Echo Factsheets - 2nd Ed - 3

Echo
Factsheets
Companion Syllabus to the
Masterclass Lectures
T. Binder / G. Goliasch / F. Wiesbauer

Echo Factsheets, 2nd Edition
A few words from the Authors
This is not a textbook, it doesn’t even provide echo images. It‘s simply a
learning aid for everyone who wants to browse through the essentials of
echocardiography and make the facts stick.
Most of all, it is the companion syllabus to our 123sonography Masterclass.

Our Masterclass is an innovative video-based course, which teaches basic
and more advanced echocardiography on the internet. You will also find
the content of this book available for download there. In general, this book
follows the content of the 20 lectures. But it also provides more in-depth
information and should be seen as a reference guide for measurements,
facts and imaging views that are important in echocardiography.
Instead of using too much text or a dull checklist format, we put the echo
facts and graphics into tables and decorated them with images that will
help you remember the facts. Do some of these images look familiar?
Well, we also used them in our Masterclass presentations. After all, we
want to help you to remember what you have learned there. :-)
The positive feedback we got so far inspired us to make this book even
more practical. We threw out what was too much and added what we
think is essential. The result is this 2nd edition.
We hope this booklet will make a difference when you learn echocardio-
graphy and will improve your echo learning experience.
Don’t forget to visit us at:
123sonography.com
Tommy Binder and the 123sonography Team

July 2012, Vienna, Austria
Table of Contents
Chapter 1: Principles of Echocardiography
Chapter 2: How to Image
Chapter 3: Heart Chambers and walls
Chapter 4: Diastolic Function
Chapter 5: Dilated Cardiomyopathy
Chapter 6: Hypertrophic Cardiomyopathy
Chapter 7: Restrictive Cardiomyopathy
Chapter 8: Coronary Artery Disease
Chapter 9: Aortic Stenosis
Chapter 10: Aortic Regurgitation
Chapter 11: Mitral Stenosis
Chapter 12: Mitral Regurgitation
Chapter 13: Tricuspid Valve

Upgrade to the Masterclass and get all 20 chapters in
our comprehensive paper Workbook
Chapter 14: Prosthetic Valves
Chapter 15: Endocarditis
Chapter 16: Right Heart Disease
Chapter 17: Aortic Disease
Chapter 18: Pericardial Disease
Chapter 19: Tumors and Masses
Chapter 20: Congenital Heart Disease

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
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.
10
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
11
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.
12
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
13
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
14
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
15
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.
16
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)
17
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
18
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
NOTES
20
002 // How to Image
CONTENTS
22 How to Move the Transducer
22 Imaging Windows
22 Image View
28 Abbreviations
21
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
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
23
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
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
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
ry
lic
te
ro
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).
26
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
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
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

29
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
30
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
31
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
32
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
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
34
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
35
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
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
37
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

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
38
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.
39
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

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
40
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
41
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
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
NOTES
44
004 // Diastolic Function
CONTENTS
46 Basics of Diastolic Dysfunction
51 Specific Situations
45
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
46
BASICS OF DIASTOLIC DYSFUNCTION NOTES
Mitral Inflow Signal PW Doppler sample volume

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

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
47
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
48
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
49
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
PAS < 30 mmHg PAS > 35 mmHg
Normal LAP Normal LAP Elevated LAP Elevated LAP
Algorithm for the estimation of filling pressures in patients with

normal 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 estimating filling pressures in patients with

reduced left ventricular function (EF <55%) according
to the ASE/EAE guidelines (2009)
50
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
51
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
005 // Dilated Cardiomyopathy
CONTENTS
54 Background
54 Echo Features
55 Specific Forms
53
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
54
ECHO FEATURES NOTES

ECHOFEATURES OF DILATED
CARDIOMYOPATHY –
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
55
NOTES SPECIFIC FORMS
Abortive forms of Takot- Taktsubo 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
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
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.
57
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
58
006 //
Hypertrophic Cardiomyopathy
CONTENTS
60 Basics
61 Echocardiographic Evaluation
59
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 HYPERTROPHIC
CARDIOMYOPATHY –apical
four-chamber view/Color
Doppler Mid-ventricular
turbulences
Turbulent flow in the LVOT
caused by systolic anterior mo-
tion of the MV. Distortion of the
MV leads to regurgitation with
a posteriorly directed jet. Flow
PMVL
acceleration is also present in the
Posterior Turbulent flow LVOT
mid-ventricular portion (addi-
tional mid-ventricular obstruc-
MR jet
tion).
60
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
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
61
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
62
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. hypothyroi-
afterload or increase in contractility dism, 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.
63
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
007 //
Restrictive Cardiomyopathy
CONTENTS
66 Basics
67 Specific Forms
65
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´
66
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
67
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
68
008 // Coronary Artery Disease
CONTENTS
70 Segmental Approach
72 Wall Motion Abnormalities
76 Patterns of Myocardial Infarction
77 Complications
69
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
70
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)
71
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
72
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).
73
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

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
74
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)
75
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
76
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
77
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)
78
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 –

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.
79
NOTES COMPLICATIONS
APICAL THROMBUS – zoomed
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)
80
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

81
009 // AORTIC STENOSIS
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
82
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.
83
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
84
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 Vmax 2
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 cm2
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
85
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
86
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.
87
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 cm2 • 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)
88
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
89
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.
90
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
91
NOTES
92
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

