use color Doppler Doppler.
• Look for aliasing to detect jets
• Reduce pulse repetition frequency (PRF) to detect low velocity
flow (e.g. ASD, PFO)
• Use higher frame rates
• Use multiple views
• Use color flow as a guide for CW/PW sample volume

27

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 002 // HOW TO IMAGE

NOTES ABBREVIATIONS

AC = acoronary cusp
AL = anterolateral papillary muscle
Ao = aorta
Asc Ao = ascending aorta
AV= aortic valve

CS= coronary sinus

Desc Ao = descending aorta

IVC = inferior vena cava

IVS = interventricular septum

LA= left atrium

LC= left-coronary cusp
LL-PV = left-lower pulmonary vein
l-PA= left pulmonary artery
LU-PV= left-upper pulmonary vein
LV = left ventricle
LVOT = left ventricular outflow tract

MV = mitral valve

PA = Pulmonary artery
PM= posteriomedial papillary muscle

RC = right-coronary cusp
RL-PV= right lower pulmonary vein
r-PA = right pulmonary artery
RU - PV= right upper pulmonary vein
RV= right ventricle

SVC = superior vena cava

TV = tricuspid valve

28

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 003 // Heart Chambers and Walls

CONTENTS
30 The Left Ventricle

32 Left Ventricular Function

34 The Right Ventricle

37 The Left Atrium

40 The Right Atrium

41 Left Ventricular Hypertrophy

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 003 // HEART CHAMBERS AND WALLS

NOTES THE LEFT VENTRICLE

Only use MMode values when Quantification of LV Diameter

your line of interrogation is PLAX MMODE Four-chamber
perpendicular to the LV cavity view
and walls.

IVS RV

Measure distances LVEDD

between the endocardial PW

borders, not the

pericardium (lateral).

LEFT VENTRICULAR DIAMETER –

apical four chamber view/2D
Endocardial border
The endiastolic diameter of the
left ventricle (LVEDD) is measured
from the lateral to the septal bor-
der of the endocardium between Epicardial border
the tips of the mitral valve and
the papillary muscle at end dias-
tole. If a septal bulge is present,
LVEDD
measure more basally.

Left Ventricular End-Diastolic (LVED)

There must be Diameter – Reference Values
agreement between
M-Mode and 2 D
measurements in Normal (mm) 42 – 59 39 – 53
regard of LV size.
Mild (mm) 60 – 63 54 – 57

Moderate (mm) 64 – 68 58 – 61

Severe (mm) ≥ 69 ≥ 62 ESC/ASE 2005

Normal chamber size LVED Diameter/Body Surface Area (BSA) – Reference Values
increases with body
surface area
(and body size). Normal (cm/m2) 2.2 – 3.1 2.4 – 3.2

Mild (cm/m2) 3.2 – 3.4 3.3 – 3.4

Moderate (cm/m2) 3.5 – 3.6 3.5 – 3.7

Severe (cm/m2) ≥ 3.7 ≥ 3.8 ESC/ASE 2005

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 003 // HEART CHAMBERS AND WALLS

THE LEFT VENTRICLE NOTES

LV End-Diastolic Volume (4-chamber view) – Volume measurements are

Reference Values superior to diameter and
area measurements.

Normal (mL) 67 – 155 56 – 104

Mild (mL) 156 – 178 105 – 117

Moderate (mL) 179 – 200 118 – 130

Severe (mL) ≥ 201 ≥ 131 ESC/ASE 2005

SIMPSON METHOD – apical

LV end-diastolic volume four-chamber view/2D

Tracing of the endocardial bor-

Papillary muscle der in end-diastole to quantify
end-diastolic volume (LVEDV).
For biplane quantification,
be sure that the length of the
ventricle matches on the four-
and two-chamber view.

LV Systolic Volume (4-chamber view) – Reference Values Do not trace the papillary
muscles. Their volumes
should be included in the
Normal (mL) 22 – 58 19 – 49 calculation.

Mild (mL) 59 – 70 50 – 59

Moderate (mL) 71 – 82 60 – 69

Severe (mL) ≥ 83 ≥ 70 ESC/ASE 2005

Pathophysiology A reduction of
longitudinal function is an
Principles of LV Function: early marker of LV
Factors influencing ejection fraction/stroke volume dysfunction.

contractility shape preload afterload

myocardial mechanics

stroke volume

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 003 // HEART CHAMBERS AND WALLS

NOTES THE LEFT VENTRICLE

Contractility, preload and Pathophysiology of LV Failure:

afterload influence myocardial Cascade and Compensatory Mechanisms
function. A reduction in
contractility is initially reduction in compensation
compensated by activation of contractility
the sympathetic nervous system sympathicus
stroke stroke
(compensatory increase in heart increased
volume volume
rate and contractility) as well as preload
(exercise) (at rest)
dilatation of the left ventricle. dilatation
Stroke volume is kept adequate increased
at rest, but cannot adapt to afterload
exercise (reduced functional
reserve). In end-stage heart
failure, stroke volume is also
reduced at rest
(decompensation).

LEFT VENTRICULAR FUNCTION

LV function and Parameters of LV Function

(longitudinal) contractility
may be reduced despite a • Fractional shortening • Contractility (dp/dt)
”normal” ejection fraction, • Cardiac output/index • Stroke volume
especially in patients with • ”Eyeballing” of LV function • Tei index
small ventricles. • Deformation parameters • TDI velocity of the myocardium
(strain, strain rate) • MAPSE (mitral annular plane
• Ejection fraction (EF) – Simpson method systolic excursion)

Fractional shortening is a Fractional Shortening – Reference Values

rough estimate of global left
ventricular function. Do not
use the Teichhholz formula
to derive the ejection Normal 25 – 43% 27 – 45%
fraction from these values.
Mild 20 – 24% 22 – 26%

Moderate 15 – 19% 17 – 21%

Severe ≤ 14% ≤ 16% ESC/ASE 2005

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 003 // HEART CHAMBERS AND WALLS

LEFT VENTRICULAR FUNCTION NOTES

Fractional Shortening – Contraindications In these settings, fractional

shortening cause
• LBBB/dyssynchrony/pacemaker • Poor image quality overestimation or
• Abnormal septal motion • ”Pseudo-shortening” of the underestimation of left
• Regional wall motion abnormalities LV (very small ventricle) ventricular function.
• Inadequate (oblique) MMode orientation

MMode LEFT BUNDLE BRANCH BLOCK

LV AV
– PLAX/Mmode
AMVL
Mmode image of the left
ventricle displaying dys-
synchrony in the left bundle
branch block. Early systolic
inward motion occurs
dissociated from the motion of
the posterolateral wall. It is not
possible to define end-diastole
and end-systole to determine
fractional shortening. Increase
your sweep speed to best
visualize dyssynchrony of the
septum. Tissue Doppler imaging
may be helpful to delineate the
time of contraction.

Ejection Fraction – Simpson Method 1) Ejection fractions tend

to be higher in small
Normal > 55 % ventricles. 2) Athletes often
have ejection fractions in the
Mild 45 – 54 % EDvol – ESvol low normal range.
EF = x 100 3) Ejection fraction does not
EDvol
Moderate 30 – 44 % predict exercise capacity or
functional reserve.
Severe < 30% 4) Ejection fraction is super-
normal in patients with
ESC/ASE 2005 reduced afterload (e.g.
mitral regurgitation).

Stroke Volume, Cardiac Output, Cardiac The calculation of these

Index – Reference Values parameters is very highly
dependent on correct
Rest Exercise
measurement of LVOT
Stroke volume 70 – 110mL 80 – 130mL width.

Cardiac output 5 – 8.5 L/min 10 – 17 L/min

Cardiac index > 2.5 L/min/m2 > 5 L/min/m2

33

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 003 // HEART CHAMBERS AND WALLS

NOTES LEFT VENTRICULAR FUNCTION

A rough estimate of Measuring Contractility – dP/dt

contractility can also be
obtained by eyeballing the Normal > 1200 mmHg/sec
slope of the MR curve. 1m/s

Borderline 800 – 1200 mmHg/sec

dP/dt
Reduced < 800 mmHg/sec
3m/s
Severely reduced < 500 mmHg/sec

Limitations: Mitral regurgitation (MR) signal needed, inexact, not completely

load independent

CW Sample
DP/DT – apical four-chamber
view/CW Doppler mitral
regurgitation
MR
The dP/dt is calculated by
measuring the slope of the initial
mitral regurgitation signal
between 1 m/s and 3 m/s.
1 m/s

dP/dt
3 m/s

THE RIGHT VENTRICLE

The geometry of the

right ventricle is more PA SVC Characteristics of the RV
complex than that of
the left ventricle: PV • The wall is thinner (< 5 mm)
it resembles a bagpipe. • Moderator band
• Strongly trabeculated
RAA
• ”Wrapped around” the left ventricle
RVOT
PV = pulmonic valve
TV RA
RVIT RAA = right atrial appendage
RVIT = right ventricular inflow tract
RVOT = right ventricular outflow tract

IVC

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 003 // HEART CHAMBERS AND WALLS

THE RIGHT VENTRICLE NOTES

Measurements of the Right Ventricle RV diameters appear

larger when the
Reference Slightly Moderately Severely transducer is too far
Range Abnormal Abnormal Abnormal cranial.
RV dimensions
Basal RV diameter (mm) 20-28 29-33 34-38 ≥ 39
Mid RV diameter (mm) 27-33 34-37 38-41 ≥ 42
Base-to-apex length (mm) 71–79 80-85 86-91 ≥ 92

Above pulmonary valve (mm) 17-23 24-27 28-31 ≥ 32

Below pulmonary valve (mm) 15-21 22-25 26-29 ≥ 30

ESC/ASE 2005

RIGHT VENTRICULAR DIAMETER

– apical four-chamber view/2D

Measurement of the basal and

mid right ventricular diameter in
end-diastole. To enhance accura-
cy use a four-chamber view that
is optimized for the right ventri-
Mid cle. The right ventricular diam-
eter will be overestimated when
the ventricle is foreshortened.

Basal

Right Ventricular Systolic Function Speckle-trackingderived

longitudinal strain of the free
Tricuspid annular plane systolic excursion (TAPSE) > 16 – 18 mm right ventricular wall may
provide additional information
TDI maximum velocity at the basal lateral wall (S‘) > 10 cm/s to quantify right ventricular
function. It also reflects RV
PW Doppler myocardial performance index > 0.4 function in the apical segments.

Tissue Doppler myocardial performance index > 0.55

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 003 // HEART CHAMBERS AND WALLS

NOTES THE RIGHT VENTRICLE

TAPSE – apical four-chamber MMode
view/Mmode RV wall

TAPSE is measured by placing

the MMode through the tricus-
pid annulus and measuring the
displacement from diastole to
systole.

Free RV Wall TAPSE

TDI
SAMPLE RA

TISSUE DOPPLER IMAGING OF

THE RIGHT VENTRICLE – apical
four-chamber view/TDI PW RV
wall

The sample volume is placed in

the basal lateral wall of the right S‘ TDI Velocity (max.)
ventricle. S’ denotes RV longitu-
dinal function.

E‘ A‘

Assessment of RV RV Diastolic Function

diastolic dysfunction is
rarely used in clinical E/A ratio < 0.8 or > 2.1
practice.
E/e‘ >6

Deceleration time (ms) < 120ms

Always look for the Causes of RV Dilatation

cause of RV dilatation.
• Dilated cardiomyopathy • Right ventricular dysplasia
• Right heart infarction • RV volume overload (e.g. atrium septal
• Myocarditis defect, pulmonic/tricuspid regurgitation)
• Pulmonary embolism/hypertension • Athletes (normal reaction to training)

36

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 003 // HEART CHAMBERS AND WALLS

THE RIGHT VENTRICLE NOTES

Fractional Area Change (FAC)– Reference Values Tracing of RV contours may

be difficult (trabeculations,
Normal 32-60 % Trace the RV contour in diastole and thin wall).
systole in an optimized 4-chamber view
Mild 25 – 31 % to obtain the areas. Calculate the
percentage of change.
Moderate 18 – 24 % (RV area end-diastole – RV area
end-systole)/RV area end-diastole *100
Severe ≤ 17 %
ESC/ASE 2005

THE LEFT ATRIUM

MMode Measurements of LA – Reference Values LA size and volume predict

adverse events (i.e. afib,
stroke) and constitute a

Normal (mm) 30 – 40 27 – 38 marker of disease severity.

Mild (mm) 41 – 46 39 – 42

Moderate (mm) 47 – 52 43 – 46

Severe (mm) ≥ 52 ≥ 47

LA Length (4-Chamber View)– Reference Values Measure the length of

the left atrium parallel to
Reference Slightly Moderately Severely the interatrial septum.
Range Abnormal Abnormal Abnormal

LA diameter (mm) 27–38 39–42 43–46 ≥ 47

LA diameter/
BSA (mm/m2) 15–23 24–26 27–29 ≥ 30

Reference Slightly Moderately Severely
Range Abnormal Abnormal Abnormal

LA diameter (mm) 30–40 41–46 47–52 ≥ 52

LA diameter/
BSA (mm/m2) 15–23 24–26 27–29 ≥ 32

ESC/ASE 2005

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 003 // HEART CHAMBERS AND WALLS

NOTES THE LEFT ATRIUM

LA Length – A Practical Scale

Normal (mm) ≤ 50

Mild (mm) 51 – 60

Moderate (mm) 61 – 70 LA

Severe (mm) > 70

LEFT ATRIAL LENGTH –apical

four-chamber view/2D

The length of the left atrium is

measured from the mitral annular
plane to the roof of the left
atrium parallel to the interatrial
septum in end-systole. Be sure
not to measure into the pulmo-
nary vein. This measurement only
LA diameter
provides a rough estimate of left
atrial size.

Pulmonary vein

LA Area – Reference Values

Normal (cm2) ≤ 20

Mild (cm2) 20 – 30

Moderate (cm2) 30 – 40
LA

Severe (cm2) > 40

ESC/ASE 2005

LEFT ATRIAL AREA –apical End-Systole

four-chamber view/2D

Tracing of LA area is performed in

LA systole. The left atrial appen
dage (if visible), pulmonary veins,
and interatrial aneurysms
(if present) are spared.

LA diameter

Pulmonary vein

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 003 // HEART CHAMBERS AND WALLS

THE LEFT ATRIUM NOTES

LA Volume – Reference Values LA volume measurements

are superior to MMode
LA Volume (Area and 2D diameter
Length Method) – measurements. LA
8 A4c x A2c Reference Values Practical Scale volumes > 200 ml denote
V= X
3 L very severe atrial
dilatation (LA volumes
may even exceed 1 liter).
Normal (mL) 18 – 58 22 – 52 <50

Mild (mL) 59 – 68 53 – 62 50 – 70

Moderate (mL) 69 – 78 63 – 72 70 – 90

Severe (mL) ≥ 79 ≥ 73 > 90

Pittfalls in Calculating LA Volume Optimize the 4-chamber

view specifically to the left
• Inclusion of pulmonary veins • Measurement not performed at end atrium to obtain best results.
• Tenting area of MV systole
• Alignment/atrial foreshortening • Oblique view of the LA
• Lateral resolution • Foreshortening of the atrium

Parameters of LA Function In most cases the Doppler

(MV inflow) signal is
• Doppler (MV inflow) sufficient to estimate LA
• Area changes systolic/diastolic function. Functional
• Pulmonary vein flow assessment of the LA is still a
• TDI/2D strain subject of ongoing research.

The area under the A-wave

correlates with the ejection
of blood from the left atrium
(atrial contraction) into the
left ventricle (booster pump
function). A small A-wave
either means there is poor
contraction, high resistance
to filling, or the greater part
of the blood has already
entered the ventricle during
the passive filling phase.

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 003 // HEART CHAMBERS AND WALLS

NOTES THE LEFT ATRIUM

The most frequent Causes of LA Dilatation

cause of LA dilatation
in the adult is • Diastolic dysfunction • Restrictive/hypertrophic cardiomyopathy
hypertension. • Mitral stenosis/regurgitation • Atrial fibrillation
• Aortic stenosis • Impaired LV function

THE RIGHT ATRIUM

The right atrium can be Causes of RA Dilatation

stretched in length when
the left atrium expands. • Pulmonary hypertension • Right ventricular failure
expands ands. • Tricuspid valve disease • Atrial fibrillation

The RA is generally RA Length – Reference Values (4 chamber view)

smaller than the LA.
However, for Reference Slightly Moderately Severely
practical reasons you Range Abnormal Abnormal Abnormal
may also apply the
simple grading scale RA minor axis
shown for the left diameter (mm) 29–45 46–49 50–54 ≥ 55
atrium.
RA minor axis
diameter/BSA
(mm/m2) 17–25 26–28 29–31 ≥ 32

ESC/ASE 2005

RIGHT ATRIAL LENGTH – apical

four-chamber view/2D

The length of the right atrium is

measured from the tricuspid
annular plane to the roof of
the right atrium, parallel to the
interatrial septum, in end-systole.
Be sure not to measure into the
vena cava.
RA diameter
RA

Vena cava

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 003 // HEART CHAMBERS AND WALLS

THE RIGHT ATRIUM NOTES

Coronary Sinus

Reference value = 4 – 8 mm (upper limit 15 mm)

Causes of a dilated coronary sinus:

• Elevated RA pressure
• V. cava sin. persistens,
• Malformation (aneurysm/diverticula), – unroofed coronary sinus

Inferior Vena Cava IVC allows estimation of RA

pressure. Dilated IVC without
Size < 17 mm, Inspiratory collapse ≥ 50% respiratory changes indicates
IVC size varies greatly, depending on fluid status and central venous pressure elevated RA pressure (> 15
mmHg).
Causes of IVC dilatation:
• Tricuspid regurgitation A large inferior vena cava does
• Pericardial tamponade constriction not always indicate a medical
• Restrictive cardiomyopathy condition. Some patients simply
• Right heart failure have a large inferior vena cava
• Scimitar syndrome (anomalous pulmonary venous return into the IVC) (even in the absence of elevated
RA pressure).

LEFT VENTRICULAR HYPERTROPHY

Forms of Left Ventricular Hypertrophy

Most patients with
Left ventricular geometry
hypertension have
RWT
concentric LVH.

Concentric Concentric
remodelling hypertrophy
0.43

Normal Eccentric
hypertrophy

LVMI

LVMI (left ventricular mass index) = LV mass/BSA

Reference adapted from Ganau et al. JACC 1992

Relative Wall Thickness (RWT)

2 x PWT
Normal values 22 – 42 % RWT =
LVID

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 003 // HEART CHAMBERS AND WALLS

NOTES LEFT VENTRICULAR HYPERTROPHY

Potential problems: the Quantification of LVH – Severity of Septal Thickness

measurements were not
performed at end diastole
(2D), RV structures interfere
with the measurement, the Normal (mm) 6 – 10 6–9
shape of the IVS (basal septal
bulge), incorrect image Mild (mm) 11 – 13 10 – 12
orientation (non-
perpendicular). Moderate (mm) 14 – 16 13 – 15

Severe (mm) ≥ 17 ≥ 16

2D measurements: end-diastole, mid-septum, 4 chamber view ESC/ASE 2005

INTERVENTRICULAR
SEPTUM – apical four-chamber
view/2D
Interventricular septum
The interventricular septum is a
prominent structure. The center
of the septum is highly echoge IVS diameter
nic. A septal bulge is frequently
observed, especially in hyper-
tensive patients. The thickness
of the bulge should be reported
separately.

May cause obstruction Sigmoid Septum

and SAM, especially
under certain clinical • Septal buldge – less than
conditions 3 cm in length
(hypovolemia, • Associated with hypertension
hyperkinesia, • Not associated with
catecholamines). hypertrophic cardiomyopathy

Buldge

42

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 003 // HEART CHAMBERS AND WALLS

LEFT VENTRICULAR HYPERTROPHY NOTES

Quantification of LV Mass (ESC/ASE 2005) LV mass better reflects the

extent of LVH than the
Measurments obtained from 2D-targeted M-mode or 2D linear LV measure- measurement of septal
ments: LV internal dimensions and wall thicknesses should be measured at the thickness. Even small
level of the LV minor dimension, at the mitral chordae level. measurement errors are
magnified. Therefore, LV mass
measurement should only be
{ [(
LV mass = 0.8 x 1.04 LVIDd + PWTd + SWTd )
3
(
– LVIDd ) ]} + 0.6 g
3
performed in patients with
good image quality.
Abbreviations:
LVIDd= left ventricular internal diameter at end diastole This formula is appropriate for
PWTd= posterior wall thickness at end diastole evaluating patients without
SWTd= septal wall thickness at end diastole major distortions of LV
geometry.

LV Mass/Body Surface Area – Reference Values

Normal (g/m2) 50 – 102 44 – 88

Mild (g/m2) 103 – 116 89 – 100

Moderate (g/m2) 117 – 130 101 – 112

Severe (g/m2) ≥ 131 ≥ 113

Additional Findings in Hypertensive Patients In a patient with these

findings, left ventricular
• Left atrial enlargement • Dilated aorta hypertrophy is likely to be a
• Right ventricular hypertrophy • Aortic valve sclerosis consequence of
• Diastolic dysfunction • Mitral annular calcification hypertension.

Athlete‘s Heart Endurance training/

isotonic exercise (such as
• Left ventricular hypertrophy (RWT • Supranormal left atrial booster pump marathon running)
≤ 45 and septum rarely > 13mm) function causes an eccentric form
• Normal or supranormal • Changes occur only after intensive of hypertrophy. Isometric
diastolic function and prolonged training exercise (such as weight
• Left and right ventricular dilatation for several years lifting) causes a more
concentric form.
Deconditioning reverses
left ventricular
hypertrophy.

43

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 003 // HEART CHAMBERS AND WALLS

NOTES

44

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 004 // Diastolic Function

CONTENTS
46 Basics of Diastolic Dysfunction

51 Specific Situations
45

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 004 // DIASTOLIC FUNCTION

NOTES BASICS OF DIASTOLIC DYSFUNCTION

Causes
Any patient with systolic
dysfunction also has diastolic • Aging
dysfunction. • Sytolic dysfunction
• Heart failure with preserved ejection fraction
Patients with diastolic • Left ventricular hypertrophy
dysfunction usually have a • Restrictive cardiomyopathy/infiltrative disease
dilated left atrium. • Coronary artery disease
• Hypertrophic cardiomyopathy
• Heart transplantation

Diastole beginns with aortic Diastole Duration

valve closure, which can be Diastole
R R
assessed with PW Doppler
sample volume in the LVOT
(end of signal).
T P

Fusion of the E- and Timing of Diastole

the A- wave may occur in
E A
tachycardia. The duration of Components
diastasis decreases with • IVRT – isovolumetric relaxation (AV
heart rate and PQ duration. closure to MV opening)
• E= rapid early (passive) LV filling
• Diastasis
• A= late LV filling – atrial contraction

IVRT Diastasis

Echo assessment of Physiology of Diastolic Function

diastolic function
Geometry
primarily reflects left Filling pressure Preload
dyssynchrony
atrial filling pressure.

Active myocardial Diastolic Percardium

relaxation function

LA compliance/ Heart rate LV compliance

function

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 004 // DIASTOLIC FUNCTION

BASICS OF DIASTOLIC DYSFUNCTION NOTES

Mitral Inflow Signal PW Doppler sample volume

should be at the tip of the
Diastolic filling
DT MV leaflets.

The deceleration time (DT)

shows the pressure decay of
early filling. In general the
E A
shorter the DT, the higher
Early filling Atrial contraction the filling pressure.

MITRAL INFLOW SIGNAL –

apical four-chamber view/
PW Doppler MV

The mitral inflow signal allows

assessment of diastolic function
as well as the timing of events
Diastolic filling (such as diastolic filling time).
The E-wave represents early
E-wave
A-wave diastolic filling while the A-wave
represents atrial contraction. It is
advisible to always use an ECG.

Early filling Atrial contraction

Mitral Inflow – Reference Values In some situations the

parameters of diastolic
16–20 years 21–40 years 41–60 years > 60 years function may be
inconsistent and difficult to
IVRT (ms) 50 ± 9 67 ± 8 74 ± 7 87 ± 7 interpret.

DT (ms) 142 ± 19 166 ± 14 181 ± 19 200 ± 29

A duration 113 ± 17 127 ± 13 133 ± 13 138 ± 19

E/A 1.88 ± 0.45 1.53 ± 0.4 1.28 ± 0.25 0.96 ± 0.18

IVRT= isovolumic relaxation time, DT = decceleration time

EAE/ASE 2009

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 004 // DIASTOLIC FUNCTION

NOTES BASICS OF DIASTOLIC DYSFUNCTION

An E/e’ ratio ≤ 8 (septal or TDI Mitral Annulus – Reference Values

lateral) indicates normal left
atrial pressure; a septal E/e’ 16–20 years 21–40 years 41–60 years > 60 years
≥ 15 or a lateral E/e’ ≥ 12
indicates elevated left atrial Septal e‘ (cm/s) 14.9 ± 2.4 15.5 ± 2.7 12.2 ± 2.3 10.4 ± 2.1
pressure.
Septal e‘/a‘ 2.4 1.6 ± 0.5 1.1 ± 0.3 0.85 ± 0.2

Lateral e‘ (cm/s) 20.6 ± 3.8 19.8 ± 2.9 16.1 ± 2.3 12.9 ± 3.5

Lateral e‘/a‘ 3.1 1.9 ± 0.6 1.5 ± 0.5 0.9 ± 0.4

EAE/ASE 2009

TISSUE DOPPLER IMAGING OF

THE MITRAL ANNULUS – apical
four-chamber view/TDI PW

E’ and a’ represent the mitral

annular velocity towards the
base of the heart during early
passive (e’) and active (a’) filling.
E/e’ is a marker of left atrial filling
pressure.

a´
e´

Situations in Which TDI at the Mitral Annulus

Should Not Be Used

• Annular calcification • Myocardial infarction

• Mitral valve prosthesis • Moderate to severe mitral regurgitation

Use right upper PV to record Pulmonary Venous Flow

the PW signal. Remember to
reduce PRF. • Peak systolic PV flow velocity (S) Isovolumic relaxation

• Peak diastolic PV flow velocity (D)

S
• Peak reverse atrial flow velocity (AR)
• AR duration

Signs of impaired diastolic function:

Decrease in systolic component, increase AR duration

in peak AR, increase in AR duration

AR

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 004 // DIASTOLIC FUNCTION

BASICS OF DIASTOLIC DYSFUNCTION NOTES

Pulmonary Veins – Reference Values Pulmonary vein flow has many

limitations and is rarely used in
16 – 20 years 21 – 40 years 41 – 60 years > 60 years clinical practice.

S/D 0.82 ± 0.18 0.98 ± 0.32 1.21 ± 0.2 1.39 ± 0.47

AR (cm/s) 16 ± 10 21 ± 8 23 ± 3 25 ± 9

AR duration (ms) 66 ± 39 96 ± 33 112 ± 15 113 ± 30

EAE/ASE 2009

Grading of Diastolic Dysfunction Left atrial filling pressure

increases with the degree
? ? of diastolic dysfunction.
Valsalva Valsalva

Grade 0 Grade 1 Grade 2 Grade 3 Grade 4

Supernormal Normal Impaired Pseudonormal Restrictive Irreversibly

relaxation restrictive

Enlarged Decreased Shortened Prolonged

Increasing filling pressures are seen in the patterns from left to right. Provocation
maneuvers such as Valsalva that unload the left atrium may cause a reversal of the
pattern (pseudonormal -> impaired relaxation and restrictive -> pseudonormal)

IMPAIRED RELAXATION
PATTERN – apical four-chamber
view/PW Doppler MV

The A-wave is taller than the

E-wave. This indicates impaired
diastolic relaxation. Large parts
of ventricular filling occur during
atrial contraction in such
patients. In addition, the
A-wave deceleration of the E-wave is
prolonged.

E-wave

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 004 // DIASTOLIC FUNCTION

NOTES BASICS OF DIASTOLIC DYSFUNCTION

Mitral E/A

E/A ≥ 1 – < 2 or E/A ≥ 2 , DT <150 ms

E/A < 1 and E ≤ 50 cm/s
E/A < 1 and E ≤ 50 cm/s

E/e’ < 8 E/e’ > 15

E/Vp < 1.4 E/Vp ≥ 2.5
S/D > 1 S/D < 1
Ar-A < 0 ms Ar-A ≥ 30 ms
Valsalva  E/A < 0.5 Valsalva  E/A ≥ 0.5
sPAP < 30 mmHg sPAP > 35 mmHg

Normal LAP Normal LAP Elevated LAP Elevated LAP

Algorithm for estimating filling pressures in patients with reduced left

ventricular function (EF <55%) according
to the ASE/EAE guidelines
(2009)

E/e’

E/e’ sep. ≥ 15 or
E/e’< 8
E/e’ 9 – 14 E/e’ lat. ≥ 12 or
(sep., lat. or av.)
E/e’ av. ≥ 13 or

LA vol. ≥ 34 ml/m2 LA vol. < 34 ml/m2

Ar-A < 30 ms Ar-A ≥ 30 ms
Valsalva  E/A < 0.5 Valsalva  E/A ≥ 0.5
sPAP < 30 mmHg sPAP > 35 mmHg

Normal LAP Normal LAP Elevated LAP Elevated LAP

LAP = left atrial pressure; sPAP= systolic pulmonary artery pressure

Algorithm for the estimation of filling pressures in patients with nor-

mal left ventricular function (EF >55%) according to
the
ASE/EAE guidelines (2009)

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 004 // DIASTOLIC FUNCTION

BASICS OF DIASTOLIC DYSFUNCTION NOTES

A Simple Approach to Diastolic Function/Rules

• Supernormal diastolic function: • DD normal vs pseudonormal:

When the echo is normal and the Look at deceleration time,
patient is young LA enlargement, and E/e‘ (≥ 8 – 12)
• Normal diastolic function: • Restrictive filling:
When the echo is normal, the patient is When E is twice of A (E/A ratio is >2),
< 45 years of age, and E>A then filling pressure elevated
• Impaired relaxation: • Perform TDI:
When A is higher than E (E/A ratio is < 1), When E/e´is > 12 – 15 then filling
filling pressure is normal or slightly pressure is elevated (PCWP > 12 mmHg)
elevated • Perform valsalva:
• Pseudonormal diastolic function: Unloading of the atrium, LA pressure
When echo is abnormal (LVH, red LVF, (LAP) drops, unmasking of pseudonor-
etc) or the patient is > 65 years of age mal filling (discrimination between
and E is higher than A (E/A ratio > 1) irreversible restrictive vs. reversible
restrictive)

SPECIFIC SITUATIONS

Beat to Beat Variations in E/A Ratio

• Changes in LV filling pressure in relation to respiration?

• COPD patients
• High normal filling pressures (E/e`= 8 – 9)

E/A Fusion

• Tachycardia
• Long systole (left bundle branch block)
• Long AV delay

EA FUSION – apical four-

chamber view/PW Doppler MV

E/A fusion can be abolished by

slowing down the heart rate – in
E/A fusion
this example by performing a
Carotid artery maneuver A-wave
carotid artery maneuver.
E-wave

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 004 // DIASTOLIC FUNCTION

NOTES SPECIFIC SITUATIONS

E L A
The presence of an L-wave L-Wave
indicates elevated filling
pressure. • Mid-diastolic filling of the LV
• Elevated filling pressure?
• Bradycardia
• Can also occur in atrial fibrillation
(difficult to detect, no A wave)

L WAVE – apical four-chamber A-wave

view/PW Doppler MV

The L-wave occurs between the

E- and the A-wave, and denotes
E-wave
mid-diastolic filling of the LV.
It is indicative of eleva-
ted LV filling pressure.

L-wave

Atrial Fibrillation/Flutter in Diastolic Dysfunction

• Often associated with • No A-wave, therefore the E/A ratio

diastolic dysfunction cannot be obtained
• Pulmonary venous flow is difficult to • Use E/e‘ and deceleration time
assess (average several beats) 

Diastolic dysfunction/LV filling Left Atrial Pressure in Mitral Valve Disease

pressure should not be
assessed in the setting of • Left atrial size does not necessarily • E-wave velocity also reflects
mitral regurgitation > grade II. reflect elevated filling pressures increased stroke volume
• Left atrial size may also be enlarged • E‘ is reduced in mitral stenosis and
Estimate filling pressure to due to volume overload + atrial elevated in mitral regurgitation
determine the severity of fibrillation
disease and how the LV can
cope with the problem
(e.g. AS, AR, cardiomyopathy).

52

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 005 // Dilated Cardiomyopathy

CONTENTS
54 Background

54 Echo Features

55 Specific Forms
53

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 005 // DILATED CARDIOMYOPATHY

NOTES BACKGROUND

Ischemic cardiomyopathy is Definition

similar to dilated • Myocardial disease (primarily)
cardiomyopathy but is, by • Impaired systolic function
definition, NOT a form of dilated • Left ventricular dilatation
cardiomyopathy. • In the absence of coronary artery disease
and significant primary valvular disease

The etiology remains unidentified Causes

in many cases because a biopsy is
not performed. • Genetic • Drug and alcohol abuse
• Congential • Certain cancer medications
About 30% of patients with • Infections • Exposure to toxins
idiopathic cardiomyopathy are
estimated to suffer from genetic
forms of the disease. In these
forms, there is frequently an
overlap between dilated and
hyptertrophic forms.

Associated Problems

• Left heart failure • Right heart failure

• Atrial fibrillation, ventricular arrythmias • Tricuspid regurgitation
• Pulmonary hypertension • Dyssynchrony
• Mitral regurgitation • Thromboembolism

ECHO FEATURES

End-stage ischemic Diagnosis

cardiomyopathy
and dilated • Reduced left ventricular function • Exclude other causes (coronary artery
cardiomyopathy look • Dilated left ventricle disease, valvular)
very similar. • Reduced right ventricular function

Right ventricular function Signs of Advanced Dilated Cardiomyopathy

correlates better with
prognosis than LVF (it • Low cardiac output (LVOT velocity • Diastolic function/filling pressure
denotes end-stage heart < 0.5 m/sec) (restrictive pattern)
failure). • Very low ejection fraction • Severe pulmonary hypertension and
• Atrial size (large atria in more tricuspid regurgitation
advanced forms) • Poor right ventricular function
• Significant mitral regurgitation • Pleural effusion

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 005 // DILATED CARDIOMYOPATHY

ECHO FEATURES NOTES

ECHOFEATURES OF DILATED
CARDIOMYOPATHY –
apical four-chamber view/
Color Doppler
Dilated LV
MR central jet Dilated left ventricle with re-
(annular dilitation) duced left ventricular function,
mitral regurgitation with a central
jet caused by annular dilatation,

Enlarged LA

Mechanisms of Mitral Regurgitation in Cardiomyopathy MR increases mortality.

(additional volume
• Annular dilatation geometry • Atrial enlargement overload of LV).
• Bileaflet restriction • Dyssynchrony
Rule out a structural cause for
The degree of mitral regurgitation may change rapidly and is related to factors mitral regurgitation. It could
such as increased afterload, preload, and volume status. point to the presence of a
primary valvular cause of
systolic dysfunction.

SPECIFIC FORMS

Ischemic Cardiomyopathy It may be difficult or even

impossible to distinguish
• Not really a form of dilated cardi- • Thin scarred walls, ventricular between dilated and ischemic
omyopathy but shares several distortion and clearly segmental cardiomyopathy on
features myocardial dysfunction suggests echocardiography.
• Most common cause of heart failure ischemic cardiomyopathy
• Occurs in large infarctions, leads to
ventricular remodeling and
global dysfunction

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 005 // DILATED CARDIOMYOPATHY

NOTES SPECIFIC FORMS

Abortive forms of Takot- Takotsubo Cardiomyopathy

subo cardiomyopathy
with more subtle wall • Stress–induced cardiomyopathy is basal segments which may cause
motion abnormalities more common in women LVOT obstruction, and right ventricular
have been reported. • Echo features include segmental wall involvement
motion abnormalities (in particular • Normal coronary angiogram
apical ballooning), hyperdynamic • Abnormalities are reversible

TAKOTSUBO
CARDIOMYOPATHY – apical
four-chamber view/2D

A typical feature of Takotsubo Apical

cardiomyopathy is apical bal- ballooning
looning. The basal segments tend
to be hyperdynamic.

Peripartum Cardiomyopathy

• A non-familial, non-genetic form of • Recovery rate > 40%

dilated cardiomyopathy associated • Often presents as acute heart failure
with pregnancy • May involve both ventricles
• Clinical presentation in the last month • Has no specific echo features
of pregnancy or 5 months
post partal

The duration of, and the Tachycardia/Arrythmia-Mediated Cardiomyopathy

heart rate needed for, the
induction of tachycardiomy- • Prolonged periods of tachycardia in • Cardiac function returns in most cases
opathy are highly atrial fibrillation or ventricular after heart rate control, but may take
variable and depend on nu- tachycardia several weeks or months
merous factors. • In arrhythmia-mediated • Assessment of left ventricular function
cardiomyopathy, frequent ectopic is difficult and is underestimated in
beats (> 17,000/24h) tachycardia. Always repeat the
echocardiogram after heart rate
control

56

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 005 // DILATED CARDIOMYOPATHY

SPECIFIC FORMS NOTES

HIV-Mediated Cardiomyopathy

• Focal myocarditis
• Most common form of cardiomyopathy in African countries (e.g. Burkina Faso)

Causes
• Myocarditis • Nutritional deficiency
• Autoimmune cardiomyopathy • Drug toxicity (e.g. zidovudine)

The severity and incidence of HIV-mediated cardiomyopathy strongly depends on

the treatment regimen (HAART reduced the incidence by 30%).
HIV-mediated cardiomyopathy has no specific echocardiographic features.
One usually finds left ventricular function without regional wall motion abnormali-
ties, and possibly pericardial effusion.

LV Non-Compaction There is a genetic link

between non–compaction
• Characterized by prominent • Congenital cardiomyopathy and hypertrophic
trabeculae and intertrabecular characterized by prominent cardiomyopathy.
recesses (sinus) trabeculae and intertrabecular
• Associated with other cardiac recesses (spongy myocardium)
abnormalities • May present at any age
• Genetic disease, risk of • May be associated with normal or
cardiomyopathy, family screening reduced left ventricular function
is important • Echocardiography is the most
• Associated with neuromuscular important diagnostic tool
disorders (alternative: MRI)

LV NON-COMPACTION –
Sinus apical four-chamber view/2D

The apical portion of the left

ventricle is strongly trabeculated
and appears spongy. Look care-
Hypertrabeculation fully and visualize all portions of
the myocardium to find hyper-
trabe culated areas. Use contrast
and color Doppler when in doubt.

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 005 // DILATED CARDIOMYOPATHY

NOTES SPECIFIC FORMS

Echo Evaluation

• The involved segments are mid • Use color Doppler with low PRF and
ventricular (especially inferior and contrast to visualize blood flow
lateral) and apical. Is usually seen best between the trabeculae
on atypical views • Use deformation imaging to detect
• Right ventricular involvement may be myocardial dysfunction (i.e. speck-
present but is difficult to differentiate le-tracking echocardiography) at the
from normal trabeculae regions of hypertrabeculation

Chagas Disease

• Trypanosoma cruzi • Caused by infection with Trypanosoma

• Megaesophagus cruzi (present in feces of reducidae e.g.
• Cardiac disease triatoma infestand = kissing bug)
• Megacolon • Most common form of cardiomyopa-
• Most common form of thy in Latin America
cardiomyopathy in Latin America • Associated with megaesophagus,
• Right heart failure is dominant megacolon induced by neural
(regional + global dysfunction) degeneration

Echo Features

• Pericardial effusion
• Regional myocardial dysfunction
with preserved global left ventricular function
• Often apical aneuryms
• Diastolic dysfunction is present
in about 20% of patients

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 006 // Hypertrophic Cardiomyopathy

CONTENTS
60 Basics

61 Echocardiographic Evaluation
59

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 006 // HYPERTROPHIC CARDIOMYOPATHY

NOTES BASICS

Cardiomyopathy may Epidemiology

differ markedly in terms of • Prevalence: 1 in 500
morphology, clinical • Annual mortality: Adults 2%
presentation and Childhood 4 – 6%
prognosis.
• Most common cause of sudden
cardiac death in athletes

The onset of disease may Cause

vary: childhood,
adolescence, or sometimes • Genetic disease (sarcomere)
late in life. • Autosomal dominant
• Associated syndromes (Noonan‘s, Friedreich ataxia, LEOPARD)
Perform family screening.

Symptoms

• Asymptomatic • Arrhythmias
• Chest pain • Sudden death
• ECG abnormalities • Dyspnea
• Syncope • Palpitations

Other causes of left When to Consider Hypertrophic Cardiomyopathy?

ventricular hypertrophy
include hypertension, • Unexplained left ventricular • Speckled appearance of
aortic stenosis, athlete‘s hypertrophy (> 15 mm) the myocardium
heart, and infiltrative • LVOT/LV gradient • Asymmetric left ventricular hypertrophy
heart disease. • ”Spade-shaped” left ventricular cavity • Turbulent flow in the LV/LVOT

OBSTRUCTIVE
CARDIOMYOPATHY – apical
three chamber view
Mid-ventricular
Turbulent flow in the LVOT turbulences
caused by systolic anterior mo-
tion of the MV. Distortion of the
MV leads to regurgitation with
a posteriorly directed jet. Flow
acceleration is also present in the
PMVL
mid-ventricular portion (addi-
Posterior Turbulent flow LVOT
tional mid-ventricular obstruc-
tion).
MR jet

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 006 // HYPERTROPHIC CARDIOMYOPATHY

BASICS NOTES

Obstructive Forms Non-Obstructive Forms There is an overlap

between obstructive and
non-obstructive forms;
the gradients may be
inconsistent.

LVOT obstruction Asymmetric

Mid-ventricular obstruction Apical

ECHOCARDIOGRAPHIC EVALUATION

Non-Obstructive Cardiomyopathy (Apical Type) Apical hypertrophy may

be difficult to detect. Use
• More common in the Asian population contrast for LV cavity
• Associated with a favorable prognosis opacification.
• ECG tends to show giant negative T-waves
•A typical echocardiographic finding: spade-
shaped left ventricle

APICAL HYPERTROPHIC
Spade sign CARDIOMYOPATHY – apical
four-chamber view/2D
Apical
hypertrophy Pronounced hypertrophy of
the apex with a spade-shaped
ventricular cavity. Atrial enlarge-
ment is also a common feature of
hypertrophic cardiomyopathy.

Views to Display SAM = Systolic Anterior Motion

(of the Anterior Mitral Valve Leaflet)

• Parasternal long-axis view • Mmode/Color MMode

• Parasternal short-axis view at MV • Five-chamber view
• Apical long-axis view

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 006 // HYPERTROPHIC CARDIOMYOPATHY

NOTES ECHOCARDIOGRAPHIC EVALUATION

SYSTOLIC ANTERIOR MOTION SYSTOLE
OF THE MV – apical three-cham-
ber view/2D Hypertrophy

Dynamic left ventricular out-

flow tract (LVOT) obstruction is
caused by anterior motion of the
mitral valve during systole.

SAM

LVO
T
AV
AM
VL
PMVL

Use Valsalva or exercise SAM (Systolic Anterior Motion) Increases With

to provoke a gradient
during the exam. • Hypovolemia
It may ”unmask” • Exercise
obstructive • Medication (i.e. nitroglycerin, diuretics)
cardiomyopathy. • Dobutamine
• Valsalva
• Post-extrasystolic

Find the site of Quantification of Obstruction

obstruction with 2D and
color Doppler (SAM), put • Measure maximal LVOT velocity • Early obstruction is hemodynamically
CW through this site. The (CW Doppler) more relevant
CW Doppler focus point • The Doppler signal is typically • It may be difficult to discern the signal
should be postioned at dagger-shaped of LVOT obstruction from that of aortic
the site of obstruction. • A late peak generally indicates obstruc- stenosis or mitral regrgitation. Use color
tion more towards the mid/apical parts Doppler for guidance
of the ventricle

LVOT FLOW ACCELERATION – SYSTOLE

apical five-chamber view/CW
Doppler

Dagger-shaped spectrum in a Systole

patient with obstructive hyper- start
trophic cardiomyopathy. In this
example maximum obstruction
occurs rather late in systole (late
peak).

Vmax

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 006 // HYPERTROPHIC CARDIOMYOPATHY

ECHOCARDIOGRAPHIC EVALUATION NOTES

Mitral Regurgitation in Obstructive Cardiomyopathy Mitral regurgitation may

also increase with
• Distortion of mitral valve geometry due to SAM) provocation and a rise in
• The jet is directed posteriorly gradients.
• The severity correlates with the degree of obstruction

Other Causes of LVOT Obstruction SAM may also occur in

diseases and conditions
• Hypertensive heart disease caused by a • Post-mitral valve repair when other than hypertrophic
sigmoidal septum the anterior mitral valve leaflet is cardiomyopathy.
• Following surgery for aortic stenosis left too long
due to the presence of left ventricular • Hypovolemia
hypertrophy and a sudden decrease in • Hypercontractile state (e.g. hyperthy-
afterload or increase in contractility roidism, fever, catecholamines)

Mid-Ventricular Cardiomyopathy Mid-ventricular and LVOT

obstruction may be
• Least common type of combined.
hypertrophic cardiomyopathy
• Often combined with LVOT
obstruction
• Rather late peak of maximum
gradient velocity
• Gradients are rarely very high

Echocardiographic Assessment in Septal thickness > 30mm =

Hypertropic Cardiomyopathy increased risk for sudden
cardiac death.
• Myocardial thickness and location of • Degree of mitral regurgitation/SAM
hypertrophy • Atrial size Because the left ventricle
• Systolic/Diastolic function • (Deformation imaging) cavity is usually small, left
• Doppler measurement of maximal ventricular function appears
gradients better than it is. In addition,
most patients have reduced
longitudinal function, especially
in those segments which are
very hypertrophic or fibrotic.

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 006 // HYPERTROPHIC CARDIOMYOPATHY

NOTES ECHOCARDIOGRAPHIC EVALUATION

Patient history, distribution of Differential Diagnosis

left ventricular hypertrophy,
other echo findings and speckle • Hypertensive heart disease • Sarcoid heart disease
tracking may be helpful in • Aortic stenosis • Athlete‘s heart
establishing the correct • Amyloid heart disease • Fabry‘s disease
diagnosis.

Also consider surgical Alcohol Septal Ablation – Recommendations

myectomy, especially in
patients who are candidates • Severe heart failure symptoms
for surgery (e.g. aortic (NYHA classes III or IV) refractory to medication
stenosis with LVOT • Subaortic Doppler gradient > 50 mmHg at rest
obstruction). or with provocation (i.e. exercise)
• Adequate coronary anatomy/echo morphology

ESC 2003

64

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 007 // Restrictive Cardiomyopathy

CONTENTS
66 Basics

67 Specific Forms
65

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 007 // RESTRICTIVE CARDIOMYOPATHY

NOTES BASICS

1) Restrictive cardiomyopathy is Definition

NOT the same as a restrictive
filling pattern. A restrictive filling • Idiopathic, systemic or
pattern may also be present in infiltrative disorder.
other forms of cardiomyopathy. • May involve the left and/or right
ventricle.
2) Subclinical systolic dysfunction • Primarily a ”diastolic disease”
(despite normal ejection fraction) of the ventricles
may be present in early stages of • Normal or slightly reduced systolic
disease. function (in the early stages).

Restrictive cardiomyopathy is Most Common Causes

the least common form of
cardiomyopathy (5% of all cases • Amyloidosis • Radiation
of primary heart muscle • Idiopathic • Chemotherapy
disease). • Sarcoid heart disease • Carcinoid
• Endomyocardial fibrosis • Hemochromatosis

Patients typically present with Pathophysiology

signs of right heart failure.
Clinical and echocardiographic • Diastolic dysfunction • Hepatomegaly
features may be similar to those • Elevated filling pressure • Peripheral edema
of constrictive pericarditis. • Stiff ventricle • Pericardial effusion
• Right heart failure • Pleural effusion

Suspect restrictive CMP in Echo Features

patients with normal left
ventricular function and • Left ventricular hypertrophy function (in the early stage)
unexplained significant • Bi-atrial enlargement • Expanded left atrial appendage
bi-atrial enlargement. • Normal left ventricular volume (in the • Dilated inferior vena cava and pulmo-
early stage) nic veins
• Normal left ventricular ejection • Tricuspid regurgitation

How to Distinguish Restriction from Constriction

(Doppler MV Inflow and TDI MV Annulus)
Normal Restrictive Constrictive
E A E E Progressive decline of
A A the E‘ wave in restrictive
CMP
DD: The E‘ wave is
preserved/exaggerated
E´ in constrictive pericardi-
tis.
E´
E´

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 007 // RESTRICTIVE CARDIOMYOPATHY

SPECIFIC FORMS NOTES

Amyloid Heart Disease – Echo Features The echocardiogram is often

so typical that it leads to the
• Ground glass pattern • Advanced diastolic dysfunction diagnosis of amyloidosis.
• Left ventricular hypertrophy • Pericardial/Pleural effusion
• Atrial enlargement • ”Apical sparing pattern” of
• Thickened interatrial septum longitudinal strain
• Thickened valves frequently with mild • Systolic dysfunction (endstage)
regurgitations • Right heart involvement

Speckled AMYLOIDOSIS – apical

myocardium four-chamber view/2D

LVH Typical features of amyloidosis,

MV
including echogenic/hourglass
TV appearance of the myocardium,
thickened valves, and enlarged
Thickened atria. This patient also received a
valves
pacemaker.
PM Thickened
leads IAS

Hypereosinophilia/Endomyocardial Fibrosis (EMF) – Eosinophilic thombi are

Echo Features found in endomyocardial
fibrosis even in the absence
• Fibrous thickening of the endocardium • Different stages (necrotic/thrombotic/ of regional wall motion
• Echogenic eosinophilic infiltrates in the fibrotic) abnormalities or global LV
left and right ventricular apex • Late-stage restrictive filling pattern dysfunction.

Sarcoid Heart Disease – Echo Features 20 – 30 % of patients with

proven sarcoidosis have
• Cardiac involvement in sarcoidosis is • Hypertrophy (segmental) cardiac involvement. MRI is
associated with a poor prognosis • Edema/Fibrosis more sensitive than echo in
• Pericardial effusion • End-stage: left ventricular dilatation, the detection of sarcoid
• Left ventricular aneurysms wall thinning and impaired left heart disease.
• Wall motion abnormalities (not related to ventricular function
coronary perfusion territories)

Segmental
SARCOIDOSIS – apical
hypertrophy four-chamber view/2D
Wall Motion
abnormality Abnormal cardiac geometry with
Fibrosis segmental wall motion abnormal-
ities, thickening, and increased
echogenicity in the region of the
mid- and distal anterior septum.
Enlarged
atria

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 007 // RESTRICTIVE CARDIOMYOPATHY

NOTES SPECIFIC FORMS

Fabry‘s Disease: Manifestation

• Rare multisystemic disease • Renal failure

• X-linked genetic disease • Angiokeratoma
• Alpha–galactosidase deficiency

Some authors suggest that the Fabry‘s Disease: Echo Features

binary sign, defined as binary
appearance of the left ventricular • Left ventricular hypertrophy
endocardial border, aids in the • Right ventricular hypertrophy
diagnosis of Fabry‘s disease. • Myocardial fibrosis
However, the sensitivity and • Diastolic dysfunction/enlarged left atria
specificity of this sign is rather low.

FABRY’S DISEASE – apical

four-chamber view/2D LV hypertrophy
Pronounced bi-ventricular hy-
pertrophy and rather speckled RV hypertrophy
appearance of the myocardium.

Speckled
myocardaum

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 008 // Coronary Artery Disease

CONTENTS
70 Segmental Approach

72 Wall Motion Abnormalities

76 Patterns of Myocardial Infarction

77 Complications
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 008 // CORONARY ARTERY DISEASE

NOTES SEGMENTAL APPROACH

Segmentation (16-Segment Model)

The left ventricle is divided

Apex
into basal (6), mid (6) and
apical (4) segments.

Mid ventricle

Base

Apical four-chamber view

Subdivision of the corresponding short-axis view (SAX). Note that the basal and mid SAX
consist of 6 segments while the apical SAX has only 4 segments (16-segment model).

The inferolateral segment is

also referred to as the
posterolateral or posterior
segment.
( )
In echocardiographic
nomenclature there is no IS= inferoseptal, AS=anteroseptal , A = anterior,
diaphragmatic segment. AL= anterolateral, IL=inferolateral, P= posterior, I=inferior, S= septal, L=lateral
ESC 2006

Definition of the individual segments on the apical views. Note that the inferior
portion of the basal septum is visible on the 4-chamber view.

as al ai aa al/pl as

(a/i)ms ml mi ma mpl

m(a)s

(i)bs bl bpl
bi ba
b(a)s

as = apical septum ai = apical inferior al/pl = apical lateral

(a/i)ms= mid inferoseptum mi= mid inferior mpl= mid inferolateral (posterior)
(i)bs = basal inferoseptum bi = basal inferior bpl = basal inferolateral (posterior)
al = apical lateral aa = apical anterior as = apical anteriorl
ml = mid anterolateral ma = mid anterior m(a)s = mid anteroseptum
bl = basal anterolateral bal = basal anterior b(a)s = basal anteroseptum

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 008 // CORONARY ARTERY DISEASE

SEGMENTAL APPROACH NOTES

Bull’s Eye Representation

Ant Ant

Sept (ant) Lat Sept (ant) Lat

Sept (inf) Inf.lat/ Sept (inf) Inf.lat/

post post

Inf Inf

16-Segment model 17-Segment model (supra-apical cap)

Coronary Supply In left dominant perfusion,

the posterior (inferolateral)
wall and even large portions
of the inferior wall are
supplied by the LCx. In right
dominant perfusion, the RCA
supplies the posterior wall in
addition to the inferior
segments.

Left anterior descending (LAD)

Right coronary artery (RCA)

Circumflex artery (Cx)

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 008 // CORONARY ARTERY DISEASE

NOTES WALL MOTION ABNORMALITIES

LV contrast study improves What Are We Looking For?

endocardial border detection.
• Lack of wall/myocardial thickening • Ventricular geometry
Try your best to obtain the • Wall motion • Echogenicity/scar
best possible image quality. • Hinge points
This is what counts most
when you are looking for
regional wall motion
abnormalities.

INFERIOR WALL ANEURYSM –

apical two-chamber view/2D Inferior
wall
Inferior myocardial infarction Anterior
leading to distortion of ventric- wall
ular geometry (aneurysm) and Aneurysm
regional wall thinning in the basal Akinetic
and mid inferior segments. myocardium

Left atrial
Mitral appendage
Coronary valve
sinus

If possible, compare Wall Motion Abnormalties

wall motion with a
reference segment.

Hyperkinesia Normokinesia Hypokinesia Akinesia Dyskinesia

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WALL MOTION ABNORMALITIES NOTES

Wall Motion in Ischemic Conditions Ischemia, hibernation

and stunning are all
Coronary artery Myocardial wall: thickness marked by hypo/akinesia
and motion at rest AND preserved wall
thickness.

Normal

Exercise-
induced
ischemia

Ischemia

Necrosis

”Hibernation”

”Stunning”

Remodeling Predisposing factors for

remodeling are large
• Progressive LV dilatation infarctions ( anterior >
• Eccentric LV hypertrophy inferior), mitral
• Distortion of geometry regurgitation, and
• Hypokinesia of normally perfused segments elevated afterload
• further increase of mitral regurgitation (hypertension, AS).

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 008 // CORONARY ARTERY DISEASE

NOTES WALL MOTION ABNORMALITIES

There is no risk of rupture in Aneurysm

chronic aneurysms. Definition: Abnormal widening of all myocardial layers during diastole

• High risk of thrombi

• Increased risk of heart failure
• Apical aneurysms are best seen
on two-chamber and atypical views
(avoid ”foreshortening”)
• The slow flow phenomenon is seen
within the aneurysm

APICAL ANEURYSM – apical END-SYSTOLE

four-chamber view/2D

Very large apical aneurysm after

anterior myocardial infarction. LV Aneurysm
The apical region is dilated and
dys-/akinetic.

The degree of wall motion Myocardial Tissue After Acute Coronary Syndrome
abnormalities depends on
the transmurality of the
infarction. Various different
wall motion abnormalities
may exist simultaneously
(akinesia, hypokinesia,
aneurysm, scars).
Transmural scar: akinesia, dyskinesia, Subendocardial scar: hypokinesia,
aneurysm, thinning, bright echo thickness is normal/mildly thinned
Look for edema (myocardial
thickening, bright echoes) in
patients with myocardial
infarction after reperfusion.

Transmural scar + viability: akinesia + Viable myocardium (Acute ischemia/

hypokinesia of neighboring segments hibernation/stunning): hypokinesia,
akinesia, wall thickness preserved
Normal Viable ischemia/stunning/hibernation Scar/fibrosis

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WALL MOTION ABNORMALITIES NOTES

Quantification of Left Ventricular Function in The Simpson method DOES

Coronary Artery Disease NOT account for regional
wall motion abnormalities
• Simpson method • 3D methods (e.g. regional in the posterior and all
• Visual assessment ejection fractions) anterior septal segments
• Wall motion scoring • Endocardial contour (segments seen on the
• Center line enhancement (contrast) apical long-axis view).

Problem Zones (Regions Difficult to Image/Interpret)

Region Solution

Supraapical • Avoid foreshortening

• Move transducer more laterally + image
towards the apex
• Use two-chamber view

Lateral • Rotate four-chamber view clockwise

• Move transducer more medially

Basal inferior • Passive or active motion?

• Hinge points?
• Wall thickness

Wall Motion Abnormalities – Other Causes

• Dyssynchrony (e.g. left bundle • Myocarditis

branch block) • Cardiomyopathy (e.g. Takotsubo)
• Pacemaker • Sarcoid heart disease
• Abnormal septal motion
(e.g. postoperative, right ventricle
pressure/volume load)

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 008 // CORONARY ARTERY DISEASE

NOTES PATTERNS OF MYOCARDIAL INFARCTION

Supra-apical and distal septal Supra-Apical Infarction Distal Septum Infarction

infarctions may also occur in
proximal LAD occlusion
when rapid reperfusion is
achieved and only the distal
portions of the ventricle are
damaged.

LAD (distal, mid., prox.), small supra- LAD (distal,mid., prox.),

apical aneurysm, low remodeling risk low remodeling risk

Patients with left main Proximal LAD Type Infarction Small Basal Inferior
myocardial infarction rarely Infarction
survive.

LAD (before 1st septal branch, left main), Difficult region to interpret, low remode-
always remodeling, poor prognosis RCA ling risk

Inferior/posterior/postero- Inferior Infarction Infero-Posterior

lateral infarctions pose an Infarction
elevated risk for restrictive
mitral regurgitation
(tethering of the posterior
leaflet) .

RCA, low-moderate remodeling risk RCA (dominant) or Cx (large, prox.),

moderate remodeling risk

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PATTERNS OF MYOCARDIAL INFARCTION NOTES

Posterolateral Infarction Infero-Posterior-Lateral

Infarction

CX, RCA, moderate remodeling risk Dominant RCA, CX (large, prox.), high
remodeling risk

Lateral Infarction When assessing the patterns

of myocardial infarction,
always consider the possibility
of multiple/sequential
infarcts!

CX, LAD (diagonal branch), difficult to interpret, low remodeling risk

COMPLICATIONS

Overview Perform serial echo

exams after infarction. It
Acute/subacute will help you to detect
• Cardiogenic shock • Right ventricular infarction potential complications
• Thrombus formation (acute) • Papillary muscle rupture earlier and assess the
• Myocardial rupture • Ischemic ventricular septal defect patient‘s prognosis and
risk of further
Chronic complications.
• ”Remodeling” chronic heart failure • Thrombus formation (late)
• Right heart failure • Mitral regurgitation

Pseudoaneurysm High risk of secondary

perforation/rupture.
• Short, narrow neck (diameter < 50% of • Outer walls formed by pericardium
the fundus diameter) and mural thrombus
• Hematoma • Often pericardial effusion

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 008 // CORONARY ARTERY DISEASE

NOTES COMPLICATIONS

Myocardial Rupture

• Mortality 95% • True incidence unknown

• Also small infarctions • Tamponade
• Hematopericardium • Urgent surgery required

The most common site of Ischemic Ventricular Septal Defect

rupture is the distal anterior
septum (anterior myocardial • Incidence 0.5 – 1% • 50% Mortality
infarction), followed by the • Within 4–5 days • Risk factors (hypertension, 1st MCI)
basal inferior septum (inferior
myocardial infarction). Echo Features
• Left ventricular volume overload • Elevated flow velocity across the
Basal VSD jets may be difficult • Disrupted/spliced interventricular pulmonic valve
to discern from a tricuspid septum • Acute pulmonary hypertension
regurgitation signal in the • Turbulent flow/jet on color Doppler
Color Doppler. • CW Doppler jet velocity depends on
the size of the VSD and pressure
Ischemic VSDs are rarely a relation between the left and right
simple hole in the septum, but ventricle
rather the result of splicing of
the interventricular septum.

ISCHEMIC VENTRICULAR VSD color Doppler

SEPUTM DEFECT (VSD) – apical VSD 2D
four-chamber view
VSD
Rupture of the interventricular
septum is visible on the 2D image
(left). Turbulent flow across the IVS
defect is seen with color Doppler
(right).

Papillary Muscle Rupture

• Incidence 1% • 5% of deaths due to myocardial

• Rupture of the posteromedial papillary infarction
muscle is more common than the • Mortality 70%
anterolateral one (which has dual • Also in small infarctions
blood supply)

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 008 // CORONARY ARTERY DISEASE

COMPLICATIONS NOTES

Echo Features Transthoracic echo assessment

• Severe mitral regurgitation • Triangular shape of the mitral regurgitati- may be difficult (due to
• Flail papillary muscle on spectrum (low systolic blood tachycardia, pulmonary edema,
• Left ventricular volume overload (LV pressure in shock and pressure lack of a distinct mitral
dilatation/hyperdynamic function) equilibration between the left ventricle regurgitation jet due to a large
• Low-velocity mitral regurgitation signal and the left atrium) regurgitant orifice and low flow
• Pulmonary hypertension velocity, mitral regurgitation) –
• Dilated pulmonary veins perform a transesophageal exam.

PAPILLARY MUSCLE RUPTURE –

apical four-chamber view/2D

The head of the papillary muscle

is detached from its body and
swings freely between the left
ventricle and the atrium attached
Chordae to the mitral valve.

ṔM head
VL
AM
PMVL

Right Ventricular Infarction Look at regional and global

RV function in EVERY patient
• 30 – 50% of inferior myocardial infarction • Poorer prognosis with inferior myocardial
• Posterior wall, posterior septum affected • Usually in proximal RCA (Cx possible) infarction. When asssessing
• Recovery of right ventricular function is the right ventricle, rotate
common after acute myocardial infarction around its axis to visualize the
entire right ventricular
Echo Features myocardium.

• Dilated right ventricle • Tricuspid regurgitation (common)

• Wall motion abnormalities (inferior) • Dilated inferior vena cava
• Global/regional reduced right
ventricular function

Mural Thrombus Thrombi may be difficult to

distinguish from prominent
• Thrombogenicity of the infarct tissue • Usually apex (aneurysm) apical trabecula. Use LV contrast.
• Low flow state in the infarcted area • Systemic embolism 2%
• More common in large anterior • Small thrombi are difficult to detect
myocardial infarction

Echo Evaluation Move the focus zone to the apex

• Visible in > 1 plane. • Assess echogenicily (fresh/old thrombus). (near field) to increase your
• Assess mobility to estimate the risk of • Measure size to monitor treatment sensitivity.
embolism. effects.

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 008 // CORONARY ARTERY DISEASE

NOTES COMPLICATIONS
APICAL THROMBUS – zoomed
apical four-chamber view/2D

The thrombus has a slightly

different echogenicity than the Apical
myocardium. Older thrombi ap- thrombus
pear more echodense.

Restriction of the posterior Mitral Regurgitation in CAD – Mechanism

leaflets is a frequent finding
in patients with inferior • Annular dilatation • Aggravation of mitral regurgitation in
infarctions (regional • Leaflet restriction pre-existing MR caused by ventricular
remodeling of the inferior • Rupture of papillary muscle (acute) distortion (combined mechanisms)
wall). Restriction of both
leaflets is a consequence of
global remodeling (and
usually combined with
annular dilatation).

Diagnosis of Posterior Leaflet Restriction

• Increase in tenting area • Posterior jet direction

• ”Y” position of anterior to • Increase in tenting area (increase
posterior leaflet of coaptation depth)
• Jet origin further within the ventricle
• Immobility of the posterior
leaflet (tethering)

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 009// Aortic Stenosis

CONTENTS
82 Basics

85 Quantification of Aortic Stenosis

88 Special Circumstances

89 Sub- and Supravalvular Aortic Stenosis

90 Indication for Aortic Stenosis Surgery/Intervention

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NOTES BASICS

Severe asymptomatic aortic Natural History of Aortic Stenosis

stenosis is generally associated
Onset of symptoms With aortic valve
with a favorable prognosis. The 100 replacement
risk increases dramatically once
symptoms occur. Asymptomic stage

PERCENT SURVIVAL
75

Without aortic
valve
50 replacement
Heart failure

25 Syncope

Angina

10 20 30
YEARS
Adapted from Ross Circulation 1968

Epidemiology

• 3rd most common form of

heart disease
• Increasing prevalence with older age
(2–6% in the elderly)
• AV sclerosis is a precursor of AS

Hemodynamics in Aortic Stenosis

Patients with aortic stenosis have an increased afterload, which results in LV

pressure overload. Left ventricular hypertrophy is a compensatory mechanism
(reduces wall stress).
Afterload

LV pressure overload

Filling pressure LVH

Left Ventricular Failure in Aortic Stenosis

Persistent pressure overload leads to deterioration of left

ventricular function and eventually heart failure.

LVF

Low output Filling pressure

Heart failure

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BASICS NOTES

Causes of Aortic Stenosis In the Western world,

the cause of severe
Congenital abnormalities of the aortic valve are a frequent cause of aortic stenosis. aortic stenosis in
In some patients a stenosis is present at birth; in others congenital abnormal valves patients <50 years is
predispose the individual to aortic stenosis later in life (accelerated aging/calcifica- almost always
tion of the valve). congenital.

< 70 Years > 70 Years
2% 2% 2%

3%

23%
18%
50% 48%

25% 27%

Degenerative Bicuspid Postinflammatory

Unicommissural Hypoplastic Indeterminate

Adapted from Passik et al. Mayo Clinic Proc 1987

Rheumatic Aortic Stenosis The aortic valve is the

second most common
• Usually mild to moderate stenosis • Often combined with aortic valve involved in
• May progress to severe aortic stensos regurgitation rheumatic heart disease.
(accelerated valve aging) • Thickened leaflets/focal calcification
• Often multivalvular disease

Congenital Abnormalities of the Aortic Valve To establish the diagnosis of a

bicuspid valve, use the short-
• Unicuspid, bicuspid, quadricuspid • May be associated with genetic axis view and observe the
• Syndromes (e.g. Down‘s, Heyde‘s) syndromes (such as Down‘s, Heyde‘s) opening motion of the valve.

Morphology of the Aortic Valve A raphe may be small and

subtle. In this setting the
Normal valve (tricuspid) Functional bicuspid valve may appear
(tricuspid with raphe) – congenital tricuspid, especially on a
still frame.

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NOTES BASICS

A dilated ascending aorta Bicuspid – congenital Unicuspid – congenital

in a young patient may
point to a congenital
aortic valve abnormality.

Echocardiographic Assessment of Aortic Valve

2D
• Valve morphology (cusps) • Atrial enlargement
• Visual assessment of aortic valve • Exclude subvalvular membrane
opening and motion • Left ventricular hypertrophy
• Degree of calcification • Measurement of the aortic annulus (for
• Left ventricular function valve sizing in TAVR)

Coronary artery disease is MMode

frequent in calcified • Eccentric AV closure
aortic stenosis. • ”Box” seperation of cusps

TRICUSPID AORTIC VALVE –

zoomed PSAX AV
PV
Calcified aortic valve with re- Calcification
duced opening (aortic valve area=
AVA) in a patient with severe
aortic stenose.

Aortic valve area

BICUSPUD AORTIC VALVE –

zoomed PSAX AV

Calcified bicuspid aortic valve

with severe stenosis. Only 2
cusps are visible. It may be
difficult to determine whether a
valve is bicuspid when it is heavily
calcified.

Cusp

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BASICS NOTES

Doppler Assessment of the Aortic Valve Check were aliasing (flow

acceleration) occurs: at
Color Doppler the valve (valvular AS),
• Color Doppler aliasing caused by high • Look for the origin of aortic stenosis jet below the valve
velocity jet (stenotic turbulences) to exclude LVOT obstruction (SAM/ (subvalvular stenosis)
membrane)? or above the valve
(supravalvular aortic
CW/PW Doppler stenosis).
• Measurement of maximum and mean • Diastolic dysfunction (filling pressure,
velocity gradient across the aortic valve indirect sign of severity, correlation
(CW Doppler) with symptoms (PW Doppler)
• Measurment of LVOT velocity (PW • Elevated pulmonary pressure is a sign
Doppler) of left heart failure (CW Doppler)

QUANTIFICATION OF AORTIC STENOSIS

Methods 220 mmHg 120 mmHg Planimetry (TTE) is usually

not possible because the
• Planimetry (TEE) valves in AS are too
• Pressure gradients  100 mmHg heavily calcified (tracing
• Aortic valve area using the aortic valve orifice
Stenosis results in a pressure gradient.
continuity equation The pressure gradient is high before the will be difficult).
obstruction and low behind the stenosis.

Evaluation of Gradients time A late peak of the

Doppler signal
• Gradient = 4 x Vmax2 indicates severe aortic
(simplified Bernoulli equation) stenosis.
velocity (m/s)

• Gradients are influenced by

heart rate and stroke volume
• Jet velocity is elevated (> 2m/s) peak velocity
when AVA < 2 – 2.5 cm 2

AORTIC STENOSIS SPECTRUM

– apical five-chamber view/CW
Doppler

Severe aortic stenosis with a peak

velocity > 5.9 m/s during systole.
The baseline is shifted upward
and the velocity range adapted
LVOT AV (8 m/s). Additionally, the LVOT
trace velocity can be seen within the
velocity
AS spectrum, indicating good
Doppler alignment.

Peak velocity

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 009 // AORTIC STENOSIS

NOTES QUANTIFICATION OF AORTIC STENOSIS

Patients with bicuspid stenosis Practical Considerations

and those with severe AS
generally have eccentric AS jets. • Try to be parallel to the stenotic jet and • Use the pencil probe.
In these patients you will usually optimize the angle. • In the setting of atrial fibrillation,
obtain the highest gradient from • Evaluate gradients from multiple average the gradients of several beats
a right parasternal approach. windows (apical, suprasternal and right and the PW-LVOT velocity.
parasternal).
High cardiac output (young or • Set the focus point of the CW Doppler
anxious patients, hyperthyroi- in the aortic valve.
dism, fever, dialysis shunts, etc.)
may cause flow velocities >2 m/s
and thus mimic AS.

RIGHT PARASTERNAL SPECTRUM

– right parasternal view/CW
Doppler CW

Doppler spectrum of severe

aortic stenosis from a right
parasternal view. The spectrum is
directed towards the transducer
and is therefore positive.

Measurement of LVOT width Calculation of Aortic Valve Area (Continuity Equation)

is most critical for
the calculation of the LVOT width is measured in the PLAX, slightly proximal to the aortic valve, exactly
aortic valve area. Small where you should also place the PW Doppler sample (5-chamber view).
measurement errors result in
large differences.

A2 x V2 Ao

A1 x V1
LV
LA

LVOT diam = A1
A2 = V1 x A1 /V2

LV=Tvel = V1

AVvel = V2

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QUANTIFICATION OF AORTIC STENOSIS NOTES

Limitations of Continuity Equation To find the optimal location

of the PW Doppler sample
• Measurement of LV may be difficult. • PW sample volume position plays an volume, place it first in the
• The true geometry of LVOT (round, important role AS jet and slowly move the
oval) is not appreciated by • Underestimation of AV peak velocity in sample volume proximally
the measurement of distances suboptimal Doppler alignment until there is a sudden
velocity drop.

LVOT DIAMETER – PLAX/2D

The LVOT diameter is measured

on a parasternal long-axis view,
IVS closely below the aortic valve. It
Aorta is advisable to slightly over-
measure the LVOT diameter and
AV thus compensate the oval shape
LVOT of the LVOT.
diameter
AMVL

Reference Values for Aortic Stenosis

Mild Moderate Severe

Mean gradient < 25 mmHg 25 – 40 mmHg > 40 mmHg

Aortic valve area > 1.5 cm2 1.0–1.5 cm2 < 1.0 cm2

Jet velocity < 3 m/s 3–4 m/s > 4 m/s

ESC 2012

Valvulo-Arterial Impedance Valvuloarterial

impedance <3.5
Zva = (SAP + MG)/SVI increases the mortality
• Z(va) = measure of global LV load • MG = mean transvalvular risk 2.3 to 3 fold.
• SAP = systolic arterial pressure pressure gradient
• SVI = stroke volume index.

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 009 // AORTIC STENOSIS

NOTES SPECIAL CIRCUMSTANCES

To differentiate between Low Gradient Aortic Stenosis

true severe and pseudo-
severe AS, you should • Mean gradient
perform a dobutamine < 30 mmHg – 40mmHg Features of AS
stress echo. • EF < 40% +
red. LVF
• AVA < 1.0 cm2

Gradient < 30–40 mmHg Gradient > 40 mmHg

Pseudo-severe AS True severe AS Severe AS

Correct classification makes Factors in Favor of True Severe

a difference. Patients with ”Low-Flow Low-Gradient” Aortic Stenosis
true aortic stenosis are
potential candidates for valve • Heavily calcified valve • LVH (in the absence of hypertension)
replacement. • Late peak of AS signal • Previous exams with higher gradients

Patients with paradoxical

low-flow low-gradient AS ”Paradoxical” Low-Flow Low-Gradient Aortic Stenosis
tend to have a higher level of
LV global afterload, which is Patients with aortic stenosis and very small ventricles/cardiac output may also have
reflected by a higher valvulo- low gradients in the setting of severe aortic stenosis.
arterial impedance.
Low gradients in severe AS/ Low stroke volume (<35ml/m2)
normal EF • Concentric LVH ?
• AVA < 1.0 cm 2
• Small, restrictive LV
• EF > 50 % • Calcified valve
• Mean gradient < 40mmHg • (Hypertension)

The gradients
overestimate AS severity Aortic Stenosis and Aortic Regurgitation
only when aortic
regurgitation is moderate • Tend to occur simultaneously
or in excess of moderate. • Common in bicuspid valves
• Significant aortic regurgitation leads to higher
gradients (overestimation of the severity of aortic stenosis)

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SPECIAL CIRCUMSTANCES NOTES

Pressure Recovery Pressure recovery

may lead to
Increase of pressure downstream from the stenosis caused by reconversion of overestimation of
kinetic energy to potential energy gradients.

Where is it relevant? • High flow rate

• Small aorta < 30mm • Bileaflet prosthesis
• Moderate aortic stenosis • Funnular obstruction

SUB- AND SUPRAVALVULAR AORTIC STENOSIS

Subvalvular Aortic Stenosis (Membranous)

• 2nd most common LV outflow obstruction

• Variable morphology (i.e. muscular ridge)
• A transesophageal study is often required

SUBVALVULAR AORTIC
STENOSIS – PLAX/2D

A muscular ridge with a mem-

brane causing obstruction is seen
in the LVOT. In some patients
AV you will need to scan through
Subvalvular the entire LVOT to detect the
Membrane membrane.

AMVL

Other Findings in Subvalvular Aortic Stenosis Subvalvular obstruction

leads to aortic valve
• Abnormal mitral valve chords destruction (jet lesion)
• Associated defects (50%) (e.g. PDA, VSD, bicuspid AV, pulmonic stenosis) and aortic regurgitation.

Echo Features
• Color flow aliasing at the site of • Membrane of varying thickness within
obstruction the LVOT, often with a small muscular
• Elevated CW velocity despite normal ridge. Best visualized on atypical PLAX
AV morphology views

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 009 // AORTIC STENOSIS

NOTES SUB- AND SUPRAVALVULAR AORTIC STENOSIS

Use other imaging modalities Types of Supravalvular Aortic Stenosis

(CT/MRI) and look for other
congenital abnormalities
(Williams syndrome).

Hourglass type Membranous type Tubular type

(most common)

INDICATIONS FOR AORTIC STENOSIS

SURGERY/INTERVENTION

When the patient does not Indications for Surgery in Severe AS (Class I/ESC 2012)
fulfill the criteria/indications for
surgery, annual follow-up • Symptomatic patients with severe AS • When other cardiac surgery
should be performed. Shorter (dyspnea, syncope, angina) is being performed (e.g. CABG;
intervals are necessary when AS • Symptomatic patients with severe AS ascending aorta)
is severe, heavily calcified or and reduced LV function (<50% EF)
when symptoms are uncertain. • Asymptomatic patients with severe AS
and abnormal exercise test

The indication for aortic Other Things to Consider in Asymptomatic Severe AS

valve surgery must be
established individually. • Valve morphology (bicuspid)
Consider age, co- • Severity of AS (very severe AS)
morbidities, the risk of • Degree of calcification
myocardial fibrosis in • Subclinical myocardial dysfunction (longitudinal function)
LVH, longitudinal • Rapid progression
dysfunction, the degree
of calcification, the
patient‘s preference and
expectations, the rate of
progression, etc.

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 009 // AORTIC STENOSIS

INDICATIONS FOR AORTIC

STENOSIS SURGERY/INTERVENTION NOTES

Transcatheter Aortic Valve Replacement (TAVR) The indications for TAVR may
change with improvements in
Consider interventional valve replacement in: methodology.
• Symptomatic/severe aortic stenosis
• High-risk patients
• Suitable anatomy (AV annulus diameter)
• Appropriate anatomical access for valve implantation (transfemoral/transapical)

TRANSCATHETER AORTIC VALVE

– PLAX/2D

The steel frame and the bovine

pericardial tissue leaflets of an
Edwards-Sapien valve are visible
in the aortic annulus.

Steel Frame
Bovine Valve

Echo Assessment for TAVR Consider alternatives for the

measurment of the aortic
• Establish the presence of • Assess the extent and valve annulus (2D/3D TEE,
severe aortic stenosi. distribution of calcification CT), as these methods are
• Assess annular dimension during • Exclude patients with bicuspid valves more accurate than 2D
systole in a zoomed PLAX for valve (an ellipitical orifice may predispose to echocardiography.
sizing Undersizing may lead to device incomplete valve deployment)
migration or significant paravalvular • Exclude patients with basal septal
aortic regurgitation. Oversizing increases hypertrophy and dynamic LVOT
the risk of underexpansion, reduces obstruction
durability, and increases vascular
access complications

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 009 // AORTIC STENOSIS

NOTES

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 010 // Aortic Regurgitation

CONTENTS
94 Basics

97 Hemodynamic Calculation of Regurgitant Volume and Fraction

97 Proximal Isovelocity Surface Area (PISA) Method

98 Acute Aortic Regurgitation

98 Indications for Surgery in Severe AR

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 010 // AORTIC REGURGITATION

NOTES BASICS

Study the morphology Cause of Chronic Aortic Regurgitation

of the aortic valve on a
PSAX view at the base. • Degenerative/Sclerosis/Aging • Postendocarditis
• Aortic dilatation • Rheumatic
• Congenital • Aortic valve prolapse/rupture

Elevated left ventricular filling Hemodynamics in Aortic Regurgitation

pressure (diastolic dysfunction)
usually denotes LV deterioration • Left ventricle volume overload
(and symptoms). • Dilated left ventricle
• Filling pressure elevated
• Afterload increased

Quantification of Aortic Regurgitation

Should be Based on

• Aortic regurgitation jet (Vena contrac- • Retrograde flow in the aorta

ta, width, flow convergence) • Indirect findings
• Deceleration time or aortic regurgitation
spectrum (PHT)

LV dilatation is usually less when Indirect Findings in Aortic Regurgitation

AS and LVH are additionally
present. • Dilated left ventricle • Slightly enlarged left atrium
In our experience the ventricle • Hyperdynamic function • Mitral regurgitation (annular dilatation)
compensates more by dilatation • Eccentric left ventricular hypertrophy • Diastolic dysfunction
than with an increase in ejection
fraction.

Look at the vena contracta and Imaging of Aortic Regurgitation Jet

PISA. Use an integrative
approach for quantification. • PLAX • Five-chamber view/
• PSAX (visualize origin of jet) three-chamber view
• Suprasternal (to determine
retrograde flow)

94

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BASICS NOTES
Left carotid artery RETROGRADE FLOW IN AR –
suprasternal view/Color Doppler
Left subclavian artery
Aortic arch Severe retrograde flow during
diastole. The red color Doppler
signal denotes flow towards the
transducer from the descending
Retrograde flow
aorta towards the the arch. Color
Doppler may be used to guide
Pulmonary positioning of the PW Doppler
artery spectrum.

PW sample RETROGRADE FLOW IN AR –

Suprasternal view/PW Doppler

Holodiastolic flow with a

maximum velocity of 0.7 m/s,
indicating severe aortic
Holodiastolic
regurgitation.
retrograde
flow

Forward flow

Aortic Regurgitation – Reference Values 1) AR may be difficult to quantify

in tachycardia and higher heart
Mild Moderate Severe rates. 2) Retrograde flow is very
important. 3) Use both color
Vena contracta < 3mm 3 – 6mm > 6mm Doppler and PW Doppler to study
retrograde flow.
Jet width (% of LVOT) < 25 25 – 65 > 65
To detect retrograde flow in
Flow convergence not visible small large the descending aorta, place
the sample volume
Pressure half-time (PHT) (PW-Doppler) at the inner
aortic regurgitation (msec) > 500 200 – 500 < 200 curvature of the cranial
portion of the descending
ESC 2013 aorta.

Holodiastolic retrograde flow in

the aorta = severe AR.

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NOTES BASICS
VENA CONTRACTA –
apical three-chamber view

Severe aortic regurgitation with

a large flow convergence zone, a
vena contracta >6 mm, and a jet
Jet
width of 70% of the LVOT. width
Vena contracta

Flow
AMVL convergence

The AR signal should have a Pitfalls

velocity above 4.5 m/second.
Otherwise the signal quality • Complex, eccentric, or multiple jets. • Calcified valves (it will be difficult to see
will be inadequate for • Poor alignment of CW Doppler with the proximal flow convergence zone)
assessment of pressure half the aortic regurgitation jet • Machine settings (PRF)
time (non-parallel jet
alignment) .

AR SPECTRUM – apical five-

chamber view/CW Doppler AR

Pressure half-time is determined

by measuring the slope of the AR
signal. Severe AR is characterized AR signal AR PHT
by a very steep slope.

Aortic Regurgitation and Other Forms of

Valvular Heart Disease

• Aortic regurgitation increases gradients • Volume overload of aortic regurgitati-

in aortic stenosis. on and mitral regurgitation add up (two
• Aortic regurgitation shortens the PHT halves make a whole).
of mitral inflow in mitral stenosis.

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HEMODYNAMIC CALCULATION OF
REGURGITANT VOLUME AND FRACTION NOTES
SV LVOT – SV MV AR vol
RF (%) = = Hemodynamic calculations of
SV LVOT SV LVOT AR are rarely used. Their main
limitation is the inaccuracy of
SVMV = CSAMV x VTIMV SVLVOT = CSALVOT x VTILVOT calculating the MV cross-
sectional area.
CSA= d2 x 0.785

CSA = cross-sectional area SV = stroke volume d=diameter (MV/LVOT)

Reference Values No one ever uses this

calculation, but you
Mild Moderate Severe can impress your
friends with it!
Regurgitant volume (ml/beat) < 30 30 – 59 ≥ 60

Regurgitant fraction (%) < 30 30 – 49 ≥ 50

PROXIMAL ISOVELOCITY
SURFACE AREA (PISA) METHOD

AR Flow – SV MV The PISA method for AR

ERO (PISA) = = quantification is rarely used,
AR vel
but you can use flow
Aortic regurgitationflow = 2 x r x Vr
2
convergence (PISA zone) for
r = radius of flow convergence, semiquantitative assessment.
Vr = corresponding aliasing velocity,
Rvel = maximum velocity of the aortic regurgitation jet,
ERO = effective regurgitant orifice

Reference Values

Mild Moderate Severe

Effective regurgitant orifice (cm2) < 0.1 0.1 – 0.29 ≥ 0.3

Regurgitant volume (ml) < 30 30 – 59 ≥ 60

ESC 2013

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NOTES ACUTE AORTIC REGURGITATION

LV size = normal or slightly Causes

dilated and hyperdynamic
(the ventricle has not had • Endocarditis • Aortic dissection
time to dilate/adapt). • Cusp rupture • Iatrogenic (trauma)

Echo Features of Acute Aortic Regurgitation

• Small/slightly dilated left ventricle • Holodiastolic retrograde flow in the

• Tachycardia descending aorta
• ”Initially” hyperdynamic left ventricle • Short pressure half-time
• Premature mitral valve closure

INDICATIONS FOR SURGERY IN SEVERE

AORTIC REGURGITATION (ESC 2012)

Surgery is indicated

• In symptomatic patients • In asymptomatic patients with severe

• In asymptomatic patients with reduced LV dilatation: (left venricular enddiasto-
resting LVF (LVEF < 50%) lic diameter=LVEDD > 70 mm, LV
• In patietnts undergoing CABG or endsystolic diameter=LVESD > 50 mm
surgery of the ascending aorta, or or LVESD/BSA >25 mm/m2))
another valve. • If EF is too poor (< 30 – 35%)
Candidates for heart transplantation


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 011 // Mitral Stenosis

CONTENTS
100 Introduction

102 Quantification

103 Mitral Valve Pressure Half-Time

104 Valvuloplasty
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NOTES INTRODUCTION

Vavular involvement is Causes

present in 2/3 of patients with
rheumatic fever. • Rheumatic (most common)
• Stenotic annular calcification
Rheumatic heart disease is very • Congenital
common in developing countries.

The Shone complex is characterized Congenital Mitral Stenosis

by a combination of congenital
mitral stenosis and other forms of • Rare (0.6% of CHD)
left-sided inflow and outflow • Combined with other congenital defects
obstructions (coarctation, valvular/ • Forms: MV annulus hypoplasia, parachute MV, double-orifice MV
subvalvular aortic stenosis).

In mitral stenosis there is Effects of Mitral Stenosis

no ”burden” on the left
ventricle (no pressure or • LA-LV gradient
volume overload). • Elevated pressure in LA
• Elevated pressure pulm. capillaries
• Pulmonary congestion/edema
• Pulmonary hypertension
• Right ventricular dilatation
• Tricuspid regurgitation
• Right heart failure
• Atrial fibrillation
The pressure difference between the left atrium
and the left ventricle as recorded with invasive
measurements. The area between the curves
corresponds to the mean gradient.

The MMode is no Echo Characteristics of Mitral Stenosis

longer used to
diagnose or quantify Valve features:
mitral stenosis. • Doming (diastolic bulging) of the
anterior mitral valve leaflet RV
LV
• Reduced valve opening
• Commissural fusion Ao
• Leaflet tip thickening
• Subvalvular involvement LA
(thickened and fused tendinae)
• Secondary calcification Doming

Doppler Features
• Color Doppler is indicative of mitral • CW Doppler is used to quantify mitral
stenosis (candle flame appearance) stenosis (gradients/pressure half-time)

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INTRODUCTION NOTES
DIASTOLE MITRAL STENOSIS – PLAX/2D

Typical features of mitral ste-

nosis: Doming of the anterior
Thickened leaflet, thickening of leaflet tips,
aortic valve thickened aortic valve (aortic
valve involvement), and enlarged
Reduced opening Dom left atrium.
i
AMV ng
Tip L
thickening

Other features of mitral stenosis/rheumatic heart disease Many of these features

• Thickened aortic valve • Pulmonary hypertension develop and progress over
• Reduced left ventricular function • Aortic regurgitation time. Also consider these
(high risk of atrial fibrillation) • Tricuspid stenosis problems in your
• Enlarged left atrium, atrial fibrillation • Left atrial thrombuss management strategy.

THROMBUS IN MITRAL STENOSIS

– PLAX/2D

Mitral Severe mitral stenosis with

stenosis large left atrial thrombus (partly
Calcified shadowed by the calcified aortic
AV valve).

Shadow

Thrombus

Risk of Thrombus Formation Most thrombi are seen in the

left atrial appendage. Thus,
• Systemic embolism in 20% of all MS patients you will miss them on
• 80% of patients with severe MS are in atrial fibrillation transthoracic echo.
• 45% have left atrial spontaneous echo contrast

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NOTES QUANTIFICATION

MV Area – Reference Values

Normal (cm2) 4 – 6 cm2

Mild (cm2) > 1.5 cm2

Moderate (cm2) 1 – 1.5 cm2

Severe (cm2) < 1 cm2 ESC 2012

MITRAL VALVE PLANIMETRY –

PSAX MV/2D

The mitral valve was investi-

gated at the tip of the leaflets, RV
where the mitral valve opening is
smallest. The image is frozen in IVS
diastole at the time when mitral
Calcified MV
valve opening is largest. Tracing-
may be difficult when the valve is
calcified. MVA

Planimetry is the most direct Problems of Mitral Valve Planimetry

method to quantify MS.
It does not rely on Mitral valve area is measured on an optimized parasternal short-axis view at the
hemodynamic assumptions. smallest mitral valve orifice.
However, it is also technically
the most challenging method. • Image quality • Atrial fibrillation
• Alignment • Incomplete commissural fusion
• Timing • Operator experience
• Calcification

Forms of Mitral Stenosis

The funnular form is usually
seen when there is strong RV
LV LV RV
involvement of the
subvalvular apparatus.
Ao Ao

LA LA

Classic form Funnular form

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QUANTIFICATION NOTES

Mitral Stenosis Mean Gradient – Reference Value Transvalvular gradients are

higher in the setting of
additional mitral
Mild (mmHg) <5 regurgitation.

Moderate (mmHg) 5 – 10

Severe (mmHg) > 10

MITRAL STENOSIS SPECTRUM –

apical view/CW Doppler

Mean gradients are obtained by

tracing of the CW Doppler mitral
MV PHT valve inflow spectrum. The decel-
MV trace eration time (pressure half-time)
is used to calculate mitral valve
area.

MITRAL VALVE PRESSURE HALF-TIME

220
MV Area = The pressure half-time method is
PHT based on hemodynamic
The rate at which the gradient between the left atrium and the left ventricle assumptions and was initially
diminishes corresponds to the size of the mitral valve orifice. The smaller the tested in young patients with
orifice, the longer is the pressure half-time. rheumatic heart disease. It
works less well in elderly and
multimorbid patients with
PHT – pitfalls additional valvular lesions, left
• Diastolic dysfunction leads to overesti- • PHT is unreliable after valvuloplasty. ventricular dysfunction and left
mation of mitral stenosis • Heavily calcified valves make PHT ventricular hypertrophy.
• Aortic regurgitation leads to underesti- unreliable
mation of mitral stenosis • Concave shape of tracing

Color Doppler, PISA and Continuity Equation

• Candle flame appearance of mitral valve

inflow with color Doppler D2LVOT VTIAortic
MVA = x
• PISA for quantification (rarely used) 4 VTIMitral
• MVA = Mitral volume flow/peak velocity
of diastolic mitral flow
• Continuity equation (does not work when aortic regurgitati-
on and mitral regurgitation are both present)

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NOTES MITRAL VALVE PRESSURE HALF TIME

Quantification of Mitral Stenosis in Atrial Fibrillation

Planimetry Several different measurements

(use average)

Mean gradients Average 5 cycles with small variations of

R-R intervals close to normal heart rate

Pressure Avoid mitral flow from short diastoles/

half-time average different cardiac cycles

VALVULOPLASTY

Indication and Results

Indication Results
Clinically significant MS (valve Good immediate results (valve area
area less than 1..5 cm ( 1.8 cm in
2 2
> 1.5 cm2 without regurgitation)
unusually large patients) can be obtained in over 80%

BALLOONVALVULOPLASTY
VL

IN MITRAL STENOSIS – TEE

AM

long-axis view PMVL

AV
Balloon
The balloon is positioned within
the mitral valve and expanded to
enlarge the mitral valve orifice.

Artefact

Suitability of Valve Morphology

• Mobility • Subvalvular thickening

• Valve thickening • Valve calcification
• Thrombus • Mitral regurgitation
• Tricuspid regurgitation

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VALVULOPLASTY NOTES

Wilkins Score For the suitability of mitral

valve valvuloplasty also look
Patients with a Wilkins score > 8 – 10 are not ideal for mitral valve valvuloplasty. at the commissural region.
Patients with calcification of
the commissures are not ideal
Grade Mobility Thickening Calcification Subvalvular
candidates.
thickening

1 Highly mobile Leaflets near A single area of Minimal

valve with only normal in increased echo thickening just
leaflet tips thickness (4-5 brightness below the mitral
restricted mm) leaflets

2 Leaflet mid and Mid-leaflets Scattered areas Thickening of

base portions normal, of brightness chordal
have normal considerable confined to structures
mobility. thickening of leaflet margins extending to
margins (5-8 one third of the
mm) chordal length

3 Valve continues Thickening Brightness Thickening

to move extending extending into extended to
forward in through the the mid distal third of
diastole, mainly entire leaflet portions of the the chords
from the base. (5-8 mm) leaflets

4 No or minimal Considerable Extensive Extensive

forward thickening of all brightness thickening and
movement of leaflet tissue throughout shortening of all
the leaflets (>8–10 mm) much of leaflet chordal
occurs in tissue structures
diastole. extending down
to papillary
muscles

Adapted from Wilkins et al. Br Heart J 1988

Complications of Mitral Valve Valvuloplasty

• Acute mitral regurgitation

• Iatrogenic atrium septal defect
• Embolism
• Tamponade (perforation following
transseptal puncture)
• Vascular access complications/
bleeding

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NOTES

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CONTENT
108 Basics

109 Quantification of Mitral Regurgitation

111 Mechanisms of Mitral Regurgitation

116 Mitral Valve Prolapse

117 Flail Leaflet

117 Other Causes of Mitral Regurgitation

118 Indications
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NOTES BASICS

Severe mitral Natural History of Severe Mitral Regurgitation

regurgitation is no
benign condition. • 10-year survival rate of 57% • The 5-year risk for cardiac events in
• The 5-year all-cause mortality in patients asymptomatic mitral regurgitation
with asymptomatic mitral regurgitation patients is 33%
patients is 22%

In the setting of Hemodynamics of Mitral Regurgitation

significant mitral
regurgitation, an ejection In acute mitral regurgitation (MR), the ejection fraction is high and the size of the
fraction of 55% to 60% left ventricle is normal or slightly enlarged (unadapted). In chronic mitral regurgita-
(which is otherwise tion the ejection fraction is ”supranormal” and the left ventricle is dilated (adapted).
considered normal) In decompensated mitral regurgitation the left ventricle is significantly enlarged
already denotes left and the ejection fraction starts to drop.
ventricular failure. EF 68% EF 83%

Normal Acute MR

EF 77% EF 30%

Chronic MR Decompensated MR

Even when mitral Consequences of Mitral Regurgitation

regurgitation is severe,
the patient may remain • Left ventricular volume overload • Tricuspid regurgitation
asymptomatic for a • Elevated left ventricular filling pressure • Reduced systolic wall stress
long period of time. • Pulmonary hypertension • Reduced afterload

Echocardiography Causes
provides important clues
as to the cause of mitral Primary (structural) causes Secondary (functional) causes
regurgitation. • Mitral valve prolapse, myxomatous • Annular dilatation
Combinations of several mitral valve disease • Restrictive leaflets
etiologies are not • Flail leaflet • Systolic anterior motion
uncommon (e.g. annular • Valve fibrosis and calcification • Atrial enlargement
dilatation and restrictive • Rheumatic heart disease
leaflets). • Congenital
• Papillary muscle rupture
• Endocarditis
• Drugs
• Systemic diseases

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QUANTIFICATION OF MITRAL REGURGITATION NOTES

Integrative Approach Your ability to image jets

is more important than
Color Doppler Jet (flow convergence, vena contracta) quantitative parameters.
Use multiple views.
2D Imaging Indirect signs

Quantification Based on Color Doppler The proximal portions of the

jet (the vena contracta and the
Mild Moderate Severe flow convergence zone) are
more important for the
Vena contracta (mm) <3 3 – 6.9 ≥7 quantification of mitral
regurgitation than jet area,
Jet area (%) Small, central jet Variable Large, central jet length or width.
(<20% of LA area) (> 40% of LA area)
Do not base the quantification
ESC 2013 of mitral regurgitation on a
single parameter.

QUANTIFICATION OF MITRAL
REGURGITATION – apical
four-chamber view/Color
Flow convergence Doppler
TV PMVL
Vena contracta Typical color Doppler features
AMVL of mitral regurgitation with a
prominent flow convergence
zone (PISA), a vena contracta ≥
7mm, and a jet area > 40%
of LA area.
Jet area

Color Doppler Confounders The PRF setting greatly

influences the size of the jet.
• Geometry of regurgitant orifice • Driving force (systolic pressure) Always use the same PRF. If
• Multiple jets • LA compliance not, you will be unable to
• Coanda effect (”wall hugging” jets) make comparisons.

The maximal mitral

regurgitation velocity (CW
Doppler) represents systolic
blood pressure and does not
correlate with the severity of
mitral regurgitation.

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NOTES QUANTIFICATION OF MITRAL REGURGITATION

The size of the left atrium Indirect Signs

does not permit
quantification of mitral • Dilated left ventricle
regurgitation. • Hyperdynamic left ventricular function
• Left atrial enlargement
• Interatrial septum bulging (towards RA)

In most instances you will Retrograde Flow in Pulmonic Veins

not need pulmonic vein
Doppler to quantify mitral
regurgitation. In addition, a
good signal can only be
obtained in 50–75 % of
patients. Interpretation is
difficult in atrial fibrillation.
Normal flow Blunted flow Systolic flow reversal

With increasing degrees of mitral regurgitation, you will first note blunted flow of
the systolic component of pulmonary venous inflow. Very severe forms of mitral
regurgitation are accompanied by flow reversal of the systolic component.

Use magnifications Proximal Isovelocity Surface Area (PISA) Method

(zoom/RES) to enhance
the accuracy of your The PISA method allows calculation of: 1) regurgitant flow 2)
measurement. regurgitant fraction 3) effective regurgitant orifice area Proximal

Aliasing
To calculate the • Flow through hemispheric surface =
regurgitant volume, you flow through the orifice
need to trace the mitral • Shift aliasing limit to lower velocity
regurgitation spectrum 20 – 40cm/s (larger hemisphere)
Orifice
obtained with CW • Effective regurgitant orifice area
Doppler. (EROA) = [(2r2 x Vpisa)/Vmr] Isovelocity
• r= PISA radius, Vpisa= aliasing velocity, shells
Vmr= peak MR velocity

Regurgitant volume= EROA x MR VTI

Regurgitant flow = Q = 2 x r2 x x Nyquist vel.
Distal

There is much controversy as Limitations of PISA

to whether PISA should be
used. New 3D echo techniques • The geometry of orifice is not truly • Difficulties in delineation of PISA
are likely to make PISA more hemispheric. • Dynamic mitral regurgitation (flow
reliable (better approximation • Multiple or excentric jets changes throughout the cardiac cylce
of PISA geometry).

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QUANTIFICATION OF MITRAL REGURGITATION NOTES

Reference Values for Parameters of Mitral Regurgitation

Mild Moderate Severe

Regurgitant volume (ml/beat) < 30 31 – 59 ≥ 60

Regurgitant fraction (%) < 30 30 – 49 ≥ 50

Effective regurgitant orifice area (mm2) < 20 20 – 40 ≥ 40

Volumetric methods MR volume = MR inflow – aortic outflow (in the absence of AR)

ESC 2013

Features that Affect the Severity of Mitral Regurgitation The severity of mitral
regurgitation may differ
• Blood pressure (afterload) • Dyssynchrony markedly in one and the same
• Volume status • Anesthesia patient, especially in cases of
• Atrial fibrillation • Exercise functional mitral
regurgitation.

Echo Signs of Acute Mitral Regurgitation Patients with acute MR are

difficult to image and
• Hyperdynamic left ventricle • Low velocity of the MR signal (shock) interpret. These patients
with a normal size • Triangular shaped MR spectrum usually have low MR
• Tachycardia • Elevated MV inflow velocity velocity jets (shock),
• Abnormal valve morphology (e.g. tachycardia, and
papillary muscle rupture, flail leaflet) tachypnea.

MECHANISMS OF MITRAL REGURGITATION

Why Is the Mechanism Important? Usually transthoracic echo is

sufficient to determine the
• Etiology • Management mechanism. If not, use
• Prognosis (reversible) • Repair? transesophageal echo.

What Should Be Examined? The extent of morphologic

abnormalities of the mitral
• Valve morphology (thickened, myxo- • Origin of regurgitant defect valve does not necessarily
matous) • Mechanism of mitral regurgitation correlate with the severity of
• Extent of involvement (which parts of mitral regurgitation.
the valve are involved?)

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MECHANISMS OF MITRAL REGURGITATION

NOTES

Do not forget to image How to Visualize Mitral Valve Segments

the commissural regions.
It is easy to miss mitral
regurgitation.
LC

A1 P1

A2 P2

A3
MC P3
4-Chamber CS
view 3-Chamber
view

Commissural view 2-Chamber

view

CS = coronary sinus LC = lateral commissure MC = medial commissure

As a general rule in MV Mitral Valve Prolapse

prolapse/flail leaflet, the jet
direction is always opposite
to the location of the defect
(i.e. anterior jet direction in a
posterior leaflet defect).

Anterior leaflet prolapse Posterior leaflet prolapse

(jet direction posterior + lateral) (jet direction anterior + medial)

Bileaflet prolapse (central jet) Commissural prolapse/defect

(jet at the origin of the commissure)

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MECHANISMS OF MITRAL REGURGITATION NOTES

PMVL PROLAPS – apical four-
chamber view/2D

Severe prolapse of the posterior

mitral valve leaflet (medial scal-
lop – P2). The valve is thickened
AMVL (myxomatous) and the left atri-
um/ventricle are enlarged.

Prolapse
PMVL

PMVL PROLAPSE – apical four-

chamber view/Color Doppler

The jet direction is typically

AMVL anterior and medial (towards the
interatrial septum).

Excentric jet
ant./med. direction

Flail Mitral Leaflet The direction of the jet may

vary throughout systole
(like a loose garden hose).

Anterior flail leaflet posterior flail leaflet

(jet direction posterior + lateral) (jet direction anterior + medial)

PMVL FLAIL – apical four-

chamber view/2D

Flail posterior leaflet; the pos-

terior leaflet protrudes behind
the anterior leaflet into the left
AMVL atrium. Small chordal structures
PMVL are seen attached to the tip of
the posterior leaflet.

Flail

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NOTES MECHANISMS OF MITRAL REGURGITATION

PMVL FLAIL – apical four-
chamber view/Color Doppler
Flow convergence
Chordal ruputure of the posteri-
or leaflet directs the jet towards PMVL
the interatrial septal and anterior AMVL
(seen best on an apical long-axis
view).
Anterior
jet

It is not uncommon to see a Mitral Valve Leaflet Restriction

combination of mechanisms
(e.g. annular dilatation and
leaflet restriction)

Restriction of both leaflets Posterior leaflet restriction

(central jet direction) ((jet direction lateral, posterior)

RESTRICTED PMVL – apical

three-chamber view/2D

Inferior infarction and change

of LV geometry restricts the Restricted
motion of the PMVL. The leaflet PMVL
AMVL
is drawn towards the apex. This
results in incomplete closure of
the mitral valve. AV

RESTRICTED PMVL – apical

three-chamber view/Color
Doppler

The jet in restricted posterior

leaflet motion is typically direc
ted posteriorly. It aligns with the AMV
L
position of the posterior leaflet. PMV
L
AV

Posterior
jet

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MECHANISMS OF MITRAL REGURGITATION NOTES

Other Causes In annular dilatation the jet

direction may be slightly off
the axis when other
conditions such as mitral
valve prolapse, asymmetric
restriction, or other
abnormalities of the valve are
present.
Annular dilatation MR in hypertrophic CMP
(central jet direction) (posterior jet direction)

Other mechanisms of mitral

regurgitation include:
annular calcification, leaflet
retraction, and leaflet
shrinkage (drugs/toxins).

Valve perforation
(jet through leaflet)

AMVL Perforation – apical

four-chamber view/2D

The anterior leaflet is thickened

and destroyed. A small gap can
be seen in the anterior leaflet.
PMVL
AMVL This patient has a perforated
mitral valve after endocarditis.

Perforation

AMVL PERFORATION – apical

four-chamber view/
color Doppler.

Jet through The color jet clearly traverses the

AMVL basal anterior leaflet through the
perforation. The most frequent
site of perforation is the anterior
leaflet.

Perforation

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NOTES MECHANISMS OF MITRAL REGURGITATION

The success of mitral valve Unfavorable Factors for Repair

repair strongly depends on the
surgeon‘s experience. •Extensive involvement (more than two segments)
•Repair of the anterior leaflet is more difficult than the posterior one
Repair techniques include •Commissural defects
quadrangular resection with •Calcification
sliding plasty, chordal transfer,
and the use of artificial chords.
Mitral valve repair usually
includes implantation of an
annuloplasty ring.

MITRAL VALVE PROLAPSE

The normal mitral valve plane is Forms of Mitral Valve Prolapse

shaped like a saddle. Do not
base your diagnosis solely on • Barlow‘s syndrome (classic mitral valve • Pseudoprolapse (small ventricles,
the four-chamber view since the prolapse, myxomatous) MV enlargement)
non-planer shape of the MV • Fibroelastic deficiency • Connective tissue disease
mimics a prolapse in this view. (e.g. Marfan, Ehlers-Danlos)

Barlow‘s syndrome is a Myxomatous Mitral Valve

structural disease of the (Floppy Valve, Barlow’s Syndrome)
mitral valve. It has many
features. Do not base • Prevalence = 2 – 3% • Billowing
your diagnosis on the • Rapid multiplication of cells • Excessive tissue
presence of a prolapsing • Rocking motion of the annulus • Segmental involvement
valve alone. • Involvement of the entire subvalvular • Elongated chords
apparatus

MITRAL VALVE PROLAPSE –

TEE 3D surgical view

A myxomatous mitral valve with

a prolapse of the posterior leaflet
(P3/P2). Chordal rupture is also Prolapse
present. 3D may be helpfu l in
localizing a prolapse or defect.

Fail

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 012 // MITRAL REGURGITATION

FLAIL LEAFLET NOTES

Etiology of the Flail Leaflet Ruptured chordae may be

found in more than 50% of
• Myxomatous mitral valve • Degenerative myxomatous valves.
• Endocarditis • Rheumatic

Echo Criteria – Flail Leaflet A flail leaflet can be very

subtle, especially when
• Chordal structures in the LA secondary chords are involved.
• Concave position of leaflet
• Double contour (parallel sign) The degree of mitral
regurgitation depends on the
location and type of chord that
is ruptured. A flail leaflet does
concave not always imply severe MR.

PARALLEL SIGN – zoomed apical

four-chamber view/2D

The ruptured leaflet always

extends behind the non-ruptured
PMVL leaflet to which it frequently lies
Parallel
parallel (as seen in the example
sign
with a ruptured AMVL). This sign
may be helpful in cases of subtle
chordal rupture.
AMVL

OTHER CAUSES OF MITRAL REGURGITATION

Degenerative/Aging Rheumatic Endocarditis

Common Doming of AMVL Valve destruction

Thickened, fibrotic MV Other features of rheumatic Perforation

heart disease are present

Annular calcification Combined MS + MR Leaflet rupture

Papillary muscle fibrosis Often leaflet restriction Leaflet shrinkage/

and thickened chords calcification

Usually mild to moderate Calcification of the

mitral regurgitation subvalvular apparat

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 012 // MITRAL REGURGITATION

NOTES OTHER CAUSES OF MITRAL REGURGITATION

Cleft mitral valve is almost Congenital Abnormalities of the Mitral Valve

always present in primum
septal defects (ASD I). • Chordal abnormalities • Cleft MV, parachute MV
• Papillary muscle abnormalities • Abnormal leaflet shape/length

INDICATIONS

Repair is better than Indications for Mitral Valve Surgery (ESC Class I)
replacement. Chordae
should be preserved • Surgery is indicated in symptomatic [LVESD]≥ 45 mm and/or left ventricular
whenever possible. patients with LVEF > 30% and LVESD ejection fraction ≤ 60%)
<55 mm • Mitral valve repair should be the
• Surgery is indicated in asymptomatic preferred technique when it is inten-
patients with left ventricular dysfuntion ded to last for a long time
(left ventricular end systolic diameter

LVF < 30%: no surgery (conservative, HTX or MitraClip procedure)

ESC 2012

MitraClip Procedure

MITRACLIP – TEE 3D
surgical view

3D echo is used to monitor the

MitraClip procedure. A central
clip was placed, resulting in two
incongruent mitral valve orifices.

Mitral valve
orifice
Mitral valve anulus

MitraClip

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 012 // MITRAL REGURGITATION

INDICATIONS NOTES

Suitability for the MitraClip procedure The MitraClip procedure is

(german society of cardiology) an interventional therapy by
which a clip is used to attach
OPTIMAL POSSIBLE the anterior leaflet to the
• Central pathology (segment 2), • Pathology in segment 1 or 3, posterior one. It is similar to
• No calcification • Calcification (mild) outside the surgical procedure know
the clip zone, as the ”Alfieri” stitch. Studies
• Post annulopasty/ring have shown that this
• MVA > 4 cm 2
• MVA > 3cm , good mobility of leaflets,
2
technique is able to reduce
• Mobile length of post leaflet > 10 mm , • Mobile length of the posterior leaflet mitral regurgitation and
7-10 mm improve symptoms in both
• Coaptation depth <11 mm, • Coaptation defect > 11 mm functional and structural MR.
• Normal leaflet thickness + mobility, • Leaflet constriction during systole, flail
• Flail leaflet width <15 mm, leaflet >15 mm (only with large MV
gap <10 mm annulus and multiple clips)

Unsuitable valve morphology for MitraClip: The indication and suitability for
the MitraClip procedure are still
• Perforated mitral leaflet/ • Mobile length of the posterior evolving. They depend on
cleft mitral valve leaflet < 7 mm operator/center experience and
• Severe calcification in • Rheumatic thickening of the leaflets the improvments of the
the clip zone and restriction in systole and diastole, technique.
• Significant mV stenosis • Barlow‘s syndrome with extensive
(mean gradient ≥ 5 mmHg) involvement

Echocardiographic Approach in Asymptomatic Patients The prognosis depends on

preoperative LVF.
• Monitor left ventricular function • Atrial size correlates with the risk of
and size. atrial fibrillation.
• Check for pulmonary hypertension. • Consider stress tests.
• Early surgery when repair is likely.

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 012 // MITRAL REGURGITATION

NOTES

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 013 // Tricuspid Valve Disease

CONTENTS
122 Basics

122 Causes of Tricuspid Regurgitation

124 Quantification of Tricuspid Regurgitation

125 Tricuspid Stenosis

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 013 // TRICUSPID VALVE DISEASE

NOTES BASICS

The posterior leaflet is Morphology

usually rather small!
ANTERIOR
• Three leaflets
The location and size of • Larger than mitral valve (3.2 – 6.4 cm2) POSTERIOR

the papillary muscles is • More apical and thinner SEPTAL

highly variable. leaflets than mitral valve

The tricuspid valve is more How to Image the Tricuspid Valve

difficult to image than the
mitral valve. Use a more RV PLAX ant. + post. leaflet RV-PLAX
cranial four-chamber view
(1 intercostal space higher). RV inflow-outflow view ant./sept. +post leaflet

RV optimized SEPTAL ANTERIOR

4 Chamber
4-chamber view sept. + ant. leaflet
POSTERIOR

RV inflow E/A wave lower than MV inflow,

velocity varies with respiration

CAUSES OF TRICUSPID REGURGITATION

Trivial (physiologic) TR is Prognosis of TR

common! (70% of adults).
Survival depends on:
TR severity is a good marker • Severity of tricuspid regurgitation
of disease progression. This is • Presence and degree of
true for many conditions pulmonary hypertension
(cardiomyopathy, valvular • Reduced left/right ventricular
heart disease, pulmonary function
hypertension etc.)

Functional (secondary) Causes of Functional Tricuspid Regurgitation

tricuspid regurgitation is
much more common than • Left heart disease
structural (primary) TR! • Mitral valve disease
• Pulmonary hypertension
• RV dilatation (e.g. atrium septal
defect/left-right shunt)
Annular dilatation

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CAUSES OF TRICUSPID REGURGITATION NOTES

Causes of Primary Tricuspid Regurgitation

• Rheumatic (TR combined with TS) • Endocarditis

• Trauma (blunt trauma, flail/rupture) • Congenital (e.g. dysplasia, Ebstein‘s
• Pacemaker lead associated anomaly)

Heart Disease and Carcinoid Tricuspid Regurgitation Left heart/valve involvement

may be found in the presence
Release of vasoactive substances (such as serotonin) leads to: of ASD or PFO.

• Endocardial fibrosis • May be associated with pulmonary

• Tricuspid leaflet restriction valve stenosis/regurgitation
• Wide coaptation defect

Morbus Ebstein The origin of the tricuspid

regurgitation jet is far in the
• Variable morphology • Leaflet tethering right ventricle, caused by
• Large anterior leaflet • Apical displacement (atrialized RV) apical displacement of the
tricuspid valve.
Associated with
• Atrium septal defect (> 1/3 of patients) • Aortic coarctation Consider a rudimentary form
• Ventricular septal defect • RVOT obstruction, of Ebstein‘s anomaly or
• Patent ductus arteriosus • Arrhythmia (e.g. WPW syndrome) tricuspid valve dysplasia. Look
for apical displacement of the
valve in the setting of
unexplained tricuspid
regurgitation.

Tricuspid dysplasia is
common in dogs (Labrador
retrievers).

EBSTEIN’S ANOMALY –
apical four-chamber view/2D

Ebstein’s anomaly is character-

ized by elongated leaflets and
displacement of the tricuspid
valve. This leads to partial atrial-
ization of the right ventricle.
Atrialized
RV
Apical
displacement

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 013 // TRICUSPID VALVE DISEASE

QUANTIFICATION OF
NOTES TRICUSPID REGURGITATION

The degree of tricuspid Quantification flow convergence (PISA) vena contracta

regurgitation may
increase with inspiration. • Flow convergence • Vena contracta
Therefore, observe • Jet area • Jet length
several beats with echo. • Eye-balling

SEVERE TRICUSPID REGURGITA-

TION – apical four-chamber view Dilated
RV optimized/color Doppler
RV
Tricuspid regurgitation with a
large flow convergence zone and
a wide vena contracta. The right
ventricle and atrium are severely
dilated (volume overload).
TR
jet

Dilated
RA

One overestimates right Tricuspid Regurgitation – Reference Values

ventricular function in the
presence of tricuspid Mild Moderate Severe
regurgitation (reduced
afterload). PISA radius (mm)
Nyquist limit 28 cm/s 5 mm 6 – 9 mm > 9 mm

Vena contracta
Nyquist limit 50 – 60 cm/s <7 mm >7 mm

ESC 2013

Right ventricular function Echo Findings in Severe Tricuspid Regurgitation

is hyperdynamic in the
initial phase, but may • Dilated right ventricle/atrium
deteriorate in later stages. • Dilated inferior vena cava without
respiratory variations
• Systolic flow reversal in hepatic veins
• Flattened interventricular septum in diastole
• Visible coaptation defect

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QUANTIFICATION OF
TRICUSPID REGURGITATION NOTES
DIASTOLE
FEATURES OF SEVERE TR –
Enlarged RV PSAX/2D

D-shaped ventricle with a

ned IVS flattened interventricular septum,
Flatte both in systole and diastole – in
severe TR and pulmonary
hypertension.

LV

Pericardial effusion

Indications for Tricuspid Valve Surgery (ESC Class I) When patients with severe TR
develop signs of right heart
• In patients with severe primary or • In symptomatic patients with severe failure (pleural effusion,
secondary TR undergoing left-sided isolated primary TR without severe peripheral edema, ascites), it
valve surgery right ventricular dysfunction may be too late for surgery
(irreversible RV dysfunction).
ESC 2012
Adding tricuspid repair, if
indicated, during left-sided
surgery does not increase the
risk of surgery.

TRICUSPID STENOSIS

Overview Look for doming of the tricuspid

valve in 2D and turbulent flow on
• In 9 % of rheumatic heart disease • Endocarditis (very rare) color Doppler.
• Congenital tricuspid stenosis (very rare) • After repair/replacement.
• Functional tricuspid stenosis due to Tricuspid stenosis may also occur
intracardiac (obstruction) or extracar- after tricuspid valve repair (under-
diac (compression) masses sizing of the annuloplasty ring).

TRICUSPID VALVE STENOSIS –

apical four-chamber view/CW
Doppler

Elevated flow velocity across

the tricuspid valve with a mean
Inspiration gradient >5 mmHg. Fluctuations
in inflow velocity, which increase
PHT
during inspiration.

TR

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 013 // TRICUSPID VALVE DISEASE

NOTES TRICUSPID STENOSIS

Symptoms of tricuspid valve Hemodynamics

may mimic those of right heart
failure. • Diastolic RA-RV gradient
• Dilatation and elevated pressure in the right atrium
You will find a significant • Dilated inferior vena cava
increase in gradients during
inspiration. Therefore, average
several beats.

Look for turbulent flow on color Quantification of Tricuspid Stenosis

Doppler across the tricuspid
valve in all patients with • Pressure half time: Tricuspid valve
rheumatic mitral stenosis. area (TVA)= 190/PHT – A TVA < 1 cm2
Doming of the tricuspid valve indicates severe TS (not validated).
may be difficult to visualize. • Mean gradient: Mean gradient
Thus, you will not miss > 5 mmHg indicates significant
associated tricuspid stenosis. tricuspid regurgitation.

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 014 // Prosthetic Valves

CONTENTS
128 Types of Valves

129 Echo Assessment of Prosthetic Valves

133 Complications

137 Mitral Valve Repair

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 014 // PROSTHETIC VALVE

NOTES TYPE OF VALVES

Consider mechanical valves in Mechanical Valves

younger patients.
• Metal case/occluders • High durability
The risk of mechanical • Types: ball cage, tilting disc, bileaflet • Composite graft (prosthesis + aortic
failure of a prosthesis • Anticoagulation necessary tube graft – Bentall procedure)
is very low.

Newer models include Open Types of Mechanical Valves – Few Examples

Pivot (Medtronic) and the OnX
mechanical valve (OnX). Manufacturer Model Year

Ball Baxter Starr-Edwards 1965

Disk Medtronic Medtronic Hall 1977

Medical Omniscience 1978
Alliance Monostrut 1982

Bileaflet St. Jude St. Jude 1977

Baxter Edwards Duromedics 1982
Carbomedics Carbomedics 1986
Sorin Biomedica Sorin Bicarbon 1990

Biological valves for the Biological Valves

elderly (but not exclusively).
• Ring (struts)/stentless valves • Autograft (pulmonic valve) – Ross
Biological valves also include • No anticoagulation operation
prosthetic material (struts, • Less durable than mechanical valves • New implantation systems for rapid
sewing ring). These can be • Homograft (cadaver) deployment (e.g. Edwards Intuity)
seen on the echo.
Types of Biological Valves (examples)

Manufacturer Model

Carpentier- Edwards Perimount

Carpentier- Edwards Magna

Medtronic Hancock

Medtronic Mosaic

Sorin Group Mitroflow

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ECHO ASSESSMENT OF PROSTHETIC VALVES NOTES

BIOLOGICAL MITRAL VALVE –
apical four-chamber view/2D

The struts (2 of 3 visible) protrude

into the left ventricle. The tissue
Struts component of the valve cusps are
seen between the struts.

Valve tissue

Assessment of Valve Prosthesis Do not forget to look at the

ventricle and systolic pulmonary
2D Assessment artery pressure in mitral valve
• Occluder/cusp motion, • Annulus (cavities, pseudoaneurysms, prosthesis.
• Rocking motion of the prosthesis thrombi/vegetation)
• Cusp thickening/calcification Obtain an early postoperative
(biological valve) baseline study for comparison
later on.
Doppler Assessment
• Maximum and mean gradients across the valve using CW Doppler
• Valvular and paravalvular regurgitation using Color Doppler

FLOW PATTERN IN MECHANICAL

VALVE PROSTHESIS – zoomed
apical five-chamber view

Typical flow pattern of a mecha

V-shaped jet nical bileaflet aortic prosthesis.
The regurtitant jets originate
within the frame of the prosthesis
(central) and the jet direction is
”V-shaped”.

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 014 // PROSTHETIC VALVE

NOTES ECHO ASSESSMENT OF PROSTHETIC VALVES

Flow Patterns in Mechanical Valve Prosthesis

Forward flow Physiologic regurgitation

Search for a view that displays
the opening/closing motion of
the occluders (mitral valve
prosthesis).

Bileaflet prosthesis

The inflow and regurgitation

pattern varies, depending on the
type of prosthesis.

Tilting disc

The motion of mechanical

valves in the aortic position is
difficult to assess.

Medtronic Hall

Common Findings

• Residues of the subvalvular apparatus • Abnormal septal motion

• Cavitations • Suture material + normal regurgitations

Use atypical views. Imaging Problems in Patients With Mechanical Valves

TEE allows visualization of the • Artefacts • Endocarditis is difficult to diagnose

atrial side of the prosthesis. TTE • Shadowing • Visualization of a thrombus is difficult
shows the ventricular side. • Limited visibility of LA • Difficult to see leaflet motion
Combine TTE and TEE if you are • Limited visibility of the left atrium in • Difficult to assess flow convergence
in doubt. patients with mitral valve prosthesis
• Limited visibility of the regurgitant jet

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ECHO ASSESSMENT OF PROSTHETIC VALVES NOTES

MECHANICAL MITRAL VALVE –
apical four-chamber view/2D

Mechanical The two mechanical leaflets are

leaflet almost parallel during diastole.
The prosthesis causes shadowing
of the left atrium.

Shadow

Reference Values for Prosthetic Aortic Valves Consider prosthetic aortic

valve dysfunction when the
Bioprosthesis Vmax (m/s) Max. gradient Mean gradient maximal velocity is > 3 m/s
(mmHg) (mmHg) and the mean gradient
> 20 mmHg.
Carpentier Edwards 2.37 ± 0.46 23.18 ± 8.72 14.4 ± 5.7
Hancock 2.38 ± 0.35 23.0 ± 6.71 11.0 ± 2.29
Mitroflow 2.0 ± 0.71 17.0 ± 11.31 10.8 ± 6.51

Stentless biopros- Vmax (m/s) Max. gradient Mean gradient

thesis (25 mm) (mmHg) (mmHg)

Biocor Stentless 2.8 ± 0.5 28.65 ± 6.6 17.72 ± 6.35

Medtronic Freestyle – – 5.35 ± 1.5
Toronto Porcine 1.74 ± 1.19 38.6 ± 11.7 24 ± 4

Mechanical Vmax (m/s) Max. gradient Mean gradient

prosthesis (mmHg) (mmHg)

St. Jude Medical 2.37 ± 0.27 25.5 ± 5.12 12.5 ± 6.35

Björk-Shiley 2.62 ± 0.42 23.8 ± 8.8 14.3 ± 5.25
Starr-Edwards 3.1 ± 0.47 38.6 ± 11.7 24.0 ± 4.0

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 014 // PROSTHETIC VALVE

NOTES ECHO ASSESSMENT OF PROSTHETIC VALVES

Consider prosthetic mitral Reference Values for Prosthetic Mitral Valves

valve dysfunction if the
maximal velocity is Bioprosthesis Vmax (m/s) Max. gradient Mean gradient PHT
 2 m/s and the mean (mmHg) (mmHg) (ms)
gradient is  8 mmHg.
Hancock 1.54 ± 0.26 9.7 ± 3.2 4.29 ± 2.14 128.6 ± 30.9
Carpentier-Edwards 1.76 ± 0.24 12.49 ± 3.64 6.48 ± 2.12 89.8 ± 25.4
Ionescu-Shiley 1.46 ± 0.27 8.53 ± 2.91 3.28 ± 1.19 93.3 ± 25.0

Mechanical Vmax (m/s) Grad.max Grad. mean PHT

prosthesis (mmHg) (mmHg) (ms)

St. Jude Medical 1.56 ± 0.29 9.98 ± 3.62 3.49 ± 1.34 76.5 ± 17.1
Björk-Shiley 1.61 ± 0.3 10.72 ± 2.74 2.9 ± 1.61 90.2 ± 22.4
Starr-Edwards 1.88 ± 0.4 14.56 ± 5.5 4.55 ± 2.4 109.5 ± 26.6

Nobody understands Pressure Recovery

pressure recovery
anyway! Just remember • Leads to overestimation of • Common in small bileaflet valves
these key issues. gradients by Doppler • Especially when high flow present
• Relevant in a small aortic
root (< 30 mm)

Prosthesis–patient mismatch Prosthesis Patient Mismatch (Aortic Valve)

leads to high transvalvular
gradients through normal • A calcified aortic annulus can make it • Associated with increased late
functioning valves. This difficult to implant adequately large mortality
influences the resolution of left valves • Think of mismatch in the setting of left
ventricular hypertrophy and may ventricular dysfunction
also influence prognosis and
exercise capacity.

Prosthetic Effective Orifice Area (EOA)

The geometric orifice in Aortic Valve Prosthesis
area is not the effective
Stroke volume
orifice area.
EOA =
VTI
VTI of AV velocity Stroke volume LVOT
Consider prosthesis-patient mismatch when the indexed prosthetic
effective orfice area < 0.85 cm2/m2

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COMPLICATIONS NOTES

Prosthetic Valve Complications Left ventricular dysfunction may

occur after valve surgey due to
• Paravalvular leaks intraoperative ischemia, residual
• Valve obstruction (thrombus/pannus) valvular defects, or ventricular
• Endocarditis dysfunction at the time of
• Mechanical failure (mechanical valves) surgery (too late). It may occur
• Degenerative changes (biological valves) several years after surgery.
• Pseudoaneurysm/fistula

Look for pseudoaneurysms

of the intervalvular fibrosa,
especially in patients with
suspected endocarditis or in
patients who have received a
prosthetic valve because of
endocarditis.

Ring abscess PROSTHETIC VALVE ENDOCAR-

DITIS – TEE short-axis view/2D

Shadow Staphylococcal infection of the

valve, resulting in paravalvular
abscess. Infectious material and
echo-free cavities suround the
prosthesis. Always look for partial
dehiscence and paravalvular
regurgitation.

Mechanical leaflet

Shadow

Predisposing Factors for Structural Failure in Bioprosthesis

• Renal failure • Adolescence (growing)

• Hemodialysis • Porcine > pericardia
• Hypercalcemia • Autoimmune disease

Bioprosthesis Obstruction – Echo Findings Compare with previous studies

and initial postoperative
• Thickened calcified leaflets • Turbulent flow gradients.
• Reduced mobility • Dilated left atrium with spontaneous
• Elevated gradients contrast (mitral prosthesis) Structural failure (obstruction)
• Prolonged pressure half-time (mitral • LV dysfunction (eventually) is unlikely when the prosthesis
prosthesis) is < 2 years old and the patient
does not have endocarditis.

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NOTES COMPLICATIONS

Use fluoroscopy to detect Mechanical Valve Obstruction – Echo Findings

mechanical valve
obstruction. • Impaired/stuck leaflet • Pathologic flow pattern on color
• Echogenicity in valve region Doppler
(thrombus?) • Elevated gradients
• Pressure half time (MV)

Quite often only the Mechanical Valve Obstruction – Pannus vs. Thrombus
surgeon can give the
answer if a thrombus or a Pannus Thrombus
pannus is present INR in the therapeutic range INR too low
Slow onset of symptoms Sudden symptom onset
Higher age of prosthesis Stroke/embolism
Stable gradients Variable gradients

THROMBUS OF MITRAL PROS-

THESIS – TEE/2D

Mechanical obstruction of a Thrombus

bileaflet prosthesis caused by
thrombus. Thrombi are difficult
to see with transthoracic echo.
They are usually located at the
atrial side of the prosthesis,
which is shadowed in the trans- Mech
thoracic exam. leaflet

Use color Doppler to Quantification of Obstruction

guide the position of the
CW Doppler (mitral valve). Aortic Valve Prosthesis Mitral Valve Prosthesis
Use several windows to Morphologic findings Morphologic findings
quantify prosthetic aortic Symptoms Symptoms
valve obstruction. Velocity > 3.0 m/sec Mean gradients (>6–8 mmHg)
Doppler Vel. Index < 0.3 PHT > 130 ms
(Doppler Velocity Index = VLVOT/VProsth valve)

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COMPLICATIONS NOTES

Regurgitation in Valve Prosthesis Some degree of

paravalvular regurgitation
• Normal/physiologic • Valvular/structural failure (bio) is always present.
• Pathologic (paravalvular) • Valvular/mechanical failure (mech)

Mitral Regurgitation and Type of Prosthesis Patients with relevant

paravalvular regurgitation
Type Valvular Paravalvular Normal/physiologic often have hemolysis.

Mechanical X (mech. failure) X X Paravalvular regurgitation of

the aortic valve is best seen
Biological X X ---- on the parasternal short-axis
view (color Doppler).
Composite X (mech. failure) ---- X

Homograft X ---- X

Table showing possible forms of regurgitation in the individual types of prostheses.

Paravalvular Regurgitation

• Prevalence: 6–32% early, 7–10% late • Predisposing factors: calcified annulus,

• More common in aortic than in mitral endocarditis, suture technique
valve prosthesis • Small atria

Mech bileaflet PARAVAVULAR LEAK – TEE/3D

prosthesis surgical view

Paravavular leak in a patient with

Paravalvular
a bileaflet mechanical mitral
orifice valve.

Sutures

Echo Evaluation of Regurgitation

• Multiple/atypical views • Parasternal short axis (aortic valve)

• Eccentric jets • CW Doppler + gradients

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NOTES COMPLICATIONS

In the setting of elevated Elevated Gradients – Considerations

gradients in mitral valve
prosthesis, measure the • Compare with baseline/ • Prosthesis mismatch?
pressure half-time. If the reference values • Presence of mobile structures
pressure half-time is high, • Likelihood of obstruction (anticoagu- (thrombi/vegetations)
prosthesis obstruction is likely. lation within the therapeutic range/ • High flow state (dialysis shunt, high
If the pressure half-time is symptoms) cardiac output, heart rate)
normal, consider significant • Presence of regurgitation (increase
mitral regurgitation or high gradients per se or as a secondary sign
flow states. of prosthetic dysfunction)

Tricuspid regurgitation tends to Other Complications

increase after left heart valve
surgery. Valve dehiscence Look for rocking valve motion

Iatrogenic ventricular septal defect Rare complication

Tricuspid regurgitation Pulmonary hypertension,

following mitral valve surgery tricuspid annular dilatation, atrial
fibrillation, prior degree of
tricuspid regurgitation

If you suspect an aortic valve Pseudoaneurysm

pseudoaneurysm, look for a
pulsatile cavity with oscillating • Often caused by endocarditis (before and after surgery).
flow in (systole) and out • Occurs in native and prosthetic valves.
(diastole) of the cavity. • May lead to the formation of fistulas.

Prosthetic Valve Endocarditis (see Chapter 15)

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MITRAL VALVE REPAIR NOTES

Mitral Valve Repair – Ring Implantation (Annuloplasty) Mitral valve repair is always
combined with ring
• Different types of rings (flexible, open, • May resemble annular implantation.
closed) calcification on echo
• Prevents annular dilatation • The posterior leaflet may appear rather Measure the mean gradient and
short after ring implantation the pressure half-time across
the mitral valve in patients after
mitral valve repair. Undersizing
of the ring may lead to mitral
valve stenosis.

MITRAL VALVE REPAIR –

apical four-chamber view/2D
Papillary
Artifical chords and annuloplasty
muscle ring after mitral valve repair.
Artificial
chords

Th Th
ick i
en PM cken
AM ed VL ed
VL

Annuloplasty
ring

Common Techniques of Mitral Valve Repair

• Annuloplasty (see above) • Chordal transfer

• Quadrangular/triangular resection • Artificial chords
(with/without sliding plasty)

Complications of Mitral Valve Repair Patients with unsuccessful

repair (if not corrected)
• Residual regurgitation • LVOT obstruction/SAM caused by have a poor prognosis.
• Obstructed left ventricular inflow redundant leaflets in the setting of
(undersizing of the ring) small hyperdynamic left ventricles
• Ring dehiscence (partial dehiscence,
the origin and path of regurgitation are
outside the ring)

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 014 // PROSTHETIC VALVE

NOTES

138

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 015 // Endocarditis

CONTENTS
140 Principles of Endocarditis

141 Native Valve Endocarditis

143 Complications of Native Valve Endocarditis

145 Right Heart Endocarditis

145 Prosthetic Valve Endocarditis

146 Pacemaker/Polymer-Associated Endocarditis

147 Non-Infective/Abacterial Endocarditis

148 Indications for Surgery

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 015 // ENDOCARDITIS

NOTES PRINCIPLES OF ENDOCARDITIS

The prevalence of Definition

endocarditis associated
with prothetic valves and Endovascular microbial infection of cardiovascular structures
pacemaker leads is on the
increase. Location
• Valves
• Large intrathoracic vessels
• Ventricular and atrial endocardium
• Prosthetic material
• Polymere associated structures (lines)
• Eustachian valve

TRICUSPID VALVE
ENDOCARDITIS – apical four-
chamber view RV optimized/2D

Endocarditis with a large

vegetation attached to the native
tricuspid valve.
Thickened
leaflets

TV vegetation

Vegetation is an infected Pathophysiology of Endocarditis

mass attached to
endocardial structures,
such as valves or implanted
intracardiac material. On 2D Embolism
echo they frequently
appear as oscillating
structures of variable size Active infection
and morphology.
Endocardial defect

Post endocarditis
Non-significant Healing with Perforation
endocardial lesion/ calcification/
fibrosis fibrosis/thickening

Principle of a ”super-infected” thrombus: The endothelial lesion initiates a

repair process which involves thrombus formation. In the presence of
bacteremia this thrombus may be super-infected. Further consequences
include repair ad integrum, tissue destruction, embolism, and defect healing.

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PRINCIPLES OF ENDOCARDITIS NOTES

Microbiology Staph. aureus infection

predisposes to abscess
Other 14% formation and
complications of
Culture negative 17% Staph. aureus 25% endocarditis!

Staph. epidermidis 13%

Enterococcus 11%
Strept. bovis 20%

MITRAL VALVE ENDOCARDITIS

AMVL – PLAX zoomed/2D

A vegetation is attached to the

tip of the anterior mitral valve
leaflet.
Vegetation

LA

Epidemiologic Facts on Endocarditis

• Large geographical variations in the • Increase in the elderly population

incidence of endocarditis (3–10 • Sclerosis and aging also predispose to
episodes/100.,000 person-years) endocarditis

NATIVE VALVE ENDOCARDITIS

Diagnosis, Symptoms and Findings Endocarditis may be manifested

in many ways, many of which
• Fever/night sweat may be atypical
• Predisposing factors In the setting of infection, heart
• Conjunctival petechiae murmur or atypical symptoms,
• Janeway lesions Echo Culture think of endocarditis. Early
• Roth spots diagnosis saves lives.
• Splinter hemorrhages
• Vegetations Blood culture and other signs of
• Regurgitations Clinics infection (CRP, leukocytes, etc.)
• Complications of endocarditis are equally important. A negative
(abscessive destruction) blood culture does NOT rule out
• Pericardial effusion endocarditis.

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 015 // ENDOCARDITIS

NOTES NATIVE VALVE ENDOCARDITIS

MITRAL VALVE ENDOCARDITIS –
TEE surgical view/3D Vegetation

Large vegetation on the posterior

leaflet prolapsing into the left
atrium

Posterior leaflet

Anterior leaflet

Follow-up studies help to make Differential Diagnosis

an accurate diagnosis
(progression?). • Fibrosis/calcification • Tangential imaging of structures
• Myxomatous degeneration (e.g. mitral • Old vegetations
valve prolapse) • Tumors/thrombi
• Lambl‘s excrescence/strands

Transesophageal Indication for Transthoracic Echo in

echocardiography is not Suspected Endocarditis
mandatory in isolated
right-sided native valve
endocarditis with good Clinical Suspicion of Endocarditis
transthoracic quality.

TTE

Poor quality Positive Negative

Prosthetic
TTE
valve,
intercardiac
Persistent clinical suspicion
device

High Low

TEE TEE Stop

If the initial TEE is negative but endocarditis is still suspected,

repeat TEE within 7–10 days

ESC guidelines 2009

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NATIVE VALVE ENDOCARDITIS NOTES

What Else to Look For? ”Healing” usually leads to some

degree of fibrosis or calcification
• Involvment of other valves • Valve obstruction (large of the affected valve.
• Regurgitations and resulting vegetations, rare)
volume overload • Coronary embolization of
• Myocardial function (right + left) vegetation leading to wall motion
• Pericardial/pleural effusion abnormalites (rare)

COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS

Complications Embolization is the primary

manifestation of endocarditis in
• Embolism • Pseudoaneurysm 28–47% of all patients. The risk
• Valve destruction • Perforation of embolization depends on the
• Regurgitation/heart failure • Fistula size (>10 mm) and mobility of
• Abscess • Mycotic aneurysm the vegetation.
Exclude endocarditis in the
setting of stroke and fever.

Types of Valve Destruction

MV perforation Fistula

Valve perforation is a hole in the cusp or leaflet which appears as an interruption in

endocardial tissue continuity, best seen with color Doppler. In contrast, a fistula is a
communication with neighbouring cavities that does not directly involve the valve
(for instance, between the aorta and the left atrium).

Pseudoaneurysm – MV pseudo-
intervalvular aneurysm
fibrosa

Pulsatile perivalvular (echo-free) cavity communicating

with the cardiovascular lumen.

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 015 // ENDOCARDITIS

NOTES COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS

Types of Valve Destruction
AV ring abscess MV annular
abscess

Perivalvular cavity filled with infectious material which has a non-homogeneous

(echodense/echolucent) appearance

AV cusp MV flail leaflet

rupture

Tear in the aortic cusp or chordal rupture, which usually

leads to excentric regurgitation jets.

PSEUDOANEURYSM IN
AV ENDOCARDITIS –
TEE long-axis view/2D
Pseudoaneurysm
A pulsating cavity surounds the
aortic valve (pseudoaneurysm).
Numerous vegetations are pre-
AV
sent at the aortic cusps.
Vegetation

Communication
to the left ventricle

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RIGHT HEART ENDOCARDITIS NOTES

Causes of TV Endocarditis Tricuspid valve endocardits is

very likely in patients with
• Intravenous drug abuse • Indwelling catheters pulmonic abscess + drug abuse
• Immunocompromised • Pacemaker + new heart murmur.

Tricuspid Valve Endocarditis – Facts

Use atypical views to image
• The most common organisms are • High recurrence rates. tricuspid valve endocarditis
Staphylococcus aureus (60–80%) • Endocarditis frequently causes a flail and also look for pleural
and Pseudomonas. tricuspid valve leaflet.. effusion (secondary to
• Pulmonary hypertension, pulmonary • Tricuspid valve endocarditis may pulmonary infection).
embolism or tricuspid regurgitation also occur in patients without
may result in right heart failure. predisposing factors.
• The prognosis is relatively good (10%
inhospital mortality), but is poor in
fungal infection.

Complications Tricuspid valve vegetations

may become very large.
• Valve destruction • Septic pulmonary embolism
• Involvement of neighbouring cardiac • Lung abscess
structures

PROSTHETIC VALVE ENDOCARDITIS

Risk Factors

• Heart failure • Valve degeneration

• Wound complications • Prior history of endocarditis
• Direct contamination during cardiac • Prosthesis thrombi (super-infection)
surgery

Differential Diagnosis Prosthetic valve endocarditis is

difficult to detect.
• Artefacts • Strands Transesophageal echo is
• Subvalvular residuals • Thrombus recommended in case of
• Surgical materials • Hematoma suspicion.
Find out which operation was
Compare your findings with previous studies. performed, talk to the surgeon.
Surgical material such as suture
material or patches may mimic
endocarditis.

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 015 // ENDOCARDITIS

NOTES PROSTHETIC VALVE ENDOCARDITIS

Prosthetic valve endocarditis Complications

is a life-threatening
condition and is associated • Periannular abscess • Valve dehiscence
with a poor prognosis. • Pseudoaneurysms • Valve obstruction
• Paravalvular leaks • Fistula

PERIANNULAR PROSTHETIC
VALVE ABSCESS – TEE short-
axis/2D

The echodense area surounding AV

the prosthesis corresponds to a vegetation
periannular abscess. Additionally,
a large vegetation is seen on the
Abscess
rim of the cusps.

PACEMAKER/POLYMER-ASSOCIATED
ENDOCARDITIS

Pacemaker lead infection is Predisposing Factors

difficult to diagnose. A negative
study does not rule out • Pouch/Pocket infection • Diabetes
endocarditis. Combine • Impaired immunity • The surgeon‘s experience
transthoracic and • Systemic infection • Advanced age
transesophageal echo to • Temporary pacing before implantation
visualize as many portions of
the leads as possible.

Clinical Presentation

• Fever, subfebrile (recurrent) • Septic shock (acute)

• Pulmonary embolism • Poor general condition
• Local complications

Lead infection usually Typical Sites of Infection

occurs at sites where
the leads are in contact • Vena cava superior • Tricuspid annulus
with the endothelium. • Right atrium
• Tricuspid valve

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 015 // ENDOCARDITIS

PACEMAKER/POLYMER-ASSOCIATED
ENDOCARDITIS NOTES
CENTRAL LINE ENDOCARDITIS
Left atrium – apical four-chamber view/2D
&TEE bicaval view/2D
a
av
nac Central line with its tip in the
Vegetation , ve right atrium. Mobile vegeta-
p
Inf. Su
tion attached to the catheter
vena cava
Mobile (thickened tip) on transthoracic
structure echo (left) and the adjacent wall

heter (right) seen in TEE.

Cat

Thickened
catheter

NON-INFECTIVE/ABACTERIAL ENDOCARDITIS

Types
• Libman-Sacks endocarditis
• Marantic endocarditis • Antiphospholipid syndrome
• Hypercoagulable state

Echo Characteristics

• Valve thickening • Small vegetations

• Mild or moderate regurgitation • Pericardial effusion

Cardiac Manifestations of Libman-Sacks Endocarditis

• Valve thickening and vegetations • Left + right ventricular dysfunction

• Mural thrombus • Pericardial effusion
• Spontaneous contrast

LIBMAN-SACKS ENDOCARDITIS –
Thickened apical three-chamber view/2D
valve
Patient with lupus and antiphos-
pholipid syndrome. Several small
vegetations are seen on the
mitral valve.

Vegetations

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 015 // ENDOCARDITIS

NOTES INDICATIONS FOR SURGERY

ESC Guidelines 2009

Recommendations for Surgery in Infective Endocarditis (IE)

Heart Failure Timing Class Level

Aortic or mitral IE with severe acute regurgitation or

valve obstruction, causing refractory pulmonary Emergency I B
edema or cardiogenic shock

Aortic or mitral IE with fistula into a cardiac

chamber or pericardium causing refractory
pulmonary edema or shock Emergency I B

Aortic or mitral IE with severe acute regurgitation or

valve obstruction and persistent heart failure or
echocardiographic signs of poor hemodynamic
tolerance (early mitral closure or Urgent I B
pulmonary hypertension)

Aortic or mitral IE with severe regurgitation

and no HF Elective IIa B

Uncontrolled Infection

Locally uncontrolled infection (abscess,

false aneurysm, fistula, enlarging vegetation) Urgent I B

Persistent fever and positive blood cultures

> 7 – 10 days Urgent I B

Infection caused by fungi or multiresistant Urgent I B

organisms elective

Prevention of Embolism

Aortic or mitral IE with large vegetations and one

or more embolic Urgent I B
episodes despite appropriate antibiotic therapy

Aortic or mitral IE with large vegetations

(>10 mm) and other predictors of complicated Urgent I B
course of disease (heart failure, persistent infection,
abscess)

Isolated very large vegetations (>15 mm) Urgent IIb B

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 016 // Right Heart Disease

CONTENTS
150 Basics of Pulmonary Hypertension

152 Echo Assessment of Pulmonary Hypertension

155 Disease of the Right Ventricle

155 Right Ventricular Infarction

156 Right Ventricular Hypertrophy

156 Arrhythmogenic Right Ventricular Dysplasia

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 016 // RIGHT HEART DISEASE

NOTES BASICS OF PULMONARY HYPERTENSION

By definition, the diagnosis of Definition and Classification of Pulmonary Hypertension

pulmonary hypertension can only
be made by introducing a right Definition: mPAP ≥ 25 mmHg at rest
heart catheter.
• Pulmonary arterial hypertension (PAH) • Chronic thromboembolic pulmonary
Left heart disease • Pulmonary hypertension owing to left hypertension
(postcapillary) is the most common heart disease (CTEPH) • Pulmonary hypertension with unclear
cause of pulmonary hypertension. • Pulmonary hypertension owing to lung multifactorial mechanisms
disease and/or hypoxia

Patients with chronic Causes of Pulmonary Hypertension

obstructive pulmonary disease
rarely develop severe forms of Left heart disease 78%
pulmonary hypertension.
Others 7%

CTEPH 1%

PAH 4%

Lung disease 10%

Look at the left heart. Hemodynamic Definition of Pulmonary Hypertension

Does it explain pulmonary
hypertension? Is LV filling Definition Characteristics Clinical groups
pressure elevated? The
echo can provide clues as Pulmonary hypertension Mean PAP ≥ 25 mmHg All
to whether pre- or
post-capillary pulmonary Pre-capillary pulmonary Mean PAP ≥ 25 mmHg PAH
hypertension is present. hypertension PCWP ≤ 15 mmHG Lung disease
CTEPH
Unclear/multifactorial

Post-capillary PH Mean PAP ≥ 25 mmHg PH due to left heart

PCWP > 15 mmHG disease

Passive TPG ≤ 12 mmHg

Reactive (out of proportion) TPG > 12 mmHg

The transpulmonary gradient is the difference between mean PAP and PCWP
PAP = pulmonary artery pressure TPG= transpulmonary gradient

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BASICS OF PULMONARY HYPERTENSION NOTES

Prognosis of Pulmonary Hypertension Pulmonary hypertension is

a disease with a poor
prognosis, especially in
advanced stages. Early
diagnosis is important.

Echocardiographic Screening for Pulmonary Hypertension Exercise Doppler

echocardiography is
Class Level currently not
recommended for
PH unlikely Tricuspid regurgitation I B screening patients for
velocity ≤ 2.8 m/s, sPAP ≤ 36 pulmonary hypertension.
mmHg and no additional
echocardiographic variables
suggestive of PH

PH possible Tricuspid regurgitation IIa C

velocity ≤ 2.8 m/s, sPAP ≤ 36
mmHg, but the presence of
additional echocardiographic
variables suggest PH

Tricuspid regurgitation IIa C

velocity 2.9–3.4 m/s, sPAP
37–50 mmHg with/without
additional echocardiographic
variables suggestive of PH

PH likely Tricuspid regurgitation I B

velocity > 3.4 m/s, sPAP > 50
mmHg, with/without
additional echocardiographic
variables suggestive of PH

Additional echo variables suggestive of pulmonary

hypertension = IVS flattening, short PVAT, PA- dilatation
ESC 2009

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 016 // RIGHT HEART DISEASE

ECHO ASSESSMENT OF
NOTES PULMONARY HYPERTENSION

systolic PAP (sPAP) =

= 4 TR Vmax2 + Right Atrial Pressure (RAP)

Normal tricuspid Quantification of sPAP and Pulmonary Hypertension

regurgitation velocity is
age dependent. The • Normal TR velocity is 1.7– 2.3 m/s
severity of TR tends to • Elevated when TR velocity > 2.8–3.0 m/s
increase with age. • sPAP = TR velocity-derived RV/RA gradient + RA pressure

Mild PHT sPAP > 40 (35) mmHg

Moderate PHT sPAP > 50 mmHg

Severe PHT sPAP > 60 mmHg

MEASUREMENT OF SYSTOLIC
PULMONARY ARTERIAL PRES- CW sample
SURE – apical four-chamber
TR signal
view/CW Doppler TR

The RV/RA gradient is derived

from the peak tricuspid regurgi-
tation velocity using CW Dop-
pler. Be sure to measure the true
maximim velocity (good signal
quality).

Peak velocity

Pulmonary hypertension Factors That Influence TR velocity/sPAP

does not imply severe
tricuspid regurgitation • Severity of tricuspid regurgitation
and severe TR does not • Pulmonary hypertension
imply severe pulmonary • Doppler/image quality
hypertension. • Alignment of the TR jet to CW Doppler
• Right ventricular function
• Inspiration (higher with inspiration)

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ECHO ASSESSMENT OF
PULMONARY HYPERTENSION NOTES

Estimation of Right Atrial Pressure In very severe tricuspid

regurgitation, the TR
RA pressure IVC (diameter) Inspiration spectrum is triangular. In this
case RAP and thus
0 – 5 mmHg small (< 1.5 cm) collapsing pulmonary artery pressure
cannot be estimated (no
5 – 10 mmHg normal (1.5 – 2.5 cm) > 50% diameter reduction gradient between RA and
RV).
10 – 15 mmHg dilated (>2.5 cm) < 50% diameter reduction
Elevated RA pressure may
> 20 mmHG IVC + liver veins dilated no diameter change lead to significant shunts
across a patent foramen
ovale, or ASD causing
RA pressure estimation based on this scale is not always reliable. undersaturation.

DILATED INFERIOR VENA CAVA –

subcostal IVC view/2D
Dilated hepatic vein
Severely dilated inferior vena
cava without respiratory fluctu-
ations in diameter and dilated
hepatic veins in a patient with
pulmonary hypertension. These
Dil
ate findings suggest right atrial pres-
d IVC RA sures > 20 mmHg.

Quantification of mPAP

mPAP = 4 x maximum pulmonary regurgitation velocity

mPAP =79–0.45 x (pulmonary acceleration time) (Mahan‘s regression equation)

Pulmonary Acceleration Time (PVAT) PVAT can be very valuable in

situations where sPAP cannot
• Shortened in elevated pulmonary artery pressure be measured due to
• May be normal in elevated right-sided cardiac output insufficient TR signal.

Should only be applied for heart rates between 60 – 100

Normal > 130 ms Mild 80 – 100 ms

Borderline 100 – 130 ms Severe < 80 ms

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 016 // RIGHT HEART DISEASE

ECHO ASSESSMENT OF
NOTES PULMONARY HYPERTENSION
PULMONARY ACCELERATION Sample volume
TIME (PVAT) – PSAX/PW PV
PA
PVAT is measured from the onset
to the peak of the RVOT/PV
outflow signal. In the abscence
of pulmonary hypertension, the Signal onset PVAT
peak is rather late and the curve
symmetrical.

Peak velocity

The normal pulmonary artery Echo Findings in Pulmonary Hypertension

is a) smaller than the
ascending aorta b) <27 mm in • Dilated right ventricle • Pulmonary regurgitation
women and <29 mm in men. • Reduced right ventricular function • Enlarged right atrium
• Right ventricular hypertrophy • Pericardial effusion
Patients with pericardial • Septal flattening (systolic) = D-shaped • Pleura effusion
effusion have a poor prognosis. ventricle • Low cardiac output
Septal flattening can be very • Dilated pulmonary artery
subtle, especially when systolic
pressure is high.

ECHO FINDINGS IN PULMONARY SYSTOLE

HYPERTENSION – PSAX/2D RV hypertrophy

Echo features of severe pulmo-

nary hypertension: D-shaped Dilated RV
left ventricle with a flattened
S
interventricular septum in systo- TV IV
le, a dilated right ventricle, right n ed
te
ventricular hypertrophy, and peri- at
cardial effusion. Fl
LV

Pericardial effusion

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DISEASE OF THE RIGHT VENTRICLE NOTES

Echocardiographic Signs of Acute The McConnell sign is

Pulmonary Embolism marked by akinesia of the
mid-free wall but normal
• The sensitivity of echo for the • 60/60 sign: Characterized by a PVAT motion of the apex. It is
detection of pulmonary embolism is below 6 0ms in the presence of a also present in right
low. In cases of typical echo findings tricuspid regurgitation maximum ventricular infarction. The
(especially dilated RV with reduced gradient above 30 mmHg but 60/60 sign is a PVAT
RV function), the patients are usually below 60mmHg below 60 ms in the
very symptomatic (large PE) • Right ventricular pressure overload: presence of a TR
• McConnel sign: Characterized by Characterized by a D-shaped right maximum gradient above
akinesia of the mid-free wall but ventricle 30 but below 60 mmHg.
normal motion in the apex (poor
positive predictive value)

DD: Pulmonary Embolism and RV Infarction The untrained right ventricle is

unable to cope with acute
• Similar symptoms pressure overload. Therefore,
• Similar ECG very high sPAP measurements
• Similar echo findings are uncommon in acute
• Look for regional wall motion abnormalities (inferior infarction) pulmonary embolism
(exceptions are patients with
recurrent pulmonary
embolism/CTEPH with
preexisting pulmonary
hypertension).

RIGHT VENTRICULAR INFARCTION

Right Ventricular Infarction The majority of patients

with RV infarction
• Associated with inferior myocardial infarction (30–50%) recover in a period of
• Poor prognosis weeks or months.
• Hypotension/shock
• Arrhythmia

Echo Findings Look at the right

ventricular wall motion in
• Global and regional reduction in • Low annular velocity (Tissue all patients with inferior
right ventricular function Doppler) and decreased longitudinal infarcts.
• Low cardiac output strain (speckle-tracking)
• Tricuspid regurgitation
• Dilated inferior vena cava

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 016 // RIGHT HEART DISEASE

NOTES RIGHT VENTRICULAR HYPERTROPHY

Use atypical views of the • Right ventricle free wall ≥ 6mm • Measurement may be difficult;
RV (2-chamber RV view, • Use a subcostal 4-chamber view to also use visual assessment
inflow/outflow RV view). image the free right ventricle wall • Right ventricle hypertrophy may also
• Consequence of pressure overload on lead to right ventricular outflow tract
the right ventricle obstruction (narrow right ventricular
• Concentric right ventricular hypertro- outflow tract)
phy in pulmonary stenosis

Causes of Right Ventricular Hypertrophy

• Chronic pulmonary hypertension • High altitude

• Pulmonic valve stenosis (including • Athlete‘s heart syndrome
congenital abnormalities, • Hypertrophic cardiomyopathy
e.g. tetralogy of Fallot) (with right heart involvement)
• Tetralogy of Fallot

ARRHYTHMOGENIC RIGHT VENTRICULAR

DYSPLASIA (ARVD)

ARVD may affect both • Usually autosomal dominant • 5–10% of sudden cardiac deaths
ventricles. Echo has rather • Fatty and fibrous replacement of (<65 years)
low sensitivity and specificity myocardium, especially in the right • Its prevalence is 3-fold higher in males
in subtle forms of ARVD -> ventricular outflow tract
MRI will be needed.

Echocardiographic assessment Echo Findings in ARVD

should always include the RVOT
(aneurysm?). Use atypical views. • Aneurysmal dilatation, usually in the • Regional wall motion
diaphragmatic, apical and infundibular abnormalities + thin wall
regions (triangle of dysplasia) • Right ventricular dyssynchrony
• Reduced right ventricular function

Carcinoid Heart Disease

• Characterized by plaque-like deposits • High circulating concentrations of

of fibrous tissue, which most com- serotonin in the heart is the underlying
monly occur on the endocardium of substrate of carconoid heart disease.
valvular cusps and the leaflet. • The right heart is most commonly
• Occurs in 50% of patients with affected because serotonin is inactiva-
carcinoid syndrome ted by the lung and therefore protects
the left heart

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ARRYTHMOGENIC RIGHT VENTRICULAR

DYSPLASIA (ARVD) NOTES

Echo Findings in Carcinoid Heart Disease If you suspect carcinoid

heart disease, tilt the
• Right ventricular enlargement • Abnormal motion of the interventricu- transducer to the abdomen
• Tricuspid valve, pulmonic valve leaflets lar septum (volume overload caused and image the liver. The
and the subvalvular apparatus are by tricuspid regurgitation). majority of patients with
thickened and rigid • Triangular CW spectrum indicative of carcinoid heart disease have
• Usually significant tricuspid severe tricuspid regurgitation. hepatic metastases.
regurgitation with restricted motion • Associated with pulmonic stenosis
of the leaflets, causing a wide (and regurgitation).
coaptation defect.

SYSTOLE CARCINOID HEART DISEASE –

apical four-chamber view RV
Prominent
optimized/2D
Moderator band
Restricted motion/position of the
Dilated RV tricuspid leaflets, leaving a wide
coaptation defect. The leaflets
are thickened (from the base) and
rigid. The endocardium
is bright. These findings are high-
Rigid ly indicative of carcinoid heart
leaflets disease.
+
Coaptation
defect

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NOTES

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 017 // Aortic Disease

CONTENTS
160 Imaging of the Aorta

161 Basics

161 Aortic Aneuryms

164 Aortic Dissection

167 Aortic Coarctation (CoA)

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 017 // AORTIC DISEASE

NOTES IMAGING OF THE AORTA

Use a modified parasternal long- How to Visualize the Aorta with

axis view (one intercostal space Transthoracic Echocardiography
cranial) to see more of the
ascending aorta.

Every echo report should

Suprasternal win-
include a description dow (aortic arch)
of the ascending aorta
(normal/dilated)
with corresponding
Three-chamber
measurements. view

Two-chamber
Four-chamber view
view
(descending aorta)
(descending
aorta)
PLAX


Even with TEE it may be Transoesophageal Echo (TEE)
difficult to see cranial
segments of the BETTER RESOLUTION MORE SEGMENTS
ascending aorta.
The esophagus is close to the TEE is much better for the
aorta. We may therefore use higher assessment of the descen-
transducer frequencies, which ding thoracic aorta
translate into better resolution.

The aortic diameter is Where and How to Measure

slightly larger in systole
than in diastole. By using several measurements (in
Aortic arch the setting of aortic dilatation), it is
also possible to determine the shape
and extension of aortic aneurysms.
Ascending
aorta
Sinotubular Descending
junction aorta

Aortic Sinus of
annulus valsalva

Leading
edge
The aorta can be measured on a long- and/or Inner
short-axis view. Most reference values were edge
obtained with the leading edge method.
However, to correlate measurments better Axial view
with other imaging modalities (CT, MRI),
measurements of the inner diameters (in-
ner edge to inner edge) are applied to an
increasing extent. The difference between Leading Inner
these measurements methods is minimal edge edge
and insignificant, thanks to improved image
resolution. Longitudinal view

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BASICS NOTES
VISUALIZATION OF
THE ASCENDING AORTA –
modified PLAX/2D

The more cranial portions of the

orta ascending aorta can be better vi-
inga sualized by moving the transduc-
nd
ce er up one intercostal space and
As
more laterally.

Size of the Aorta The size of the aortic is

strongly related to body
Diameter Diameter/BSA surface area (in particular
hight) and age.
Aortic annulus 20-31mm 13 mm/m2

Sinus of valsalva 29- 45mm 19 mm/m2

Sinotubular junction 22-36mm 15 mm/m2

Ascending aorta 22-36mm 15 mm/m2

Aortic arch 22-36mm

Descending aorta 20- 30mm

Abdominal aorta 18- 28mm

ESC 2010

AORTIC ANEURYMS

Definitions

True aneurysm
Localized dilatation > 50% of the reference
segment (circumscribed or diffuse aneurysms)

Aortic ectasia
Arterial dilatation of less than 150% of the
normal arterial diameter

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NOTES AORTIC ANEURYMS

Any increase in the diameter Incidence – Facts

of the aorta is related to
(blood) pressure, the size of • Death – aneurysm = • No difference between prevalence
the aorta, and the thickness 0.7/100,000 per year in men and women
of the wall (law of Laplace). • Death – dissection = • Thoracic aneurysms >6 cm are subject
1.5/100,000 per year to a rupture and dissection risk
of 6.9% per year.

To quantify aneurysms of the Forms of Aneurysms

ascending aorta, always use a
parasternal long- and short-axis
view. In the presence of an
aneurysm of the ascending aorta,
also image from a suprasternal
window to determine whether
the aortic root is involved.
Ascending aortic aneurysms are
sometimes visualized best from a
right parasternal approach.
Pure ascendens type ”Sausage” type Bulbus type (Marfan)
Look at the shape of the
ascending aorta: something is In the setting of aneurysms the aorta changes its orientation
wrong when there is no (to the right); it may even be elongated.
narrowing at the sinotubular
junction.

ANEURYSM OF THE ASCENDING

AORTA – PLAX/2D

Patient with bicuspid valve, aortic

stenosis and aneurysm of the
aortic root and the ascending
aorta. There is no narrowing at Aortic
the sinotubular junction. Calcified
aneurysm
aortic valve

Progressive dilatation of the Bicuspid Aortic Valve and Aneurysm

aorta continues even after
aortic valve replacement in • Dilatation of the aorta may be present in patients with
patients with bicuspid valves. congenital abnormal valves (e.g. bicuspid).
Follow such patients closely. • 9-fold higher risk of dissection in the presence
of bicuspid valves.
• 6–10% of all dissections occur in the setting
of bicuspid valves.

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AORTIC ANEURYMS NOTES

Inherited Disorders Affecting the Aorta Inherited disorders

also include so called
• Marfan • Annulo-aortic ectasia ”overlap syndromes”.
• Ehlers Danlos (type IV) • Loeys-Dietz syndrome
• Familial forms of connective tissue
disorders

Marfan Syndrome – Cardiac Manifestations Aortic disease/dissection

is the main cause of
• Aortic dilatation • Mitral valve prolapse morbidity and mortality in
• Aortic dissection • Pulmonary artery dilatation Marfan syndrome.
• Aortic regurgitation (annular dilatation) • Large aortic valve cusps

Inflammatory Diseases of the Aorta Infections may trigger

non-infectious vasculitis by
• Syphilis • Giant cell arteritis generating immune complexes
• Staph. aureus infection • Takayasu arteritis or by cross-reactivity.
• Kawasaki disease Inflammation may result in
aortic dilatation and ostial
stenosis of major branches.

Risk of Rupture – Stratification Based on Aortic Size

Low risk ≤ 2.75 cm/m2 4%/year

Moderate risk 2.75 – 4.25 cm/m2 8%/year

High risk ≥ 4.25 cm/m2 20%/year

Indications for Aortic Surgery (ACC Class I) Use other imaging

modalities (mitral
• Asymptomatic patients with an • Patients with a growth rate of more regurgitationI and CT)
ascending aortic diameter or an aortic than 0.5 cm/year in an aorta for precise
sinus diameter ≥ 55mm less than 5.5 cm in size measurements and for
• Patients with Marfan syndrome with an • Patients undergoing aortic decision-making. Use
aortic diameter between 40-50 mm valve repair, with an aortic the technique you are
aneurysm ≥ 4.5 cm in size most familiar with.

ACC 2010

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NOTES AORTIC DISSECTION

The false lumen is usually Aortic Dissection

larger than the true lumen,
with slower flow, and often Characteristics:
with thrombi. • Intima (media) disruption/
intimal flap – true + false
Thrombus
Intimal flaps may prolapse lumen Tear
through the aortic valve. • Spiral-shaped dissections may
Flap
Also look for intimal flaps occur, sometimes involving True lumen
in the aortic arch (using a branches (coronaries!!, False lumen
suprasternal window). supraortic branches)
• 2.6–3.5 cases per 100,000
persons/year
• 2/3 males

Classifications of Aortic Dissection

Stanford classification

A A B
Ascending Descending
Type A involves the ascending aorta, type B only the descending aorta

DeBakey classification

I II III
Ascending Ascending Descending
Descending
Type I involves the ascending and the descending aorta, type II only the ascending
aorta and type III only the descending aorta.

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AORTIC DISSECTION NOTES

Risk Factors for Dissection Untreated dissection of the

ascending aorta is associated
• Aortic aneurysm • Atherosclerosis with a mortality rate of 90%
• Marfan + other connective tissue • Iatrogenic (e.g. left heart catheter, heart within 1 year (rupture into the
disorders surgery cannulation) pericardium, mediastinum, or
left pleural cavity).

Aortic Dissection The intima/media is

detached (flap), and
Classic dissection Complications of dissection divides the aorta into a
• Aortic rupture true and a false lumen.
• Branch vessel dissection (coronaries)
true • Expansion
• Intramural hematoma
• Aortic regurgitation
false • Rupture with pericardial tamponade
• Leriche syndrome

TTE in Aortic Dissection Beware of reverberations of

the aortic wall or adjacent
• Sensitivity = 77–80% structures. They may mimic
• Specificity = 93–96% an intimal flap. A true intimal
Always confirm dissection by using other imaging modalities. flap is marked by motion
independent of the aortic
Aortic regurgitation wall.
in dissection
• Dilatation of the root
• Bicuspid valves
• Prolapse of the intimal flap

DISSECTION OF THE ASCENDING

AORTA – PLAX/2D

Highly mobile intimal flap in the

ascending aorta, denoting aortic
dissection. This flap is almost cir-
cumferential and thus visualized
both anteriorly and posteriorly.
Intima
flap

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NOTES AORTIC DISSECTION

Aortic Syndromes

Intramural hematoma Rupture

Bleeding into the aortic wall (such as Plaque rupture, penetrating ulcers,
after plaque rupture) causes an intramu- and intramural hematoma may lead to
ral hematoma. aortic rupture.

Localized dissection ”Healed” dissection

Localized dissection is usually a result The false lumen of dissection may

of atherosclerosis. Dissection is limited thrombose and eventually heal.
to a circumscript region.

Aortic syndromes are no benign Penetrating ulcer Intraluminal thrombus

condition. The bear a high risk
of rupture. Further evaluation
with CT/mitral regurgitation is
mandatory.

Rupture of an atherosclerotic plaque Regional thickening of the aorta > 7 mm

results in a penetrating ulcer. (circular shape) (DD: thrombus in false
lumen, intramural hematoma)

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AORTIC DISSECTION NOTES

Aortic Plaque Plaque size is important

for risk stratification.
• Patients with artherosclerotic plaques • Increased risk of embolism/stroke When the plaque size is >
in the aorta are subject to a high risk of (plaque in the ascending aorta/aortic 4 mm, the risk of stroke is
coronary artery disease and arch). significantly increased.
myocardial infarction. • Increased risk of aortic dissection. (OR=9.1)
• Increased risk of aortic syndromes.

Typical Locations of Plaques in the Aorta TTE is also Capable of

demonstrating plaques /especially
• Aortic arch in the ascending aorta). Capable of
• Cranial segments of the demonstrating plaques/especially
descending aorta in the ascending aorta).

AORTIC COARCTATION (COA)

Facts Kinking may lead to flow

turbulence (seen in color
• 5–10% of all congenital defects Doppler), thereby
• Predominantly men mimicking CoA =
• Higher blood pressure at the upper extremities pseudocoarctation
compared to the lower extremities
• Located distal to the subclavian artery
• Increased risk of intracranial hemorrhage

Echo Features The suprasternal view is the

most valuable window to
• Left ventricular hypertrophy identify coarctation.
• Narrowing of the aorta Quantification is based on the
• Turbulent flow is visible on color Doppler maximal velocity/gradients
• Elevated CW Doppler gradient in the aorta (measured with CW Doppler)
• The presence of a systolic and an additional diastolic gradient and the presence of a systolic
denotes hemodynamic significance of obstruction AND diastolic gradient.

Doppler measurments usually

overestimate gradients in
comparison to hemodynamic
assessment.

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 017 // AORTIC DISEASE

NOTES AORTIC DISSECTION

AORTIC COARCTATION –
ery
suprasternal view/Color c art
ali ery
and CW Doppler ep
h art
hio
c tid
ac aro
Br nc
Turbulent flow in the descending
m mo ry
aorta (left) denotes the location CW sample volume co rte
ft na
Le ia
of coarctation. The Doppler c lav
ub
spectrum (right) shows a systolic ft s
Systolic + diastolic Le
and diastolic gradient (>4 m/s),
Aortic
suggesting severe coarctation. gradient
coarctation
Jet

Patients with hemodynamically Coarctation – Associated Abnormalities

relevant forms of CoA also
have left ventricular • Bicuspid aortic valve
hypertrophy. • Persistent ductus arteriosus/ventricular septal defect
• Hypoplasia of the aortic arch
• Left ventricular outflow tract obstruction

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 018 // Pericardial Disease

CONTENTS
170 The Pericardium

170 Pericardial Effusion

173 Pericardial Tamponade

175 Pericardial Constriction

176 Other Diseases of the Pericardium

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NOTES THE PERICARDIUM

The pericardium consists of a The Pericardium – Importance

visceral and a parietal layer.
• Limits distension
Patients with an open • Facilitates interaction and coupling
Pericardial cavity
pericardium or chest (cardiac of the ventricles/atria
surgery) have an abnormal • Facilitates twist and torsion Fibrous layer
contractile pattern. • Normal quantity of Myocardium
pericardial fluid < 50ml Endocardium
Parietal layer

Visceral layer

PERICARDIAL EFFUSION

Bacterial infection Forms of Pericardial Effusion

(especially tuberculosis)
predisposes to Transudative Hemorrhagic
constriction. Congestive heart failure, myxedema, Trauma, rupture of aneurysms, malig-
nephrotic syndrome nant effusion, iatrogenic
Exudative effusion is
characterized by fibrous Exudative Malignant
strands. Tuberculosis, spread from empyema Often hemorrhagic

Causes of Pericardial Effusion

The cause of pericardial effusion • Idiopathic: no cause is found despite • Autoimmune disease: particularly:
depends on the setting of your lab full diagnostic investigation systemic lupus erythematodes,
and the part of the world you practice • Infectious: common in viral infection rheumatoid. arthritis., systemic
in (e.g. tuberculosis in developing (direct + immune response) sclerosis
countries, iatrogenic when • Iatrogenic: pacemaker, catheter • Radiation: 20% develop constriction
interventions and cardiovascular procedures, biopsy, cardiac surgery • Rheumatic: usually small
surgery are performed at your • Neoplastic: often hemorrhagic, pericardial effusion
center). denotes poor prognosis • Traumatic: contusio cordis or heart/
• Myocardial infarction: myocardial aortic rupture
The cause of effusion may remain rupture, epistenocardic (early) + • Endocrine disorder: e.g. myxedema
unclear because the diagnosis would Dressler syndrome (late) • Pulmonary hypertension: the
require peri-and/or myocardial • Renal failure: uremia- or dialysis- mechanism is unclear (poor prognosis)
biopsy as well as cytological, associated • Post cardiac surgery: usually hemat-
histoimmunological, and oma, often localized
microbiological analysis of the fluid. • Aortic rupture: hemorrhagic
effusion, pericardial effusion in 45%
of dissections.

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PERICARDIAL EFFUSION NOTES

Echo Diagnosos of Pericardial Effusion The pericardium is

highly reflective in
• Echo-free space measured in end-diastole. echocardiography.
• Use multiple views, especially
subcostal views.
• Use atypical views; specifically visualize
the surroundings of the right ventricle.

Liver
PERICARDIAL EFFUSION –
Pericard subcostal four-chamber view/2D
ial effusio
n Fibrin strand Large circumferential pericardial
effusion with fibrin strands. The
RV image loop shows swinging heart
motion.
LV

Facts Talk to the patient.

Thorough history-taking
Large effusion Regional effusion often helps to clarify the
Neoplastic Postoperative cause of effusion.
Uremic Trauma
Tuberculosis Purulent
Myxedema

Differential Diagnosis Pericardial effusions are

anterior to the descending aorta
• Pleural effusion while pleural effusions are
• Epicardial fat posterior to it.
• Pericardial cyst
• Ascites If you are still not sure, make the
patient sit up and image the
pleura (from the back). Here you
will see whether a pleural
effusion is present or not.

Epicardial Fat Epicardial fat is common in

obese patients, diabetes, atrial
• Follows the normal motion • Absent above the right atrium and fibrillation and coronary artery
of the pericardium usually very prominent in the atriovent- disease. Epicardial fat is seen
• Is related to the presence of abdominal fat ricular groove as well as around the better in the presence of a
• Is not completely echo-free (low- atrial appendages pericardial effusion.
intensity echos)

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NOTES PERICARDIAL EFFUSION

EPICARDIAL FAT – subcostal
four-chamber view/2D

A patient with a small pericardial

effusion and pronounced epicar-
dial fat. Epicardial fat is promi- Pericardial effusion
nent in the AV groove and absent
in the region of the right atrium. Epicardial fat

Epicardial border

Localized effusions occur Location of Pericardial Effusion

in the setting of fibrinous
and iatrogenic
(hemorrhagic) pericardial
effusion.

Large circumferent Localized

Small circumferent

Localized

The separation of Quantification of Circumferential Pericardial Effusion

pericardial layers can be
detected on echocardiography, Small < 1 mm 300 ml
when pericardial fluid exceeds
15–35 ml. Moderate 10–20 mm 500–700 ml

Follow-up of pericardial Large > 20 mm > 700 ml

effusion requires using the
same views. Always measure in Very large > 30 mm + compression
the same region and also assess
pericardial efussion visually.

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PERICARDIAL EFFUSION
NOTES
SEQUENTIAL IMAGES OF PERI-
CARDIAL EFFUSION – PSAX/2D

Changes in the size of a peri-

cardial effusion can be best
appreciated by recording similar
images and displaying them in
split-screen format. The effusion
in this patient clearly diminishes
over time.

Quantification of Volume Volume quantification is

best performed from a
Subtract the volume derived by tracing the cardiac contour from subcostal view.
the volume derived by tracing the epicardial contour (+ pericardial effusion).
The difference is the volume of the pericardial effusion.

Importance of Echo in Pericardial Effusion Always look for other echo

features which may reveal the
• Establish the diagnosis • Hemodynamic importance cause of effusion (e.g.
• Help to find its cause? • Direct pericardiocentesis myocardial infarction,
pulmonary hypertension,
endo-myocarditis).

PERICARDIAL TAMPONADE

Definitions Tamponade, constriction and

effusive constriction share many
Tamponade: Intrapericardial fluid common features.
Constriction: ”Stiff” pericardial sac Tamponade is a medical
Effusive constricitive: ”Stiff” pericardial sac + fluid emergency, and occurs when
fluid accumulates rapidly.

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 018 // PERICARDIAL DISEASE

NOTES PERICARDIAL TAMPONADE

Use a respiratory curve Pathophysiology of Tamponade –

while imaging the patient Interventricular Interdependence
to determine the phase of
inspiration and expiration.

RV LV RV LV

RA LA RA LA

Tamponade – expiration Tamponade – inspiration

In tamponade, systemic venous return is shifted towards inspiration. The heart is

unable to adapt to the increase in volume of the right heart during diastole, especi-
ally during inspiration. To accomodate the volume, the septum shifts to the left
(septal shift) during inspiration.

Echocardiography is Hallmarks of Tamponade

important for the diagnosis of
tamponade, but a tamponade • Systemic venous return shifted to inspiration
is also a clinical diagnosis. • Impaired filling of the left ventricle during inspiration
• Interventricular interdependence

Symptoms Signs

Pain Tachycardia

Dyspnea Edema

Shock Low blood pressure

Triggers of Tamponade in Chronic Pericardial Effusion

• Hypovolemia – low pressure tamponade

• Paroxysmal tachyarrhythmia
• Intercurrent pericarditis

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PERICARDIAL TAMPONADE NOTES

Echo Signs of Tamponade Use multiple views to

assess septal shift and
• Right atrial collapse (early sign, alone • Swinging heart phenomenon (usually use respiratory curves.
usually does not denote relevant associated with some degree of
tamponade) hemodynamic relevance of effusion) Tamponade is often a
• Dilated inferior vena cava and • Septal shift towards the left ventricle ”stagewise” process. It
hepatic veins during inspiration (indicator of hemo- may occur gradually.
• Right ventricular collapse (difficult to dynamic significance)
assess in swinging heart due to out of • Respiratory changes in PW Doppler
plane motion of the right ventricle, but mitral valve inflow (Changes > 30% are
if present usually associated with indicative for hemodynamic significan-
symptoms) ce), Apply with caution in atrial
• Left ventricular collapse (severe fibrillation
tamponade, emergent pericardiocenti- • Exaggerated respiratory changes in
sis required) tricuspid valve inflow (PW Doppler)
• PW Doppler flow reversal in hepatic
veins
.
VARIATIONS OF MITRAL VALVE
INFLOW– apical four-chamber
view/PW Doppler

Respiratory variations (>25%) of

Max. the mitral inflow in pericardial
Expiration Inspiration tamponade. Inflow velocities are
less during the first beat follow-
ing inspiration.
Min.

PERICARDIAL CONSTRICTION

Pericardial Constriction – Characteristics Patients with radiation-

associated constriction
• Pericardial calcification/fibrosis/ • Venous distention have a poor prognosis.
scarring • Edema
• Subacute/chronic disease • Hepatomegaly
• Normal systolic function • Ascites
• Impaired filling

Causes of Pericardial Constriction Constriction may be local,

but in most cases it
• Inflammation (bacterial/tuberculosis) • Connective tissue disease causes impairment of
• Radiation • Idiopathic biventricular filling.
• After cardiac surgery

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NOTES PERICARDIAL CONSTRICTION

Types of Constriction

• Annular form • Global form + myocardial atrophy

• Left-sided form • Global form + perimyocardial fibrosis
• Right-sided form • Restrictive cardiomyopathy

To confirm constriction, it is Echo Features of Pericardial Constriction

sometimes necessary to use
hemodynamic catheter studies • Dilated inferior vena cava and • Septal shift (pronounced shift of the
(dip and plateau pressure drop hepatic veins intervenricular septum towards the left
between the left ventricle and • Predominant forward flow in early ventricle during inspiration)
right ventricle during diastole (pronounced E-wave) • Distorted heart contour, especially in
inspiration). (PW Doppler) regional forms of constriction
• Exaggerated trans-tricuspid flow • Poor image quality
The size of the right ventricle during inspiration (PW Doppler) • Echogenic pericardium
increases in the phase of septal • Expiratory flow reversal in hepatic • Rather small ventricle/atria
shift. veins (PW Doppler) • Pleural effusion
In our experience, the easiest • Septal bounce (oscillating septum)
and best way to diagnose
constriction is by displaying
inspiratory septal shift and
septal bounce. This can be
done in any view that depicts
the interventricular septum.

OTHER DISEASES OF THE PERICARDIUM

Pericardial cysts may be Pericardial Cyst

quite large and are often first
suspected on a chest X-ray. Benign tumor: 6% of mediastinal masses and 33% of mediastinal cysts

Failure of fusion of mesenchymal lacunae that form the pericardial sac

• Usually asymptomatic
• Unilocular/multilocular
• Typically located at the right cardiophrenic angle

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OTHER DISEASES OF THE PERICARDIUM NOTES

PERICARDIAL CYST –
apical four- chamber view/2D

RV Incidental finding of a large peri-

cardial cyst located in the right
cardiophrenic angle.

RA

Pe
ric
ar
d
cy ial
st

Differential Diagnosis: Pericardial Cyst

• Localized pericardial effusion • Diaphragmatic hernia

• Hepatic/renal/mediastinal cyst • Atrial diverticula
• Echinococcal cyst • Aneurysmatic vessels

Malignant Disease of the Pericardium Symptomatic pericardial

effusion in malignancy
• Primary malignancy • Pericardial involvment is associated has a poor prognosis
• Metastasis with pericardial effusion (hallmark) (median survival,
• Pericardial carcinosis 4 months).
Even in patients with a
malignancy and
pericardial effusion, the
former is not always
related to the latter.

Congenital Absence of the Pericardium Consider the absence of

the pericardium in
• 1/10.000 autopsies • Higher risk of traumatic dissection patients with unusually
• Various forms (total/left/right absence • Potential complications include shaped ventricles with
of the pericardium) herniation or entrapment of cardiac abnormal contractile
• Often asymptomatic or chest pain chambers (e.g. left atrial appendages) motion.

Echo Features of Congenital Absence of the Pericardium Use MRI or CT to confirm

the diagnosis.
• Displacement of the heart • Enlargement of the left atrial
• Excessive cardiac motion appendage
• Abnormal septal motion

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NOTES

178

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 019 // Tumors and Masses

CONTENTS
180 Pseudotumours

181 Masses
179

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 019 // TUMORS AND MASSES

NOTES PSEUDOTUMOURS (STRUCTURES THAT MIMIC A MASS)

If you have the Pseudotumors of the Right Atrium

opportunity, attend an
autopsy and see what • Pectinate muscles • Prominent (lipomatous) tricuspid valve
these structures really • Eustachian valve annulus
look like. • Chiari network • Catheters/pacemakers
• Crista terminalis • PFO/ASD occluders
• Lipomatous hypertrophy of interatrial
septum (dumbbell sign)

EUSTACHIAN VALVE – zoomed

apical four-chamber view/2D

Very prominent and long Eusta-

chiian valve in the right atrium.
The Eustachian valve typically
arises from the inferior vena cava.
TV

Eustachian
valve

Structures of the Left Atrium

• Pectinate muscles • Calcified mitral annulus

• Lipomatous hypertrophy of interatrial • Ridge between the left superior
septum pulmonary vein and the left atrial
• PFO/ASD occluders appendage

LIPOMATOUS INTERATRIAL
SEPTUM – TEE bicaval view/2D

A lipomatous interatrial septum Se Left atrium

pt m
is best seen with TEE. The fossa um du
se n
ovalis is typically spared, resulting
cu cu
in a ”dumbbell”. nd se a
um um av
pt c
Se na
ve
rior
pe
Lipomatous Su
interatrial
septum

Right atrium

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 019 // TUMORS AND MASSES

PSEUDOTUMOURS NOTES

Pseudotumors of the Right Ventricle These structures can also

be visualized from
• Catheters (ICU) • Trabeculations subcostal views – use
• Pacemakers • Moderator band them.
• Muscle bundles

Pseudotumors of the Left Ventricle Elongation of chords may be

mistaken for vegetations. They
• Abberant/artifical chords may also mimic systolic anterior
• Trabeculations motion and falsely suggest the
• Papillary muscles presence of hypertrophic
obstructive cardiomyopyopathy.

ABBERANT CHORD –
apical four- chamber view/2D

Abberant chord that traverses the

left ventricle from the septum to
the lateral wall.

Aberrant
chord

MASSES

Distinguish between

Thrombi Tumors Endocarditis

Fever/infection X

Located on native valves X X

Embolism X (X) X

Expansive growth located

in > 1 chamber X

Spontaneous contrast x

Combine clinical and morphological clues to determine the etiology of the mass.

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 019 // TUMORS AND MASSES

NOTES MASSES

Mural thrombi have an Risk Factors for Thrombus Formation

overall incidence of 20%. In
large infarctions with Atria Left ventricle
aneurysms the incidence is • Atrial fibrillation • Reduced left ventricular function
as high as 60%. The risk of • Mitral valve replacement • Aneurysm (apex)
systemic embolization is 2%. • Mitral stenosis • Acute myocardial infarction
• Reduced left ventricular function • First week after STEMI

The appearance of thrombi Echocardiographic Aspects of Thrombus

may vary greatly, ranging
from fibrotic/solid/high • Size • Mobility
echogenicity to soft/jelly- • Echogenicity (fresh vs. old) • Location
like/low echogenicity.
Always describe these aspects of a thrombus for better comparison over time.

Tumors of the Heart

THROMBUS IN LEFT
ATRIAL APPENDAGE/atypical api-
cal four-/two-chamber view/2D

This rare example shows that it LV

may be possible to detect left
atrial appendage thrombi with Thrombus
transthoracic echo, especially
when using atypical views.
LAA

PV
LA

Metastatic lesions of the Common Sources of Metastatic Lesions

heart are almost 20 times
more common than • Melanoma • Esophageal cancer
primary cardiac tumors. • Soft tissue sarcoma • Renal carcinoma
• Thyroid cancer • Hepatocellular carcinoma
• Lung cancer • Secondary involvement with leukemia
• Breast cancer and lymphoma

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MASSES NOTES

Benign Primary Cardiac Tumors About 75% of all primary

cardiac tumors are benign.
Adult Child

3 % 5 % 1 % 13 %

2 %
5  % 15 %

16 %
46 % 15  %
46  %
21 %

Myxoma Lipoma Fibroelastoma Rhabdomyoma

Fibroma Hemangioma Teratoma

Myxoma – Echo Facts Given a typical

presentation, the echo
• More common in the left atrium than • Myxomas are typically pedunculated study is virtually
the right atrium (typically located at the (often short stalk), either round/oval diagnostic. If uncertain
fossa ovalis of the interatrial septum) with a smooth surface, or villous in perform TEE or MRI.
• Less common in other heart chambers appearance
or on valves • Large myoxomas may cause
valvular obstruction
• Systemic embolism or microembolism
may occur

MYXOMA – zoomed
MV
apical four- chamber view/2D

Myxoma A typical myxoma originating

from the interatrial septum. Its
surface is rather smooth, it has a
very short stalk and is homoge-
neous. Myxomas may be much
larger, filiform, and more inho-
LA mogeneous.

IAS

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 019 // TUMORS AND MASSES

NOTES MASSES

Do not confuse a lipoma Lipoma

with lipomatous
hypertrophy of the • Second most common benign • May be found in the intramyocardial
interatrial septum. cardiac tumor region
• Common locations: LV, RA, IAS • CT & MRI: high specificity for fat

When valvular Papillary Fibroelastoma

dysfunction is present,
think of endocarditis • Most frequently located on the aortic • Rarely causes valvular dysfunction
rather than papillary valve, followed by the mitral valve (DD: endocarditis)
fibroelastoma. • Its mobility predicts the risk of • Usually located on the downstream
embolism side of the valve
• May cause coronary occlusion (rare)

FIBROELASTOMA (AORTIC
VALVE) – apical three-cham-
ber view/2D
Fibroelastoma
Small mass on the ventricular
aspect of the aortic valve,
which was histologically AMVL
proven to be a fibroelasto-
ma. Fibroelastomas may also
appear as pedunculated or
berry-like structures. AV

Malignant Cardiac Tumors

Various percentages have been
reported. Some authors claim Adult Child
that up to 95% of malignant

primary cardiac tumors are
6%
sarcomas. Irrespective of the

true underlying number, 33 %
11 %
sarcomas are certainly the most 33 % 44 %

common malignant primary

neoplasms in adults. 16 %

If a tumor involves the wall of 21% 11 %
more than one chamber, it is
usually malignant (invasive
growth). Malignant tumors are
frequently associated with Angiosarcoma Rhabdomyosarcoma Mesothelioma
pericardial effusion. Fibrosarcoma Lymphoma Osteosarcoma
Malignant teratoma

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 019 // TUMORS AND MASSES

MASSES NOTES

Imaging Tips for the Evaluation of Masses Malignant tumors of the right
atrium tend to grow along the
• Use atypical views focusing on the whether the tumor is vascularized and interatrial septum. Look closely
mass whether there is flow within the tumor. at this structure when you see a
• Do not be too focused on the tumor • Use echo contrast. It helps to delineate mass in the right atrium.
– perform a complete exam the tumor and determine whether the
• Use different gain settings. In- tumor is vascularized.
tramyocardial tumors are sometimes • Do not forget to point the transducer
difficult to see. to the liver, the inferior vena cava, and
• Use color Doppler. It may help to tell the pleura.

Complications of Malignant Tumors

• Local compression • Spread to surrounding structures

• Obstruction • Arrhythmias
• Pericardial effusion with tamponade • Valvular dysfunction

MALIGNANT MASS (RHABDO-

MYOSARCOMA) – atypical apical
four-chamber view/2D

Tumor masses in the left atrium.

The structure of the tumor is
AMVL inhomogeneous and it is causing
Tumor inflow obstruction into the left
ventricle.
Left atrium

Consequences/Therapeutic Options To determine changes in size of

a tumour/mass or thrombus
• If you are not certain whether it is a • If it is a thrombus., anticoagulate and compare images side by side.
tumor, perform other imaging modali- repeat study. It should become smaller. This is often more reliable than
ties (i.e. TEE, MRI, CT) and perform • If it is a malignant tumor, determine comparing measurements.
follow-up exams. what it is (biopsy of primary tumor,
• In benign tumors, consider surgical pericardial tap, lab., etc.) Some tumors
removal when the tumor is in the left respond well to treatment with
heart. LV tumors are subject to a high radiation or chemotherapy (such as
risk of embolization (e.g. lymphoma).
fibroelastoma). Small and very mobile masses
are difficult to see on MRI.
Echo is superior because its
frame rate is much higher.

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 019 // TUMORS AND MASSES

NOTES

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 020 // Congenital Heart Disease

CONTENTS
188 Basics

188 Atrial Septal Defect (ASD)

191 Patent Foramen Ovale (PFO)

192 Ventricular Septal Defects (VSD)

194 Patent Ductus Arteriosus (PDA)

195 Coronary Fistulas

196 Tetralogy of Fallot

197 Transposition of the Great Arteries

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 020 // CONGENITAL HEART DISEASE

NOTES BASICS

20% of all congenital Prevalence (Adults)

defects are atrial septal 20% have a
right-to-left shunt
defects. • Complex jet lesions:
418 per million 45% have a left-to-right shunt


35% have no shunt

ATRIAL SEPTAL DEFECTS (ASD)

Severe pulmonary Hemodynamics of Atrial Septal Defects

hypertension is rare in the
setting of isolated atrial • Right ventricular volume overload • Reduced compliance of the left
septal defects. • Pulmonary hypertension ventricle
• Potential for paradoxical embolism

75% of all atrial septal Types of Atrial Septal Defects

defects are secundum Secundum defect
defects.
Sinus venosus Atrial appendage
defect (sup.)

Primum defect
Coronary sinus defect

Sinus venosus
defect (inf.)

Patients with a primum ASD tend to Associated Lesions

have left axis deviation and a long PQ
interval on the ECG, whereas patients ASD I (primum defect) Sinus venosus defect
with a secundum ASD have right axis • Cleft mitral valve (always) • Partial anomalous venous return
deviation and RBBB. • Inlet ventricular septal defect • Overriding superior vena cava
• Septal aneurysms
A patent foramen ovale and a
secundum ASD (ASD II) are not the ASD II (secundum defect) Coronary sinus septal defect
same entitiy. A patent foramen ovale is • Mitral valve prolaps • Unroofed coronary sinus
a shunt across a ”channel” (between a • Pulmonic stenosis • Left superior vena cava persistence
septum primum and secundum) while • Partial anomalous venous return • Partial/total anomalous venous return
an ASD II is a hole in the septum.

It is possible to have both, an

ASD and a PFO.

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ATRIAL SEPTAL DEFECT (ASD) NOTES

COMPLETE ATRIOVENTRICULAR
CANAL DEFECT – apical four-
chamber view/2D
IVS
VSD Improperly formed atrioventricu-
lar valve (shared atrioventricular
valve). Both an ASD (primum
MV
TV type) and a VSD are present.

ASD I
LA

RA

Views to Detect an ASD Transesophageal

echocardiography (TEE) is
• Slanted four-chamber view • Subcostal views superior in quantifying the size
• Parasternal SAX view • Not all ASD‘s can be detected with TTE and morphology of an ASD (two
orthogonal planes). TEE is also
required to diagnose a sinus
venosus defect.

SECUNDUM ATRIAL SEPTAL

Color jet DEFECT – slanted apical four-
ASD II chamber view/color Doppler

Moving the transducer medially

allows more parallel alignment
to the Doppler and therefore
better visualization of the ASD jet.

Difficulties in Detecting Shunts The intertrial septum may show

dropouts that mimic an ASD.
• Poor image quality ASD signal during systole
• Suboptimal angle to shunt flow • Shunt flow depends on left and right
• Low flow velocity ventricular compliance
• Inferior vena cava inflow • Elevated right heart pressure may
may mimic ASD reduce left-to-right shunt
• Tricuspid regurgitation may obscure the

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 020 // CONGENITAL HEART DISEASE

NOTES ATRIAL SEPTAL DEFECT (ASD)

An ASD must be excluded When to Suspect an ASD:

in every patient with an
enlarged RV. • Enlarged right ventricle • Elevated flow in the pulmonary
• Dilated pulmonary artery artery (VTI >25 cm)
The absence of a color jet • Positive contrast study • Patient history (arrhythmias,
across the IAS and even a • Abnormal septal morphology dyspnea, atrial fibrillation + ECG +
negative contrast study do not (aneurysm, discontinuity of the right ventricle enlargement)
entirely rule out an ASD. It could interatrial septum, etc.)
be a sinus venosus defect and it
may be possible that, despite an
ASD, there is only a left-right
shunt (negative contrast study).

The size of the ASD is Quantification of Atrial Septal Defects

quantified with a balloon
during intervention. This Large > 10 mm
”stretched size” of the ASD is
relevant for device sizing. Small 5–10 mm

No relevant shunt < 5 mm

A warning note: Even small defects can generate significant left-to-right shunts
when the gradient between the left and the right atrium is high.

The measurement of Quantification of Shunt Flow

LVOT/PA diameter is most
critical for shunt Flowpulm = (PA diameter/2)2 .  . VTI PA/RVOT
Qp/Qs =
calculation (measurement
Flowsystem = (LVOT diameter/2)2 .  . VTI LVOT
errors may have grave
consequences). PA = pulmonary artery, RVOT= right ventricular outflow tract,
LVOT= left ventricular outflow tract, VTI = velocity time integral

Suitabilty for Interventional Closure

The guidelines recommend interventional closure in patients with a stretched

diameter <38 mm and a sufficient rim > 5 mm towards the aorta.
ESC 2010

ASD closure must be avoided Indications for ASD closure (ESC Class I)
in patients with Eisenmenger • Patients with significant shunts (signs • Device closure is the method of
(right-to-left shunt) of RV volume overload) and pulmo- choice for secundum ASD closure
syndrome (ESC Class III). nary vascular resistance < 5 Wood when applicable.
units, regardless of symptoms.
ESC 2010

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ATRIAL SEPTAL DEFECT (ASD) NOTES

Suitabilty for Interventional Closure Intervention should be

monitored with the help
Ideal < 20 mm of echo (TEE, intracardiac
ultrasound).
Uncertain 20 – 25 mm

Too large > 25 mm

ASD OCCLUDER – subcostal

four-chamber view/2D
Liver
The left and the right atrial disks
of an Amplatzer occluder are
visible. The interatrial septum is
RV captured in between.

LV

RA

Amplatzer

Echo Assessment following Interventional ASD Closure

• Look for a residual shunt using color • Location and stability of the device
Doppler (reduce PRF) and echo • Thrombus on the device
contrast • Pericardial effusion

PATENT FORAMEN OVALE (PFO)

PATENT FORAMEN OVALE –

TEE bicaval view/2D
LA
Separation between the primum
PFO and the secundum septum form-
ing a patent foramen ovale (PFO).
The primum septum overlaps the
secundum septum and the PFO is
a channel rather than a hole.
SVC
RA

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 020 // CONGENITAL HEART DISEASE

NOTES PATENT FORAMEN OVALE (PFO)

Epidemiologic Facts

• 25% of the general population have a PFO.

• In patients with cryptogenic stroke the prevalence increases to 40%.

Perform a Valsalva maneuver Echo Assessment of Patent Foramen Ovale

when looking for PFO in the
contrast study and reduce PRF • Frequently associated with mobile and • Small jet into the right atrium seen with
for color Doppler assessment. aneurysmatic interatrial septum color Doppler (usually close to the
• Positive contrast study – contrast aortic rim)
A negative transthoracic appearance in the left atrium within 3 • For color Doppler assessment, use a
contrast study does not rule out heart cycles after opacification of the subcostal view or a slanted four-cham-
a patent foramen ovale. You right atrium ber view to improve Doppler alignment
need a transesophageal exam. • For contrast study use a four-chamber
view

VENTRICULAR SEPTAL DEFECTS (VSD)

The prevalence of VSD is Ventricular Septal Defect Types

10% of all congenital
lesions of the heart in the
adult population.
PA Subarterial or supracristal
Perimembranous VSD is ventricular septal defects
Ao
the most common type.

Membranous Muscular ventricular

ventricular septal defect
septal defect
RA

Inlet or canal-type ventricular septal defect

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 020 // CONGENITAL HEART DISEASE

VENTRICULAR SEPTAL DEFECTS (VSD) NOTES

Views and Locations of the Various VSD Types If you are not sure
whether a VSD is present
use the good old
RVOT RVOT
stethoscope!
TV
Ao
LV PV
RA
MV
LA PA
LA

LV LV
RV RV
RV
TV MV TV MV
LV
Ao
RA LA RA LA

Perimembranous
Outlet infracristal
Outlet supracristal
Inlet
Trabecular
Perimembranous or Outlet

PERIMEMBRANOUS VENTRIC-
ULAR SEPTAL DEFECT – PSAX/
color Doppler

Typical jet origin and direction

VSD of a perimembranous VSD. The
jet defect is located below the aortic
valve. The jet is directed more
towards right ventricular inflow.
Perimembranous
VSD Ao

LA

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 020 // CONGENITAL HEART DISEASE

NOTES VENTRICULAR SEPTAL DEFECTS (VSD)

Contrast is not helpful in VSD Quantification

ventricular septal defects.
• Left ventricular volume overload • Restrictive VSD has a high velocity
• Use atypical views to visualize the (> 4.5 m/sec) and occurs in small or
myocardial discontinuation medium-sized defects
• Color Doppler detection of flow • Non-restrictive VSDs have a low
across the interventricular septum velocity (< 4.5 m/sec), indicating
a large defect

Aneurysmal Transformation in VSD

• Partly or completely sealed VSD by • Best visualized on a five-chamber view

fibrous tissue proliferation of the septal • No risk of rupture
leaflet of the tricuspid valve

Interventional VSD Associated Lesions

closure is only possible in
muscular VSD with a Membranous VSD Supracristal VSD Inlet VSD
distance > 3mm from the
aortic valve. Septal aneurysms Aortic valve prolapse ASD I

Subaortic stenosis Cleft mitral valve

Double chambered RV

PATENT DUCTUS ARTERIOSUS (PDA)

PDA is present in 2% of the adult Hemodynamics of PDA – Different Presentations

population and is often
associated with coarctation and • Variable, depending on size • Elevation of pulmonary artery pressure
VSD. Always suspect a PDA in • Left-to-right shunt • Eisenmenger reaction
the setting of a dilated • Left ventricular volume overload • Hemodynamically insignificant (small)
hyperdynamic left ventricle in
the absence of other forms of LV
volume overload.

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 020 // CONGENITAL HEART DISEASE

PATENT DUCTUS ARTERIOSUS (PDA) NOTES

Visualization of the Patent Ductus Arteriosus Patients with high-

velocity PDA jets are
• Parasternal short axis (pulmonary artery • Dilatation of the pulmonary artery is candidates for closure
bifurcation) common (exception: small
• Suprasternal view • 2D (suprasternal view) often allows asymptomatic PDA).
• Systolic + diastolic flow in spectral and measurement of PDA size
color Doppler

PATENT DUCTUS ARTERIOSUS –

PDA jet PSAX/Color Doppler

Shunt (color jet) between the

aorta and the pulmonary artery at
Ao its bifurcation. The jet is present
during systole as well as diastole.
r-PA

Ao

CORONARY FISTULAS

Coronary Fistulas Coronary fistulas are

found in 0.2% of coronary
• Abnormal communication between • RV volume overload angiograms.
coronary artery and heart chamber • Coronary steal
• 90% into right ventricle

Echo Features of Coronary Fistulas The hemodynamic

presentation greatly
• Dilated coronary artery (> 0.6 cm) depends on the degree of
• Enlargement of heart chambers RV outflow obstruction.
• Turbulant flow In the setting of a VSD
• Continous flow (shunt) to right heart with a left-to-right shunt,
it may prevent pulmonary
hypertension and
eventually shunt reversal
(right to left) and the
Eisenmenger reaction.

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 020 // CONGENITAL HEART DISEASE

NOTES TETRALOGY OF FALLOT

The hemodynamic presentation

greatly depends on the degree
of RV outflow obstruction. In
the setting of a VSD with a left-
to-right shunt, it may prevent Overriding aorta
pulmonary hypertension and
RVOT obstruction
eventually shunt reversal
(right to left) and the Eisen-
menger reaction. Large ventricular
septal defect
Right ventricular
hypertrophy

• Stenosis of the pulmonary artery (right • Deviation of the origin of the aorta to
ventricular outflow obstruction) the right (overriding aorta)
• Ventricular septal defect • Concentric right ventricular
hypertrophy

In patients with a more severe Echocardiographic Assessment in Fallot

RVOT obstruction, PW and col-
or Doppler will demonstrate a Ventricular septal defect and overriding aorta
significant right-to-left shunt at • Assess the characteristic and large VSD • The extension of the defect from the
the VSD. In patients with a large on multiple views and define the membranous septum is best seen in
left-to-right shunt, left atrial location and number of VSDs the parasternal short axis
and left ventricular dilatation • The degree of aortic override is best • Assess the relationship between the
will be present. assessed on parasternal long-axis and defect and the tricuspid and aortic
apical views. valve.
Right ventricular outflow
obstruction tends to occur at Right ventricular outflow tract obstruction
multiple levels - infundibular, • Use parasternal short-axis views. • The pulmonary valve annulus is often
RVOT, often hypoplastic annu- • Assess the infundibulum and pulmo- hypoplastic (important information in
lus valve abnormalities nary vale. regard of a transannular patch).
(bicuspid valve). • Infundibular muscle bundles often • The pulmonary valve tends to look
contribute to the RVOT obstruction thickened and may be dome-shaped.
When assessing patients after
Fallot repair, look for residual Hemodynamic assessment
pulmonary regurgitation. • A large and generally unrestricted • The direction and degree of shunting
defect permits equalization of right and strongly depend on the severity of right
left ventricular pressures. ventricular outflow tract obstruction.

Aortic arch and coronary arteries

• Use suprasternal views to investigate • The anatomy of the proximal coronary
the aortic arch and exclude the arteries should be assessed using
presence of aortopulmonary colla- parasternal short-axis views
terals and the presence of a patent • Exclude a right aortic arch (present in
ductus arteriosus. 25%)

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 020 // CONGENITAL HEART DISEASE

TETRALOGY OF FALLOT NOTES

TETRALOGY OF FALLOT ­–
VSD PLAX/2D
A patient with a tetralogy
of Fallot, a large VSD and an
overriding aorta.

Overriding aorta

TRANSPOSITION OF THE GREAT ARTERIES

In D-TGA a shunt on the
atrial/ventricular/great
vessels (PDA) is required to
AO live, either present at birth or
Ao
PA PA artificially created (e.g.
LA LA
Rashkind’s procedure)
RA

RA Tricuspid
LV valve
Mitral valve
RV RV
LV

D-TGA L-TGA

• Lesion in which the aorta arises from corrected TGA. Venous blood returns Patients with L-TGA are at
the right ventricle and the pulmonary from the correctly located right atrium risk for (systemic) heart
artery from the left ventricle. to the discordant left ventricle via the failure because the morpho-
• Its prevalence is 4.7 per mitral valve and into the lung via the logical right ventricle (which
10,000 live births. pulmonary artery. Oxygenated blood was not formed to sustain a
• It is not associated with any flows through the pulmonary veins to high pressure system)
common gene abnormality. the left atrium into the discordant right supplies the systemic
• The most common form is the dextro ventricle, and via the tricuspid valve into circulation.
type (D-TGA), in which the aorta arises the systemic circulation through the
from the right ventricle and the aorta (atrioventricular and ventriculoar-
pulmonary artery from the left ventricle terial discordance).
(ventriculoarterial discordance). • The D-TGA leads to cyanotic heart
• Levo- or L-looped transposition of the disease while L-TGA usually does not
great arteries (L-TGA) is very rare and is present with cyanosis (unless the
commonly referred to as congenitally patient has associated cardiac defects).

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 020 // CONGENITAL HEART DISEASE

NOTES TRANSPOSITION OF THE GREAT ARTERIE

Cardiac Lesions Associated With D-TGA

• A ventricular septal defect in any • Abnormalities of the mitral and

region of the ventricular septum tricuspid valve, e.g. straddling tricuspid
(50% of patients). valve (septal chordal attachment of the
• Left ventricular outflow tract tricuspid valve extending into the left
obstruction (25%) ventricle), overriding valves.
• Coronary abnormalities

Echocardiographic Assessment in D-TGA

• Subcostal views show the pulmonary • Parasternal short-axis views show the
artery arising from the posterior left aorta rising anteriorly from the right
ventricle. ventricle.
• Look for associated cardiac lesions.

Cardiac Lesions Associated With L-TGA

• Ventricular septal defect (70-80% of • Tricuspid valve abnormalities (90% of

patients), most commonly perimem- patients) e.g. tricuspid valve regurgitati-
branous VSD. on, Ebstein-like malformation of the
• Pulmonary outflow (i.e. left ventricular) tricuspid valve accompanied by right
tract obstruction (30- 60% of patients). ventricular dysfunction and failure
The obstruction is commonly subval- (20- 50% of patients).
vular due to an aneurysm of the • Mitral valve abnormalities (50% of
interventricular septum fibrous tissue patients) e.g. abnormal number of
tags or a discrete ring of subvalvular cusps, straddling chordal attachments
tissue. of the subvalvular apparatus resulting
in outflow tract obstruction, mitral
valve dysplasia.

L-TGA ­–
Apical four-chamber view/2D

Since the tricuspid valve and the

Mitral valve
mitral valve are in opposite posi-
tions, the valve on the left side of RV
the screen is more apical (lower
in the screen) than the valve on LV
the right. This is one of the key
features that help to identify
L-TGA. The right ventricle is in
the position of the left ventricle. Tricuspid valve
It can be identified because it is RA
heavily trabeculated.
LA

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 020 // CONGENITAL HEART DISEASE

TRANSPOSITION OF THE GREAT ARTERIE NOTES

Echocardiographic Assessment in L-TGA The diagnosis of L-TGA is

often missed at adult cardiac
• Systemic location of the tricuspid valve • Subcostal imaging usually provides the echo laboratories!
and morphologic right ventricle. It is clearest view of the pulmonary artery
best seen on an apical four-chamber arising from the morphologic left
view or parasternal short-axis views. ventricle.
• Look for associated cardiac lesions.

L-TGA – Atypical long-axis view,

subpulmonic ventricle/2D
Pulmonic valve
The subpulmonic ventricle, which
is anatomically the left ventricle,
LV ensures pulmonary circulation.

PA

RA

Mitral valve

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 020 // CONGENITAL HEART DISEASE

NOTES

200

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 021 // Stress Echocardiography

CONTENT
202 Indications and Echocardiographic Features

203 Clinical Targets of Stress Echocardiography and Stress of Choice)

204 Stress Echocardiography – an Easy Approach

206 Stress Echo and “Other Echo Modalities”

207 Ischemia Testing

208 Viability Testing

209 Stress Echo in Low-Flow Low-Gradient Severe Aortic Stenosis

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 021 // STRESS ECHOCARDIOGRAPHY

INDICATIONS AND ECHOCARDIOGRAPHIC

NOTES FEATURES
Indication Clinical question Echo features of
Stress echo will help to specific interest
improve your imaging skills.
Ischemia Does the patient have CAD? New wall motion abnormalities
Stress echo for coronary
artery disease is operator Viability Are akinetic segments viable Improvement of contractility
dependent. Therefore you (hibernating myocardium)? with low-dose dobutamine
need a lot of experience in
imaging and interpreting wall Low-flow Is aortic stenosis severe? An increase in gradients driven
motion abnormalities to low-gradient AS by an increase of contractility
obtain valid results. (cardiac output) under stress

Asymptomatic Should mitral valve surgery Increase of ejection fraction

moderate/severe be performed? with stress or occurrence of
mitral regurgitati- symptoms (=adequate
on functional capacity)

Symptomatic Is dynamic mitral regurgita- Increase of mitral regurgitation

moderate/mild tion present? severity increases during stress
mitral regurgitati-
on

Aortic regurgita- Should aortic valve surgery Increase of ejection fraction

tion be performed with stress or occurrence of
symptoms (=adequate
functional capacity)

Mitral stenosis Should valvuloplasty or Excessive increase in transmit-

with unclear mitral valve replacement be ral gradients (>18 mmHg) or
severity/ performed? systolic pulmonary artery
symptoms pressure (sPAP) (>60 mmHg)
or occurrence of symptoms

Pulmonary Detection of early disease Increase in sPAP with exercise*

arterial
hypertension

Hypertrophic Is LVOT obstruction present? Exercise tolerance and an

cardiomyopath Indication for myectomy or increase of the gradient during
septal ablation stress > 50 mmHg

Dyspnea Is dyspnea related to the Exercise tolerance, increase of

heart (dilated cardiomyopa- ejection fraction during
thy, coronary artery disease) exercise, wall motion abnor-
malities suggesting coronary
artery disease

*Stress echo is currently no diagnostic criterion for pulmonary hypertension

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 021 // STRESS ECHOCARDIOGRAPHY

INDICATIONS AND ECHOCARDIOGRAPHIC

FEATURES NOTES
STRESS REACTION – PSAX Quad
view/2D

Quad view comparing four differ-

ent levels of dobutamine stress
from baseline (left upper corner)
to 40 mcg/kg/min (right lower
corner). The global contractility
of the left ventricle is increased
(see moving image).

CLINICAL TARGETS OF STRESS ECHO- The choice of the stress

CARDIOGRAPHY AND STRESS OF CHOICE test depends on the
indication/relative
Clinical Pathophysio- Stress of Echo variable
contraindication, and the
condition logic target choice
stress form your laboratory
Coronary artery Myocardial Exercise, Wall motion abnor- is most familiar with.
disease ischemia dobutamine, malities (see cine loop at
dipyridamole www.123sonography.com/
echofacts)
Dilated cardi- Contractile Dobutamine Wall motion abnor-
omyopathy reserve (exercise, malities
dipyridamole)

Diabetes, hyper- Coronary flow Dipyridamole PW Doppler Left

tension, hypertro- reserve (dobutamine, anterior descending
phic cardiomyo- exercise) (LAD)
pathy

Transmitral Increase in Exercise, PW/CW Doppler

gradient cardiac output dobutamine mitral valve

Transaortic Increase in Exercise, CW Doppler aortic

gradient cardiac output dobutamine valve

Pulmonary Pulmonary Exercise CW Doppler tricuspid

hypertension congestion/ regurgitation
vasoconstriction

EAE Guidelines 2008

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STRESS ECHOCARDIOGRAPHY –
NOTES AN EASY APPROACH

Rest Stress Myocardium

Normokinesia Normo-, hyperkinesia Normal

Normokinesia Hypo-, A-, Dyskinesia Ischemic

Akinesia Hypo-, Normokinesia Viable

A-, Dyskinesia A-, Dyskinesia Necrotic

EAE Guidelines 2008

ISCHEMIA

Dyskinesia Hypokinesia Akinesia

Normokinesia

NORMAL

Hyperkinesia

NON VIABLE

Akinesia Dyskinesia

Akinesia

VIABLE

Hypokinesia Normokinesia Hyperkinesia

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STRESS ECHOCARDIOGRAPHY –
AN EASY APPROACH NOTES

Forms of Stress It is easier to image patients

when you use a
• Semisupine exercise • Adenosine pharmacological stressor. You
• Dobutamine (antidote: beta-blocker) • Pacing will have less hyperventilation,
• Dipyridamole (antidote: aminophylline) tachycardia and chest motion.
However, exercise is a more
physiological stressor.

Exercise Stress

• The patient pedals against an increa- • Workload is escalated in a stepwise

sing workload at a constant cadence manner
(60 rpm)

Dobutamine Stress
Atropine (0.25 mg x 4)
An ischemic response may
occur late after stress – record
40 images post stress!
30
20
10
5

Dobutamine (g/kg/min)  -Blockers

0 3 6 9 12 15 18 21
Time (min)

VIABILITY TESTING – Apical

four-chamber view/2D & PW
Doppler

Patient with akinesia of the

septum (top left) with low LVOT
velocity at rest (top right), There
is no change in the contractility
of the septum during dobutamine
stress (bottom left). The segment
is not viable. The residual myo-
cardium increases its contrac-
tility (non-ischemic). This is also
reflected by the increase in LVOT
velocity (bottom right).

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STRESS ECHOCARDIOGRAPHY –
NOTES AN EASY APPROACH

Aminophylline (240mg Dipyridamole Stress

intravenously) should be
available for immediate Infusion of 0.56 mg/kg dipyridamole over 4 minutes
use in case of
dipyridamole-related
adverse events. 4 minutes of no dose

0.28 mg/kg over 2 minutes (if the stress test is still negative)

Atropine doses of 0.25 mg to maximum 1 mg (if the stress test is still negative)

Adenosine Stress

• Typically infused at a maximum dose of 140 mcg/kg/min over 6 minutes.

Pacing

• Pacing is started at 100 bpm and increased every 2 minutes by 10 bpm until the
target heart rate (85% of age-predicted maximal heart rate) is achieved.

STRESS ECHO AND “OTHER ECHO MODALITIES”

Speckle tracking is a Speckle tracking Assessment of longitudinal function during stress

promising technique,
especially for the assessment Contrast Improves the visibility of endocardial borders, simplifies
of contractile reserve in the assessment of global and regional myocardial
patients with valvular heart function
disease.
3D Quicker data acquisition, multislice approach

3D RECONSTRUCTION–
short-axis views/3D

Live 3D Reconstruction of
short-axis views for the analy-
sis of contractility during stress
echocardiography (see moving
image)

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ISCHEMIA TESTING NOTES

Facts Acquire several RR

intervals and be careful not
• Changes in wall motion (hypokinesia, • Use parasternal (long and short axis) as to record image loops
akinesia) during stress strongly suggest well as apical views (four- three-, and during ectopic beats.
significant coronary artery disease and two chamber). Use atypical views if the
are more accurate than ECG changes. image quality is better there.
They are also more specific than • Make sure the images you record
perfusion abnormalities. during stress testing closely corres-
• Worsening of wall motion in at least pond to the ones you recorded at
two adjacent segments is required for baseline (use specific stress acquisition
a positive outcome of the test. protocols that allow simultaneous
• Clear endocardial delineation is crucial review, such as split/quad screens).
– use contrast to enhance the visibility • Blood pressure measurements (each
of the endocardium. stage) and 12-lead ECG (every minute)
should be recorded.

Endpoints in Ischemia Testing Stress echo is a safe

procedure. Nevertheless, you
• Maximal dose or exercise level reached • Hypotension (drop by more need to have a defibrillator/
• Achievement of target heart rate than 40 mmHg) advanced life support
• Obvious positivity of the test (echo • Occurrence of supraventricular equipment in your lab!
and/or ECG) arrhythmias (supraventricular
• Severe chest pain/Severe dyspnea or tachycardia, new atrial fibrillation)
other symptoms • Occurrence of ventricular arrhythmias
• Hypertension (systolic hypertension (ventricular tachycardia, polymorphic
≥ 220 mmHg, diastolic hypertension premature ventricular beats)
≥ 120 mmHg)

Coronary Flow Reserve

• Transthoracic echo allows imaging of • By comparing the velocities with those
the left anterior descending (LAD) and obtained during pharmacologic stress
posterior descending (PD) coronary (infusion of adenosine), it is possible to
arteries. calculate coronary flow reserve.
• With the help of coronary PW Doppler
one can measure blood flow in the
coronary arteries.

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NOTES VIABILITY TESTING

Myocardial segments can be viable even when they do not contract (akinesia). This
phenomenon occurs in the setting of stunning or hibernation.

Phenomena Definition/Cause

Stunning Segmental dysfunction which persists for a variable

period of time - about two weeks - even after ischemia
has been relieved

Hibernation Abnormal contractility caused by inadequate blood

supply (chronic stable angina, unstable angina, silent
ischemia)

The function of viable

Stenosis after Occlusion
segments may be restored thrombolysis
when revascularization
(PCI or CABG) is achieved.

Necrosis Necrosis

Stunning Hibernation

Stunning: Reversible reduction of Hibernating: Downregulation of

function of heart contraction after myocardial function to match chronic
reperfusion reduced blood flo

It is meaningless to look Viability Response

for viability in segments
that are obviously scarred • Sustained improvement during stress • Biphasic response (improvement at
(thin, echodense). The low-dose dobutamine, deterioration
dyskinesia that occurs in at peak levels)
such segments during
stress should not be
mistaken for viability. It is a
passive phenomenon
related to the increase in
intraventricular pressure.

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STRESS ECHO IN LOW-FLOW LOW-GRADIENT

SEVERE AORTIC STENOSIS NOTES

Low-Flow Low-Gradient Severe AS - Definition Stress echo can be used to

Severe aortic stenosis in the setting of reduced left ventricular function and a valve distinguish true (severe) low-
area ≤1.0 cm2, where the aortic velocity is <4.0 m/s or the mean transvalvular flow low-gradient aortic
pressure gradient is ≤30-40 mmHg. stenosis from “pseudo-severe”
low-flow low-gradient aortic
Principle of Stress Testing in Low-flow stenosis. Patients with left
Low-gradient Aortic Stenosis ventricular contractile reserve
Augmentation of stroke volume with dobutamine should increase flow across the and true severe low-flow
aortic valve and cause a significant increase in gradients without a change in aortic low-gradient aortic stenosis
valve area (<1.0 cm2). have an acceptable surgical risk.
Valve replacement is
recommended in the majority of
these patients and usually
improves their functional status
and survival.

Changes in Echo Parameters During Stress Even moderate aortic stenosis

can be relevant when patients
True severe AS Pseudo-severe AS have ischemic or dilated
cardiomyopathy. The increased
Stroke volume (LVOT + + afterload in aortic stenosis is an
velocity) additional burden to the
ventricle.
Transvalvular gradients +++ (+)

Aortic valve area - (+)

Patients with pseudo low-flow low-gradient AS have a small aortic valve area
because the low stroke volume does not push the valve open. In contrast, in
patients with true severe aortic stenosis the aortic valve area is fixed and does not
increase when stroke volume rises.

LOW-FLOW LOW-GRADIENT
AORTIC STENOSIS – apical
four-chamber view/CW & PW
Doppler

Increase on LVOT velocity and

AV velocity in a patient with true
low flow low gradient AS

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STRESS ECHO IN LOW-FLOW LOW-GRADIENT

NOTES SEVERE AORTIC STENOSIS

Dobutamine Protocol in Low-Flow Aortic Stenosis

• Start with a low dobutamine dose (at • Duration of each step: 3-5 min
5 μg/kg/min) • Monitor blood pressure and ECG
• Increase stepwise (+2.5–5 μg/kg/ (arrhythmias, ischemia)
min) to maximum of 20 μg/kg/min

The differentiation Echocardiographic Examination

between true severe and
pseudo-severe aortic Parameter Applied for
stenosis may be improved
by calculating the LVOT diameter (at rest) Aortic valve area (AVA) (continuity equation)
projected aortic valve area
(the aortic valve area that
would be present if the LVOT velocity signal (PW Doppler) AVA (continuity equation), stroke volume
flow rate were normal).
Doppler signal aortic valve (CW Maximum and mean gradient, AVA continu-
More detailed information Doppler) ity equation
can be found in Blais et al.
Circulation 2007 Representative 2D images Visual assessment or calculation of ejection
fraction/contractile reserve

(Color Doppler of mitral Dynamic mitral regurgitation?

regurgitation)

Stroke volume can actually Endpoints in Low-Flow Aortic Stenosis

drop when heart rate increases
excessively. This will also affect • The maximum dobutamine dose has • Ventricular arrhythmias (ventricular
the gradients and can lead to been reached (20 μg/kg/min) tachycardia/increasing frequency of
misinterpretation. Sometimes • Obvious inotropic response and polymorphic ectopic beats
submaximal stress provides the positive outcome of the test • (Increase in heart rate ≥ 10-20 beats/
highest gradients. min)

A dobutamine response is Things to Consider

present when the forward
stroke volume increases by • An increase in mitral regurgitation • Difficulties in obtaining adequate
≥20% (= 20% increase in the under stress can counterbalance an Doppler signals during stress may lead to
velocity time integral). increase in cardiac output during an underestimation of the increase in
stress. gradients
• Tachycardia during stress may offset • Determine the average of several beats
an increase in stroke volume in the presence of atrial fibrillation

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 022 // Contrast Echocardiography

CONTENT
212 Principles

213 Contrast Agents

215 Applications of Echo Contrast

215 Right Heart Contrast

219 Quantification of Left Ventricular Function

221 Myocardial Perfusion Imaging

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NOTES PRINCIPLES

Injected air or gas bubbles can generate a very strong ultrasound signal
when hit by an ultrasound wave. This signal is used to opacify (contrast)
the blood pool during echocardiography.

Contrast agents are micro-bubbles, which consist of an outer shell and

encapsulated inner gas.

Intravenous injection of contrast results in pronounced contrasting

of right heart chambers. Contrast agents with the following characteri-
stics have been developed to achieve adequate opacification of the
left heart as well:

• Small bubble size (1-8 μm) • Strong ultrasound reflectors

• To allow passage through the • Contrast effects that last for 3-10
pulmonary circulation and myocar- minutes; the contrast medium can
dial microcirculation be applied as a bolus, repeat bolus,
• A durable shell and gas with high or an infusion.
density, high molecular weight, and • Can be destroyed with high-power
low solubility ultrasound To study replenishment of
• Non-toxic contrast in myocardial micro-
• No side effects circulation
• High echogenicity

Reactions of Bubbles to Ultrasound

Linear At low acoustic Compression and No special contrast

oscillation power (MI<0.2) rarefaction are equal signal is achieved
in amplitude

Non-linear At intermediate Ultrasound waves Micro-bubble-spe-

oscillation acoustic power are created at cific signal
(MI 0.2–0.5) harmonics of the
delivered frequency

Destruc- At high acoustic Bursting of the Intermittent imaging

tion power (MI >0.5) bubbles, resulting in allows visualization
transient emission of of capillary refill
a high-intensity
signal

MI = mechanical index – the power of the signal to which the bubbles (or any
tissue) are exposed.

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PRINCIPLES NOTES

Acoustic Power and Microbubble Responses Some destruction of

micro-bubbles is always
High Power (MI >0.5) present, even at a lower
acoustic power.
Low Power
(MI 0.2–0.4)

Very Low Power

(MI <0.1)

Very low power does not affect the contrast bubbles (no signal). Inter-
mediate power causes the bubbles to resonate and generate a signal.
High-power ultrasound leads to the destruction of bubbles, generating a
very strong return signal.

Imaging of (Left Heart) Contrast Requires Special Settings Low mechanical real-time
imaging is used to study left
Low mechanical index Less bubble destruction, weak tissue signal, simultaneous ventricular function.
(real-time imaging) assessment of function and perfusion is possible

High mechanical index Intentional destruction of bubbles to generate high-inten-

(ECG-triggered sity signals and study replenishment
intermittent imaging)

CONTRAST AGENTS

Right Heart Contrast Agents

(Do not cross the pulmonary circulation)

Agent Dose

Agitated saline (+blood and air) 8 ml 0.9% saline (+1 ml blood

+ 1 ml air)

Dextrose 5% water 10 ml

D-galactose microparticle solution (Echovist®) 5–10 ml

Urea-linked gelatin (Haemaccel®) 10 ml

Oxypolygelatine (Gelifusin®) 10 ml

Sonicated albumin (5%) 10 ml

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NOTES CONTRAST AGENTS

Left Heart Contrast Agents

(Cross the pulmonary circulation and enter the myocardial microcirculation)

Agent Dose Bolus Dose Infusion

Perflutren 0.5 ml, < 1 ml/s, flush of Not more than 5ml in a
protein type A 0.9% sodium chloride 10-min period and do not exceed
microsphere injection, or 5% dextrose the maximum cumulative dose of
(Optison®) injection, maximum dose 8.7 ml per study
8.7 ml in any patient

Perflutren lipid 10 microliters (microL)/kg Activated Definity® via intra-

microsphere of the activated product venous infusion of 1.3 mL added
(Definity®) by intravenous bolus to 50 mL of preservative-free
injection within 30-60 saline. The rate of infusion should
seconds, followed by a be initiated at 4 mL/minute, but
10-mL saline flush titrated as necessary to achieve
optimal image enhancement;
should not exceed 10 mL/minute.

Potential Side Effects

• Back pain • Rarely: anaphylactic reactions (estimated

• Headache rate of 1 per 10,000)
• Urticaria • Modern

The ultrasound return signal Contraindications for Left Heart Contrast Agents
generated by micro-bubbles
is several million times more • Hypersensitivity to Perflutren • Hypersensitivity to blood or albumin (for
effective in scattering ultra- • Intra-arterial injection Optison only)
sound than red blood cells. • Right to left or bidirectional intracar-
diac shunts

Thirty minutes of monitoring is required only for patients with pulmonary hyper-
tension and unstable cardiopulmonary disease.

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APPLICATIONS OF ECHO CONTRAST NOTES

Vascularized tumors show

Interrogation Effect
opacification when contrast is
applied.
Detection of ASD Washout, contrast passage through the ASD
shunts

PFO Contrast into the left atrium through PFO

Intrapulmo- Rapid contrasting of LA via pulmonic veins

nary shunt (≥ 4 cycles)

Doppler signal Tricuspid Enhancement of the signal, measurement of

enhancement regurgitation maximum TR velocity

Cavity Ventricular Enhanced endocardial delineation

delineation function

Heart tumor Better delineation of the masses;

and masses flow within the mass?

Congenital Persistent Contrast injection via a left cubital vein results in

abnormalities vena cava sin. contrasting of the right atrium via the coronary
sinus.

RIGHT HEART CONTRAST

Patent Foramen Ovale (PFO)

A patent foramen ovale is a channel/flap between the septum secundum and the
septum primum that allows oxygenated blood from the mother to bypass the
pulmonary circulation and reach the systemic circulation of the infant during fetal
development.
Patent foramen ovale
SVC

Primum
septum
Secundum septum
Left
Right atrium
atrium

Eustachian valve

IVC

Schematic representation of a PFO.

The communication between the right
and the left atrium is formed by a channel/flap between
the primum and the secundum septum.

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NOTES RIGHT HEART CONTRAST

Paradoxical embolism may •A PFO persists in approximately 30% •Migraine and vascular headache are
be associated with acute of adults. more common in the setting of a
pulmonary embolism. The •Its prevalence declines with age. patent foramen ovale with right-to-left
presence of a deep vein •The prevalence of PFO is higher in cardiac shunting.
thrombosis and a sudden (young) patients with cryptogenic •Decompression sickness in scuba
rise in right atrial pressure stroke (paradoxical embolism). divers may lead to air embolism
predisposes to right-to-left •Atrial septal aneurysms are frequently through a patent foramen ovale.
shunting. associated with PFOs and/or atrial •Paradoxical embolism through a PFO
septal defects (ASDs). may also occur into the coronaries,
•A prominent Eustachian valve or Chiari renal arteries, retinal arteries, or other
network favors the persistence of PFO. sites of systemic vascular circulation.

Overlap zone AO
(primum + SVC
secundum
septum)
PV

TV

FO

CS
RV
IVC

Fossa ovalis (FO) and a patent foramen ovale as seen from the right
atrium. The connection between the right and the left atrium occurs
through an “overlap” zone between the secundum and the primum sep-
tum, which is located cranially in the fossa ovalis.

Elevated right atrial pressures The degree and direction of the shunt
(as they occur in pulmonary depend on the following factors:
hypertension) may cause
significant right-to-left shunt •Size of the PFO •Mechanical factors; distortion of
and hypoxemia. •Pressure gradient between the right cardiac anatomy (interatrial septum)
and the left atrium may increase the degree of shunting
•Respiratory phase (influences pressure (i.e. platypnea-orthodeoxia syndrome)
Patients with high left atrial gradient from left to right)
pressures have pure left-to-right
shunts. In this setting the con-
trast study will be negative (even
using a Valsalva maneuver), but
the condition can be seen with
color Doppler.

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RIGHT HEART CONTRAST NOTES

CONTRAST IN PFO – TEE bicaval
LA LA view/2D & contrast

Large PFO and hypermobile

PFO Contrast swirl interatrial septum; the separa-
tion between the primum and
secundum septum is visible in 2D
SVC (left side). Pronounced contrast
RA opacification of the left atrium
RA
occurs after the injection of oxy-
polygelatine (right side).

Detection of a Patent Foramen Ovale with Color Doppler Right atrial inflow from the
inferior vena cava “bounc-
•Best seen on a slanted four-chamber •Size of color jet (degree of shunting) ing” off the interatrial
view and a modified parasternal may vary with respiration septum may mimic an ASD/
short-axis view •Not always possible to differentiate PFO jet.
•Located cranial portion of the interatri- between a PFO and a small atrial
al septum in proximity to the aortic septal defect
valve and superior vena cava

COLOR DOPPLER in PFO – slant-

ed apical four-chamber view/
color Doppler

A small jet (PFO) is passing

through the interatrial septum

PFO jet

How to Perform an Adequate Transthoracic Contrast Consider hepatopulmonary

Study for Identification of a Patent Foramen Ovale syndrome in the setting
of severe hepatic disease,
•Use an apical four-chamber view. •Perform a bolus (intravenous) injection volume overload, and low
•The interatrial septum and the right of contrast. oxygen saturation. Right
upper pulmonic vein should be visible. •Look for contrast crossing the contrast echo can detect
interatrial septum. intrapulmonary shunts
(pronounced contrasting
Contrast that enters the left atrium via the pulmonic circulation (normal) usually of the left heart via the
comes late and bubbles appear smaller. A negative transthoracic contrast study pulmonic veins after
does not rule out a PFO. The sensitivity and specificity is much lower than that of a ≥ 4 cardiac cycles).
transesophageal contrast study.

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NOTES RIGHT HEART CONTRAST

POSITIVE TRANSTHORACIC
CONTRAST STUDY – apical
Bubbles in
four-chamber view/2D contrast
the LV
Positive contrast study with Oxy-
polygelatine (Gelifusin®) used as
contrast agent. A small “cloud” of
contrast enters the left atrium via
the interatrial septum.

Contrast
crossing

Contrast injection may aid If Negative, Repeat the Study using a Valsalva Maneuver
procedures such as pericar-
diocentesis (position of the •Use a four-chamber view (image from •Let the patient release the “Valsalva
needle in the pericardium or as far medial as possible to avoid lung pressure” as soon as contrast appears
the heart). interference when the patient inhales). in the right atrium.
•Let the patient exhale. •Let the patient inhale (to a normal
•Ask the patient to perform a Valsalva level) – too vigorous inspiration will
maneuver. result in poor image quality.
•Inject contrast.

PERSISTENT LEFT SUPERIOR

VENA CAVA – apical four-cham-
ber view/2D & contrast

Patient with a dilated coronary

sinus (right); contrast (Oxypoly-
gelatine - Gelifusin®) injected via
a left cubital vein demonstrates
contrasting of the right atrium Dilated coronary
via the coronary sinus, suggestive
sinus
of a persistent left superior vena
cava.

Platypnea-Orthodeoxia Syndrome

Right-to-left shunt that leads to dyspnea and oxygen desaturation when patients
are brought into upright position. The upright position increases the degree of
shunting by anatomically stretching the interatrial communication.

Predisposing Factors

•Aortic dilatation/aneurysm •Pulmonary emphysema, diseases of

•Chest surgery (pneumectomy) the pericardium

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QUANTIFICATION OF
LEFT VENTRICULAR FUNCTION NOTES

Left heart contrast opacification greatly enhances the visibility of the endocardial
border and thus improves assessment of global and regional function.

IMPROVEMENT OF IMAGE
QUALITY USING CONTRAST –
apical four-chamber view/2D &
contrast

Difficult assessment of global

and regional left ventricular
function in a patient with very
poor image quality (left). The
contrast study greatly improves
image quality (right).

Contrast Settings

•Harmonic imaging mode •Compression in the medium

•Low mechanical index – real-time to high range
imaging (MI = 0.5) •Image focus at the level of the mitral
valve or below

CONTRAST AND WALL

MOTION – apical four-cham-
ber view/2D & contrast

Contrast study to assess re-

gional wall motion. Akinesia
of the anteroseptal region is
clearly visible with contrast
(see cine loop - www.123so-
nography.com/echofacts)

Practical Issues Apical swirling of contrast is a

result of excessive destruction
•When injecting intravenously, contrast •Titrate the contrast dose to achieve of contrast in the near field by
will first appear in the right heart. optimal filling. ultrasound.
•Consider that too much contrast will •Bolus injection is adequate for rest
cause attenuation of those regions studies, whereas continuous infusion of Contrast echocardiography
more distal from the transducer (basal contrast should be given preference greatly enhances the accuracy
parts of the left ventricle when imaging during stress studies. of detecting regional wall mo-
from the apex). •Freeze the image intermittently to reduce tion abnormalities, both at rest
•Contrast in the right ventricle may bubble destruction and allow refilling of and during stress.
shadow the left ventricle and lead to the ventricle when contrast is low.
deterioration of image quality when •Contrast may be combined with 3D
parasternal views are used. echocardiography.

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QUANTIFICATION OF
NOTES LEFT VENTRICULAR FUNCTION
3D CONTRAST STUDY – apical
multiplane image acquisition/3D

Contrast study with multiplane

3D, four- (upper left) two- (up-
per right) and three-chamber
views (lower left). The lower right
image shows the corresponding
cut planes.

Other Indications for Left Heart Contrast

•Aneurysms and pseudoaneurysms •Masses (increased echo contrast due

•Apical hypertrophy to vascularization of the mass)
•Ventricular non-compaction •Pericardial cysts
•Apical thrombus (contrast filling •Coronary aneurysms and fistulas
defects are visible)

CONTRAST AND APICAL THROM-

BUS – apical four-chamber
view/2D & contrast
Thrombus
Patient with suspected apical
thrombus (left). Contrast injec-
tion demonstrates a filling defect
at the apex of the left ventricle,
denoting a thrombus (right).

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MYOCARDIAL PERFUSION IMAGING NOTES

Principle

Imaging of contrast within the vascular bed permits assessment of myocardial

perfusion at rest and during stress.

Limitations

•Feasible only in patients with very •Rapid destruction of bubbles (slow

good image quality flow in the capillary bed, destruction
•Low concentrations of contrast enter caused by high intramural pressure)
the coronary perfusion bed (5-10% of •Difficult to discern contrast from
cardiac output) myocardial tissue

How to Perform Myocardial Perfusion Imaging Consider that segments closer

to the transducer are destroyed
•Perform power Doppler imaging (high •Look at the replenishment of myocardi- more readily, and that this may
mechanical index). al contrast opacification as an indicator mimic a perfusion defect.
•Perform intermittent imaging (one of perfusion.
frame imaged every 1-8 cardiac cycles). •Perfusion defects appear as darker areas. Several studies have shown that
myocardial contrast echocar-
diography correlates well with
coronary flow reserve. It also
predicts recovery of systolic
function after reperfusion thera-
py. However, myocardial con-
trast echo is technically demand-
ing and involves a learning curve.

MYOCARDIAL PERFUSION IMAG-

ING – apical four-chamber view/
contrast

Intermittent ECG-triggered
imaging. Bubble destruction (left)
and replenishment with homoge-
nous contrasting of the myocar-
dium (right) in a healthy patient
without perfusion defects.

221

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 022 // CONTRAST ECHOCARDIOGRAPHY

NOTES MYOCARDIAL PERFUSION IMAGING

Myocardial Perfusion Imaging in Septal Ablation

Contrast injection into the coronary arteries may be used to study myocardial
perfusion. This is applied to define the target perfusion area during alcohol septal
ablation therapy in obstructive hypertrophic cardiomyopathy.

CONTRAST AND SEPTAL AB-

LATION – apical four-chamber
view/coronary contrast.

A contrast agent (Optison) is in-

jected into the first septal branch
of the LAD during an alcohol
septal ablation procedure, result-
ing in opacification of the basal
septum.

Contrast opacification

222

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 023 // 3D Echocardiography

CONTENT
224 Basics of Three-Dimensional Echocardiography

224 Forms of 3D Echocardiography

227 3D Image Acquisition

227 Clinical Applications of 3D Echocardiography

223

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 023 // 3D ECHOCARDIOGRAPHY

BASICS OF THREE-DIMENSIONAL
NOTES ECHOCARDIOGRAPHY

Despite advances in 3D What is 3D/4D Echocardiography?

technology, 2D image quality is
always better with a 2D transducer 3D echo permits 3-dimensional analysis and display
than with a 3D transducer. Never of ultrasound data. The term 4D echo is sometimes
base clinical decisions on 3D echo used to introduce time (moving 3D images) as the
assessment alone. “fourth dimension”.

How it is done

Data acquisition is achieved by imaging with 3D matrix array transducers.

El
th ev
mu at th
Azi io mu
n Azi

2D vs. 3D matrix array transducers

3D transducers acquire a pyramidal volume set using more than 3000
independent piezoelectric elements. The beams are formed to a large
extent within the transducer. The imaging frequency of transthoracic
3D transducers is between 2 and 4 MHz. In contrast, 2D transducers
only scan a two-dimensional sector.

FORMS OF 3D ECHOCARDIOGRAPHY

3D-dimensional image “pixels” Description Advantage Disadvantage

are known as voxels.
Real time Structures are Immediate results; Small sector or
(live) 3D displayed in 3D can be used for zoom mode, low
format while imaging. monitoring spatial and temporal
Acquisition of procedures; can resolution (frame
multiple pyramidal be used when RR rate), orientation
datasets per second. intervals vary (e.g. sometimes difficult.
atrial fibrillation).

Triggered A complete dataset is Higher temporal Post-processing

multi-beat required during and spatial required, time
(full volume) several heartbeats. resolution, more consuming,
3D possibilities of stitching artifacts.
acquisition quantification, Only works in sinus
analysis and rhythm.
display.

224

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 023 // 3D ECHOCARDIOGRAPHY

FORMS OF 3D ECHOCARDIOGRAPHY NOTES

3D Image Representation

Volume rendering Rendering algorithms that create the impression of

three-dimensionality on a 2D screen (ray casting, shear
warp etc.)

Surface rendering Surfaces are displayed as solid structures or wire frames (i.e.
cast of the ventricular cavity).

2D tomographic slices 3D dataset is sliced to reconstruct 2D cut planes (multipla-

ne)

Screen 3D rendering algorithms

Virtual
light “recode” the original ultrasound
source pixels/voxels to create a sense
of depth (distance shading,
gray-level gradient coding etc.).
View ray Shadow ray
Therefore we lose information
concerning the density of tissue
and tissue characteristics. In
other words, we cannot
distinguish fibrosis or
calcification from other less
echogenic tissue.

US structure

Principle of ray casting (volume rendering technique). Ray tracing is

an algorithm that simulates the effects of light as it would be seen by the
observer (eye) while it passes through a voxel space.

SURFACE AND VOLUME REN-

DERING – apical four-chamber
view/3D

Combination of left ventricular

surface and volume rendering
with segmental analysis (com-
parison of two regional volumes).
The curves in the right lower
quadrant represent the regional
volume curves during the cardiac
cycle. The bull’s eye shows the
selected segments (mid lateral
segment= green, mid septal seg-
ment= orange) in the left lower
quadrant.

225

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 023 // 3D ECHOCARDIOGRAPHY

NOTES FORMS OF 3D ECHOCARDIOGRAPHY

MULTIPLANAR REPRESENTATION
– apical views/3D

Simultaneous display of four-

(upper right), two- (upper left),
and three-chamber views (lower
left). The right lower corner
shows the corresponding cut
4 Ch view 2 Ch view
planes.

3 Ch view

3D color Doppler is still 3D Color Doppler

limited by rather low frame
rates and small color • Possible with live 3D and multi-beat • Permits better appreciation of flow
Doppler volumes. full volume acquisition convergence, vena contracta, and jet
• Still has limited spatial and temporal geometry
resolution • Color jets can also be displayed
• 3D color Doppler with TEE is given through reconstructed multi-slice cut
preference over TTE planes

3D COLOR DOPPLER – apical

full-volume acquisition/3D

The color jet is seen in various

cut planes, including a short-ax-
is view (left lower corner), and
additionally visualized in 3D (right
lower corner).

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3D IMAGE ACQUISITION NOTES

• Make sure you have a good • Select an adequate gain Cropping techniques (software
ECG signal (R-wave). (mid-range) threshold to discern algorithms) allow the operator to
• Aim for best possible 2D image true structures from noise. “cut away” structures that obscure
quality (trash in, trash out). • Choose the smallest necessary one’s view of the structure of
• Try to limit the number of beats in sector width to achieve the highest interest (i.e. cut away parts of the
order to reduce stitching artifacts. possible frame rate. left ventricle to view the mitral
• Check for stitching artifacts by • Use 2D images as a reference. valve or the septum).
viewing a cut plane perpendicular • For better orientation on the 3D image,
to the sweep plane. recapitulate cardiac anatomy and You can reconstruct in 3D only
• Acquire images during breath hold to topography. those structures that can also be
reduce motion and stitching artifacts. visualized in 2D.

THROMBUS IN THE RIGHT UPPER

PULMONARY VEIN – cropped
image/3D TEE

Patient after lung transplantation.

Cropped image techniques were
Pulmonary vein used to cut away the left atrium
and permit visualization of the
right upper pulmonary vein, in
which a highly mobile thrombus
is seen.

Thrombus

CLINICAL APPLICATIONS OF
3D ECHOCARDIOGRAPHY

APICAL THROMBUS –
apical multiplanar image acquisi-
tion/3D TTE
Thrombus
3D echocardiography showing a
highly mobile apical thrombus.

LV

LA

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 023 // 3D ECHOCARDIOGRAPHY

CLINICAL APPLICATIONS OF
NOTES 3D ECHOCARDIOGRAPHY

Live 3D – TEE imaging employs • Calculation of true volumes • Display structures (e.g. valves) in a more
higher frequencies (5- 7 MHz) (heart chambers) realistic format (volume rendering)
and has better spatial resolution • Calculation of myocardial mass • 3D display of color jets
than transthoracic 3D echo. It is • Display several cut planes simulta- (quantification of regurgitant lesions)
the method of choice to neously (multiplane) • Monitor interventional
monitor interventional • Reconstruction of imaging planes procedures on live 3D
procedures (e.g. MitraClip, that cannot be displayed with • 3D deformation imaging
ASD closure, left atrial conventional 2D echocardiography (strain, strain rate)
appendage occlusion).

LEFT ATRIAL APPENDAGE OC-

CLUDER – 3D TEE
Rim of the LAA LAA occluder
An Amplatzer Cardio Plug System
is deployed in the left atrial ap-
pendage.

Aortic valve

Mitral valve

Advanced Quantification Tools

3D speckle tracking Calculation and visualization of 3-dimensional

deformations

Heart chamber segmen- Semi-automated methods for endocardial border

tation algorithms detection (ventricles, atria)

Regional wall motion Allows calculation of regional ejection fraction and

analysis regional timing of contraction

Parametric display Color-coded display of various parameters, such as

wall motion, contraction timing, strain, etc.

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 023 // 3D ECHOCARDIOGRAPHY

CLINICAL APPLICATIONS OF
3D ECHOCARDIOGRAPHY NOTES
ENDOCARDIAL SURFACE REN-
DERING – apical full volume
acquisition/3D

Surface rendering is performed in

accordance with semi-automated
endocardial tracing on apical and
short-axis views. The resulting
volume (bag) is seen in the right
lower corner.

Calculation of Ejection Fraction and While the accuracy of

Volumes of the Left Ventricle semiautomated endocardial
border detection algorithms
• 3D volumes do not require geometric • Semi-automated edge detection has been greatly improved, it is
assumptions and are superior to all algorithms are usually employed to often still necessary to
other echocardiographic methods define endocardial borders manually correct the contours.
• 3D volume assessment can be • Foreshortening of the left ventricle
combined with contrast to enhance affects volume computations
endocardial border delineation • Exclude trabeculations when tracing
• 3D volume computation also allows the LV cavity
computation of “regional” ejection
fractions

Assessment of Dyssynchrony There is currently no

recommendation to select
• Regional volume curves are plotted • The systolic dyssynchrony index is a patients for cardiac
against time. These plots are used to measure of dyssynchrony. It is resynchronization therapy
determine the time difference bet- calculated as the standard deviation of based on 3D analysis of
ween the individual segments to regional ejection times (time to dyssynchrony.
minimal volumes (end-systole). The minimal regional volume).
degree of dispersion of timing • Dyssynchrony can also be visualized
correlates with the degree of dyssyn- by dynamic tracking of regional
chrony contraction on a bull’s eye display.

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CLINICAL APPLICATIONS OF
NOTES 3D ECHOCARDIOGRAPHY
TIMING OF CONTRACTION –
apical full-volume acquisition/3D

Timing of contraction in a normal

patient. All segments reach their
lowest volume (end systole) at
(almost) the same time.

Currently the major 3D Stress Echocardiography

limitation of 3D in stress
echo is its low frame rate. • Facilitates image acquisition by • Is limited by its low frame rate
multiplane imaging • Can be combined with contrast
• Better visualization of the apex

Assessment of Right Ventricular Function

• 3D volume computation of the right • Right ventricular volume and function
ventricle is superior to 2D methods computations with 3D have clinical
(complex morphology of the right impact (diagnosis and prognostic
ventricle). information) in many diseases (e.g.
• Semi-automated edge detection cardiomyopathy, atrial septal defect,
algorithms are applied to detect the tetralogy of Fallot, pulmonic regurgita-
endocardial border. tion).

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 023 // 3D ECHOCARDIOGRAPHY

CLINICAL APPLICATIONS OF
3D ECHOCARDIOGRAPHYS NOTES
3D RIGHT VENTRICULAR VOL-
UMES – apical RV full-volume
acquisition/3D

Regional volumes are divided into

outlet (yellow), inlet (green) and
apical (red) parts, which allows
regional volume computations
(curves in the right lower corner)

Mitral Valve Morphology in 3D Echocardiography The mitral valve is best

studied from a surgical view
• 3D valve assessment can be perfor- • May be useful in patients who have (en face view from the left
med with 3D- TTE and 3D-TEE undergone mitral valve replacement atrium).
• 3D TEE is superior to 3D TEE and repair (e.g. detection of paravalvu-
• Allows detection of structural defects lar leaks) While 3D imaging of the aortic,
and lesions (prolapse, flail, restriction, • Is used to select patients for the tricuspid, and pulmonic valves is
vegetations) MitraClip procedure and monitor them feasible and may sometimes
• May be combined with 3D color during the procedure provide relevant information,
Doppler • Allows the investigator to study the the 3D image quality of these
• Can define the exact location (leaflet motion and geometry of the mitral valves is usually inferior to that
scallop) of the defect valve apparatus of the mitral valve.

3D RECONSTRUCTION OF THE
MITRAL VALVE – apical full-vol-
ume acquisition/3D  

The mitral valve is viewed from

the left ventricle.

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 023 // 3D ECHOCARDIOGRAPHY

CLINICAL APPLICATIONS OF
NOTES 3D ECHOCARDIOGRAPHY
3D MITRAL VALVE PROLAPSE –
3D TEE Prolapse

Visualization of mitral valve

prolapse in the medial posterior
leaflet (P2) using 3D TEE.

Always try to get the aortic (Postero)medial P2

(Antero)medial
valve on the 3D image; it P3 A2
P1
permits you to determine the
A3 A1
orientation (medial or lateral)
of the mitral valve. CS

LAA
NC AV LC
Clockwise

RC
Counterclockwise

The anterior mitral leaflet is always adjacent to the aortic valve and is
quadrangular in shape. The posterior mitral leaflet is shorter, but arises
from a larger circumference than the anterior leaflet. The (postero-)me-
dial portion of the valve is always oriented clockwise to the aorta while
the (antero-)lateral portion is positioned counterclockwise from the
aorta. The left atrial appendage is always adjacent to the (antero-) lateral
commissure.

RECONSTRUCTION OF MITRAL
VALVE PROLAPSE –
3D reconstruction of a mitral
valve prolapse in the medial pos-
terior leaflet (P2).

This technique allows calculation

of mitral valve distances (com-
missural diameter), areas (leaflet
area), angles, and volumes (tent-
ing volumes).

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 023 // 3D ECHOCARDIOGRAPHY

CLINICAL APPLICATIONS OF
3D ECHOCARDIOGRAPHY NOTES

Further Clinical Applications of

3D Volume Rendering of Structures

• Endocarditic vegetations and • Complex congenital abnormities

complications • Intra-cardiac masses
• Pacemaker lead interference • Measurement of the aortic root/
with tricuspid valve closure annulus (e.g. TAVR evaluation)
• Atrial septal defects – quantification
of defect size

LEFT ATRIAL MASSES – 3D TEE

Mitral valve
masses Two large masses originating
from the left atrial appendage,
which extend towards the mitral
valve.

Future Perspectives

• Improvements in temporal and spatial • Refined analysis tools

resolution • Fusion imaging
• Smaller transducers/footprint • 3D strain

FUSION IMAGING – CT and 3D

echocardiography

Fusion of cardiac CT data (show-

ing coronary arteries) with a left
ventricular Beutel generated by
3D echo. The LV “Beutel“ shows
the area of latest contraction in a
color coded way (red is the area
of late contraction).

233

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 023 // 3D ECHOCARDIOGRAPHY

NOTES

234

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 024 // Myocardial Deformation Imaging

CONTENT
236 Principles of Myocardial Mechanics

236 Measures of Myocardial Deformation

238 Tissue Doppler Imaging

241 Speckle Tracking Echocardiography

247 Clinical Applications of Myocardial Deforming Imaging

235

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 024 // MYOCARDIAL DEFORMATION IMAGING

NOTES PRINCIPLES OF MYOCARDIAL MECHANICS

• The orientation of myocardial fibers in the

l
n tia left ventricular wall ensures equal distribution
re
fe of regional stress and strains.
um
rc
Ci • The left ventricle undergoes a twisting
motion, which decreases the radial, circum-
ferential and longitudinal length of the left
ventricular cavity.
l • During isovolumetric contraction, the apex
Radial na
i
it ud initially performs clockwise rotation.
g
L on • During the ejection phase the apex then
rotates counterclockwise while the base
rotates clockwise when viewed from the
apex.
• In diastole, relaxation of myocardial fibers
and subsequent recoiling (clockwise apical
rotation) contributes to active suction.

MEASURES OF MYOCARDIAL DEFORMATION

Displacement

• Displacement is the distance the • Displacement is measured as a

myocardium (or any cardiac structure) distance and therefore expressed in
travels between two consecutive centimeters.
image frames.

Tissue Velocity

• The speed (displacement per unit of • Tissue velocity is reported in cm/s

time) of movement of a myocardium
(or any cardiac structure)

Strain and Strain Rate

• Strain is defined as the fractional • Strain values can be obtained for each
change in the length of a myocardial segment (segmental strain), as an
segment. average value for all segments (global
• Three perpendicular axes (i.e. longitu- strain), or for each of the theoretical
dinal, circumferential, and radial) vascular distribution areas (territorial
represent different directions of left strain).
ventricular myocardial contraction. • Strain rate is the rate of change in
Strain is not expressed in units; it is strain and is usually expressed as 1/
usually expressed as a percentage. second.

236

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 024 // MYOCARDIAL DEFORMATION IMAGING

MEASURES OF MYOCARDIAL DEFORMATION NOTES

Strain represents
the change in fiber
V1 length compared to
its original length
(right side, yellow
L0 L arrow), whereas
strain rate is the
difference in tissue
d velocities at two
distinct points in
relation to their
distance (left side,
purple arrows).
V2 L

(L - L0) L (V1 - V2)

Strain = = Strain rate(ST) =
L0 L0 d

Rotation Basal rotation changes from

counterclockwise in infancy to
• Rotation is defined as angular displa- • It reflects rotational displacement; clockwise in adults.
cement of a myocardial segment on a myocardial rotation is expressed in
short-axis view around the LV longitu- degrees.
dinal axis, measured in a single plane. • The base and the apex of the ventricle
rotate in opposite directions.
5°
Rotation

Basal rotation
0°

-5°

Aplical rotation
-10°
Basal and apical myocardial rota-
tion in a healthy patient. The basal
-15° segment rotates clockwise, whereas
the apical parts rotate more and more
-20° counterclockwise.

Twist/Torsion The twist angle increases

significantly with age.
• It is defined as the net difference • The normal peak LV twist
between apical and basal rotation angle is approximately 7.7°
and is expressed in degrees. (Takeuchi et al. JASE 2006).
• It is calculated from two short-axis • The torsional gradient (degree/cm)
cross-sectional planes of the left is defined as the twist/torsion
ventricle. normalized to ventricular length
from base to apex, and accounts
for the fact that a longer ventricle
has a larger twist angle.

237

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 024 // MYOCARDIAL DEFORMATION IMAGING

NOTES MEASURES OF MYOCARDIAL DEFORMATION

Rotation of the Left Ventricular Apex and Base

During the Heart Cycle

Apical segment Apical segment

Rotation

Length Length
(diastole) (systole)

Rotation
Basal segment

Basal segment

Diastole Systole

TISSUE DOPPLER IMAGING

• Tissue Doppler velocity estimation of • A wall filter is used to distinguish

myocardial motion employs the between signals from tissue and
same principle as pulsed-wave and blood flow.
It is contrary to conventional color Doppler echocardiography for • Strain and strain rate can be
(blood flow encoding) blood flow. calculated.
Doppler. TDI focuses on lower
velocity frequency shifts.

TISSUE VELOCITY TRACINGS –

apical four-chamber view/TDI S'

Color tissue Doppler imaging of

a normal patient with velocity
tracings of the basal septal and
basal lateral segments

Sample volume

A´

E´

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 024 // MYOCARDIAL DEFORMATION IMAGING

TISSUE DOPPLER IMAGING NOTES

Tissue Doppler Image Acquisition Use the sector tilt function on

your scanner; it permits better
Spectral Doppler alignment of the tissue Doppler
• Place the sample volume in the region • Reduce the gain. sample volume with the
of interest of the myocardium. Make • Align the beam to the direction of the direction of myocardial motion.
sure that the sample volume is inside interrogated motion.
the myocardium throughout the • On apical views, tissue velocity
cardiac cycle. measurements are performed at the
• Adapt your sweep speed (slow annulus and the basal end of the basal
sweep speed for the assessment and mid levels of the different walls.
of peak values in several beats and
high sweep speed for measuring
slopes in a few beats).

Color Doppler
• High frame rates are needed • Avoid reverberation artefacts.
(> 100 frames/sec). • Record at least 3 beats.
• Reduce depth and sector width (of
both gray scale and Doppler sector)
to improve frame rates.

TISSUE DOPPLER MMODE –

PSAX/TDI & MMode

MMode for a parasternal

short-axis view at the papillary
muscle level, combined with
tissue Doppler imaging. This
form of display can be used to
accurately time the start of volu-
metric contraction and relaxation
(arrows).

Contraction Relaxation

239

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 024 // MYOCARDIAL DEFORMATION IMAGING

NOTES TISSUE DOPPLER IMAGING

With the advance of Clinical Applications of Tissue Doppler Imaging

speckle tracking, TDI has
Clinical Setting Measure
lost much of its appeal. It is
only used for few
indications. Diastolic function Spectral TDI at the mitral valve annulus (medial + lateral)
for the assessment of filling pressures (E/E’)

Right ventricular Spectral TDI on the lateral side of the tricuspid valve
function annulus for the assessment of basal right ventricular
function (S’)
Global longitudinal
contractile function can also Constriction vs. Spectral TDI at the mitral valve annulus shows a large E’
be assessed with the Restriction in constriction (> 8cm/s) vs. a small E’ in restriction
conventional MMode, by (usually below 3cm/s)
measuring the excursion of
the mitral annular plane Dyssynchrony Spectral and color Doppler TDI help to quantify and
during systole (MAPSE). visualize dyssynchronous motion between various
segments

CURVED MMODE – apical Apex

four-chamber view/curved
MMode & TDI

Curved M-mode is a color dis- Contraction

play format in which functional
information (such as velocities,
strain, strain rate) concerning
different segments of the heart
(such as the 4-chamber view) are
displayed along an M-mode line,
which follows the myocardial Relaxation
walls. The M-mode line „curves“
around the myocardium. Starting
at the basal inferior segment, it
moves to the apex and back to
the basal lateral wall. The func-
Base
tional information is color coded.

Modified image views Limitations of Tissue Doppler Imaging

should be used whenever
necessary to achieve the • Tissue Doppler velocities may be • The position of the baseline is
optimal imaging angle. influenced by global heart automatically defined as the value at
motion or by the movement of the beginning of the QRS complex
adjacent structures. and might therefore be incorrect
• Imaging artifacts may interfere under certain conditions (e.g. bundle
significantly with TDI accuracy. branch block, suboptimal ECG, atrial
fibrillation).
• Tissue Doppler is angle dependent.

240

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SPECKLE TRACKING ECHOCARDIOGRAPHY NOTES

• Speckles on the 2D image are stable • Speckle tracking is an offline technique Subendocardial function is
and have unique myocardial features. applied to recorded 2D images. largely regulated by longitudinal
• Speckles result from interference due • Different components of contraction contraction, and may be
to the backscatter of the ultrasound (longitudinal, circumferential and radial impaired before the
wave from structures smaller than the motion) can be studied separately. circumferential or radial
length of the wave. • Peak systolic strain is generally used to component deteriorates. Thus,
• Speckles can be tracked from frame to quantify contractility. It is defined as longitudinal function serves as
frame and provide information about the maximal shortening (at any region an early marker of left
local displacement, from which of the myocardium) during systole. ventricular dysfunction.
parameters of myocardial function
(e.g. strain, strain rate) can be derived.

ILLUSTRATION OF MYOCARDIAL
SPECKLES – apical four-chamber
view/2D

Speckle tracking imaging mon-

itors the local displacement of
myocardial speckles and uses
the obtained information to
derive parameters of myocardial
function.

2D Image Acquisition for Speckle Tracking Make sure you have a good ECG
Echocardiography signal. Avoid ectopic beats.

• Longitudinal strain is calculated from • Adjust sector depth and width to

apical views and circumferential strain include as little as possible of the areas
from short-axis views. outside the region of interest.
• Frame rates around 80 frames/sec are • Avoid artifacts (any artifact that looks
advised. Low frame rates result in the like a speckle pattern will influence
loss of speckles, whereas high frame the quality).
rates reduce spatial resolution and • Avoid apical foreshortening
image quality. (apical views) and oval images
• Position the focus point at an (short-axis views).
intermediate depth.

241

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 024 // MYOCARDIAL DEFORMATION IMAGING

NOTES SPECKLE TRACKING ECHOCARDIOGRAPHY

When aortic valve closure cannot Analysis of Speckle Tracking Images

be seen accurately, use a Doppler
signal (PW or CW) of the left • Assessment of speckle tracking strain • Define end systole (aortic valve
ventricular outflow to determine is a semiautomatic method, but closure as seen on the apical
aortic valve closure. requires manual definition of the long-axis view).
endocardial border of the • Speckle tracking strain can be
For strain representation on a myocardium. obtained for both ventricles and the
bull’s eye display, you need to • The region of interest should cover atria.
assess all apical views. All acquired most of the myocardial wall thick- • Strain can be obtained for each
views should have approximately ness. The pericardium should be individual segment (segmental strain)
the same cycle length. This may avoided. by averaging all segments (global
be a problem even in normal • Adjust the region of interest strain), or for each of the theoretical
(usually young) individuals who manually until optimal tracking is vascular distribution areas (territorial
have sinus arrhythmia. accomplished. strain).
• Segmental strain is typically shown in
a bull’s eye representation.

BULL’S EYE REPRESENTATION –

apical views/2D STE

Bull’s eye representation of seg-

mental peak systolic longitudinal
strain in a patient with anterior
myocardial infarction. Longitu-
dinal contraction is significantly
impaired in the apical region, the
anterior wall and the anterior
septum, with preserved longitu-
dinal contraction in the remain-
ing segments. The global average
longitudinal strain is reduced
(-10%).

Advantages of Speckle Tracking Echocardiography

over Tissue Doppler

• STE is angle independent • Easy to perform

• Only reflects active contraction (no • All components of myocardial
tethering effects) deformation can be assessed
• More robust and less influenced by
frame rate

Strain and strain rate are Limitations of Speckle Tracking Echocardiography

not load independent.
• Low image quality, imaging artifacts (e.g. acoustic shadowing, reverberations)
and suboptimal tracking of the endocardial border may lead to underestima-
tion of myocardial deformation.

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SPECKLE TRACKING ECHOCARDIOGRAPHY NOTES

Three-Dimensional Speckle Tracking Be sure to include the entire

Echocardiography LV cavity in the pyramidal
3D full-volume, and always
• Speckles can be tracked irrespective of consecutive cardiac cycles during optimize the automatically
their direction. breath hold. detected myocardial borders
• 3D STE results correlate well with • Information about left ventricular manually.
strain values derived from MRI motion (e.g. displacement, rotation)
• Relatively low temporal and spatial and deformation (e.g. longitudinal/ 3D strain is still in its infancy. Its
resolution. circumferential/radial strain) is calcula- major limitations are low frame
• 3D STE can be assessed in apical 3D ted automatically. rates, stitching artifacts, and
full-volume samples acquired over vendor dependency.

3D TIME TO PEAK
CONTRACTION –
Full-volume acquisition/3D

3D full-volume acquisition may

be used to assess peak longi-
tudinal function as well as the
timing of contraction. The time
to peak contraction is shown in
this patient.

Directions of Contraction using Speckle Tracking

Echocardiography

Longitudinal Radial Circumferential

Three perpendicular axis (i.e. longitudinal, circumferential, and radial)

represent the main directions of left ventricular myocardial contraction.

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NOTES SPECKLE TRACKING ECHOCARDIOGRAPHY

Longitudinal Strain

GLOBAL LEFT VENTRICULAR 4ch view 2ch view

LONGITUDINAL STRAIN – apical
views/2D STE

Global left ventricular longitu-

dinal strain is calculated using
two-, three-, and four-chamber
views. Bull’s eye representa-
tion (lower right corner) shows
normal longitudinal contraction,
indicated in red.
3ch view Bullseye

As a simplified approach, just Reference Values of Left Ventricular Longitudinal Systolic Strain
remember that normal
longitudinal systolic strains are
All levels Apical Mid Basal
usually ≥ 18%.

The assessment of longitudinal All walls −18.6 ± 5.1 −20.2 ± 5.6 −18.7 ± 3.8 −17.0 ± 5.2
strain is more robust than radial
and circumferential strain. Anterior −19.5 ± 4.2 −19.4 ± 5.4 −18.8 ± 3.4 −20.1 ± 4.0
Currently it has the greatest
impact on clinical Anteroseptal −18.8 ± 4.2 −18.8 ± 5.9 −19.4 ± 3.2 −18.3 ± 3.5
echocardiography.
Inferior −20.0 ± 4.5 −22.5 ± 4.5 −20.4 ± 3.5 −17.1 ± 3.9
Longitudinal strain is usually
higher in the apical region than Lateral −18.3 ± 4.7 −19.2 ± 5.4 −18.1 ± 3.5 −17.8 ± 5.0
in the basal region (apical to
basal gradient), and higher in Posterior −16.3 ± 6.3 −17.7 ± 6.0 −16.8 ± 5.0 −14.6 ± 7.4
subendocardial layers.
Septal −18.3 ± 5.3 −22.3 ± 4.8 −18.7 ± 3.0 −13.7 ± 4.0
Some propose that
quantification of subendocardial
longitudinal strain should be the Marwick et al. JACC Cardiovasc Imaging 2009
preferred method to study
subclinical dysfunction.

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SPECKLE TRACKING ECHOCARDIOGRAPHY NOTES

SUBENDOCARDIAL TRACKING –
apical four-chamber view/STE

Selective quantification of
longitudinal strain of the
subendocardial (inner) layers
of the myocardium.

Subendocardial layer

Circumferential Strain

CIRCUMFERENTIAL STRAIN –
PSAX apical/2D STE

Circumferential strain of the

apical part of the left ventricle in
a normal patient. Peak systolic
segmental circumferential strain
values are shown in the lower
left corner.

Reference Values of Left Ventricular Systolic Circumferential strain is usually

Circumferential Strain higher in apical and mid-
ventricular segments compared
Segment Mean peak systolic
to the left ventricular base.
circumferential strain (%)

Anterior -24±6

Lateral -22±7

Posterior -21±7

Inferior -22±6

Septal -24±6

Anteroseptal -26±11

Reference: Hulburt et al. Echocardiography 2007

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NOTES SPECKLE TRACKING ECHOCARDIOGRAPHY

Radial Strain

RADIAL STRAIN –
PSAX mid-ventricle/2D STE

Radial strain of the apical part of

the left ventricle in a normal pa-
tient. Peak segmental radial strain
values are shown in the lower left
corner.

Radial strain is higher in the Reference Values of Left Ventricular

subendocardium compared Systolic Radial Strain
to the subepicardium.

Segment Mean peak systolic

radial strain (%)

Anterior 39±16

Lateral 37±18

Posterior 37±17

Inferior 37±17

Septal 37±19

Anteroseptal 39±15

Hulburt et al. Echocardiography 2007

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CLINICAL APPLICATIONS OF
MYOCARDIAL DEFORMATION IMAGING NOTES

Myocardial Deformation in the Assessment The use of right ventricular

of Right Ventricular Function strain has not been fully
validated for clinical practice.
Principles
• Normal right ventricular contraction is • Right ventricular longitudinal strain and
a peristaltic wave directed from the strain rate correlate well with radio-
inflow tract to the infundibulum. nuclide right ventricular function.
• Longitudinal shortening is the key • A right ventricular longitudinal strain ≥
component in overall right ventricular 25% or a right ventricular longitudinal
performance, with equal contributions strain rate ≥ -4 sec-1 indicates normal
of the free RV wall and the right ventricular function.
interventricular septum.

RIGHT VENTRICULAR LONGI-

TUDINAL STRAIN – optimized
four-chamber view/2D STE

Longitudinal strain of the right

ventricle in a normal patient with
a mean longitudinal strain of
-24.8%. Peak systolic longitudinal
strain values are shown in the
lower left corner.

2D Image Acquisition for Speckle-Tracking of the Right Ventricle

• Use an apical four-chamber view optimized for the right ventricle.

RV STRAIN IN PULMONARY
HYPERTENSION - optimized
four-chamber view/2D STE

Reduced right ventricular lon-

gitudinal strain in a patient with
severely reduced right ven-
tricular function due to severe
pulmonary hypertension. Peak
systolic longitudinal strain val-
ues are shown in the lower left
corner; the mean longitudinal
strain is -7.2%.

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CLINICAL APPLICATIONS OF
NOTES MYOCARDIAL DEFORMATION IMAGING

Myocardial Deformation Imaging in

Various Clinical Settings

An increasing body of data Aortic Stenosis

shows that deterioration of • Decreased longitudinal strain • Global longitudinal strain correlates
longitudinal strain is an early (especially in the basal regions) and with the severity of aortic stenosis and
marker of left ventricular increased circumferential strain exercise tolerance
dysfunction, and that it could • Reduced left ventricular twist • Impairment in longitudinal contraction
be an important parameter for is partly reversible after aortic valve
the timing of valve surgery (such replacement
as surgery for aortic stenosis).

AORTIC STENOSIS – apical

views/2D STE

Bull’s eye presentation of seg-

mental longitudinal strain in a
patient with severe asymptom-
atic aortic stenosis and normal
systolic left ventricular function
(ejection fraction > 60%). Global
longitudinal systolic function is
significantly reduced, especially
in the basal segments.

Aortic Regurgitation
• Reduction in longitudinal and radial strain and strain rate
• Reduction improves after aortic valve replacement

Mitral Regurgitation
• Early left ventricular dysfunction is • Reduction of longitudinal, circumfe-
characterized by a reduction of global rential and radial strain rate
longitudinal strain • Delayed untwisting motion of the left
ventricle

Use speckle tracking if you are Coronary Artery Disease

uncertain about the presence • Longitudinal strain is compromised at after aortic valve closure is a common
of wall motion abnormalities. an early stage in coronary artery finding in acute ischemia
In some cases it might even be disease • Residual longitudinal strain in akinetic
superior to the naked eye. • Simplifies the detection of regional wall or severely hypokinetic regions
motion abnormalities indicates sustained viability
• Pronounced post-systolic shortening

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CLINICAL APPLICATIONS OF
MYOCARDIAL DEFORMATION IMAGING NOTES

Hypertrophic Cardiomyopathy In hypertrophic

• Longitudinal function is reduced, • Regional heterogeneity (typically basal cardiomyopathy, longitudinal
whereas circumferential and radial and mid septal longitudinal strains most strain is most severely reduced
function is elevated affected) in areas of pronounced wall
• Often paradoxical systolic lengthening thickness and fibrosis.
detectable

APICAL HYPERTROPHIC
CARDIOMYOPATHY – apical
views/2D STE

Typical strain pattern in a patient

with apical hypertrophic cardio-
myopathy. Strain is reduced at
the apex in the region of hyper-
trophy.

Dilated Cardiomyopathy
• Reduced strain in all directions
• Reduced left ventricular twist/torsion

Restrictive Cardiomyopathy
• Reduced longitudinal strain, but preserved circumferential strain
• Preserved left ventricular twist/torsion

AMYLOIDOSIS – apical views/

2D STE

Typical longitudinal strain pattern

in a patient with amyloidosis.
Longitudinal strain is preserved
at the apex and severely reduced
in (most of) the mid and basal
segments.

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CLINICAL APPLICATIONS OF
NOTES MYOCARDIAL DEFORMATION IMAGING

Constrictive Pericarditis
• Preserved longitudinal function but reduced circumferential strain
• Reduced left ventricular twist/torsion

Dyssynchrony
• Allows quantification of dyssynchrony and has the potential to optimize
cardiac resynchronization therapy (CRT)

Left Atrial Deformation

• Correlates with the recurrence of atrial fibrillation after radiofrequency catheter
ablation

Patients with hypertensive Hypertensive Heart Disease

heart disease and left • Reduced basal longitudinal strain
ventricular function • Reduced strain, especially of the basal anterior septum
frequently show reduced
longitudinal function despite
a normal ejection fraction.

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NOTES

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