93
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
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.
95
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.
96
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= d x 0.785
2
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
Effective regurgitant orifice (cm2) < 0.1 0.1 – 0.29 ≥ 0.3
Regurgitant volume (ml) < 30 30 – 59 ≥ 60
ESC 2013
97
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
98
011 // Mitral Stenosis
CONTENTS
100 Introduction
102 Quantification
103 Mitral Valve Pressure Half-Time
104 Valvuloplasty
99
011 // MITRAL STENOSIS
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)
100
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
101
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
102
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)
103
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 cm2 ( 1.8 cm2 in > 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
104
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
105
NOTES
106
012 // Mitral Regurgitation
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
107
012 // MITRAL REGURGITATION
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
108
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.
109
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).
110
QUANTIFICATION OF MITRAL REGURGITATION NOTES
Reference Values for Parameters of Mitral Regurgitation
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?)
111
NOTES MECHANISMS OF MITRAL REGURGITATION
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)
112
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 Anterior 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
113

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
114
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

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
115
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
116
FLAIL LEAFLET NOTES
Etiology of the Flail Leaflet

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

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
117
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
118
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 cm2 • MVA > 3cm2, good mobility of leaflets, 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.
119
NOTES
120
013 // Tricuspid Valve Disease
CONTENTS
122 Basics
122 Causes of Tricuspid Regurgitation
124 Quantification of Tricuspid Regurgitation
125 Tricuspid Stenosis

121
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
122
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 –
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
123
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
124
QUANTIFICATION OF
TRICUSPID REGURGITATION NOTES
DIASTOLE
FEATURES OF SEVERE TR –
Enlarged RV PSAX/2D
D-shaped ventricle with a

S
ned IV 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
125
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.
126
014 // Prosthetic Valves
CONTENTS
128 Types of Valves
129 Echo Assessment of Prosthetic Valves
133 Complications
137 Mitral Valve Repair

127
Alles_EchoFacts_140821_KD.indd 127 28.08.14 21:13

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
128

ECHO ASSESSMENT OF PROSTHETIC VALVES NOTES

BIOLOGICAL MITRAL VALVE –
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”.
129

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
130

ECHO ASSESSMENT OF PROSTHETIC VALVES NOTES

MECHANICAL MITRAL VALVE –
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
131

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
132

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.
133

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)
134

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
135

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)
136

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 –

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)
137

NOTES
138

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

139
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.
140
015 // ENDOCARDITIS
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.
141
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
142
015 // ENDOCARDITIS
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.
143
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
144
015 // ENDOCARDITIS
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.
145
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
146
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-
Inf. Sup
tion attached to the catheter
vena cava
Mobile (thickened tip) on transthoracic
structure echo (left) and the adjacent wall
he ter (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
147
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
148
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

149
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
150
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
variables suggestive of PH
PH likely Tricuspid regurgitation I B

velocity > 3.4 m/s, sPAP > 50
mmHg, with/without
variables suggestive of PH
Additional echo variables suggestive of pulmonary

hypertension = IVS flattening, short PVAT, PA- dilatation
ESC 2009
151
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)
152
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
153
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
154
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 (Ttssue all patients with inferior
right ventricular function Doppler) and decreased longitudinal infarcts.
• Low cardiac output strain (speckle-tracking)
• Dilated inferior vena cava
155
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
156
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
157
NOTES
158
017 // Aortic Disease
CONTENTS
160 Imaging of the Aorta
161 Basics
161 Aortic Aneuryms
164 Aortic Dissection
167 Aortic Coarctation (CoA)

159

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
160

BASICS NOTES
VISUALIZATION OF
THE ASCENDING AORTA –
modified PLAX/2D
The more cranial portions of the

a
aort ascending aorta can be better vi-
ing 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
161

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.
162

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
163

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.
164

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
165

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)
166

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.
167


AORTIC COARCTATION – ry
rte
suprasternal view/Color ca
ali ery
and CW Doppler ce
ph art
hio tid
ac aro
Br onc
Turbulent flow in the descending m
CW sample volume om ery
aorta (left) denotes the location ft c art
Le via
n
of coarctation. The Doppler cla
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
168

018 // Pericardial Disease
CONTENTS
170 The Pericardium
170 Pericardial Effusion
173 Pericardial Tamponade
175 Pericardial Constriction
176 Other Diseases of the Pericardium

169

018 // PERICARDIAL DISEASE
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.
170

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 effusi
on
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)
171

NOTES PERICARDIAL EFFUSION

EPICARDIAL FAT – subcostal
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.
172

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.
173

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
174

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
175

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
176

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
177

NOTES
178

019 // Tumors and Masses
CONTENTS
180 Pseudotumours
181 Masses
179

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

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
ovalis is typically spared, resulting se un
in a ”dumbbell”.
cu
n sec
du m va
m tu ca
ep a
S en
rv
rio
pe
Lipomatous Su
interatrial
septum
Right atrium
180

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 –
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.
181

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
182

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
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
183

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
184

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
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.
185

NOTES
186

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

187
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.
188
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
189
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 = (PA 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
190
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

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
191
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
192
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
193
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.
194
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.
195
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%)
196
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).
197
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
198
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
199
NOTES
200

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Echo

T. Binder / G. Goliasch / F. Wiesbauer

A few words from the Authors

Most of all, it is the companion syllabus to our 123sonography Masterclass.

Don’t forget to visit us at:

Tommy Binder and the 123sonography Team

Chapter 1: Principles of Echocardiography

Chapter 2: How to Image

Chapter 3: Heart Chambers and walls

Chapter 4: Diastolic Function

Chapter 5: Dilated Cardiomyopathy

Chapter 6: Hypertrophic Cardiomyopathy

Chapter 7: Restrictive Cardiomyopathy

Chapter 8: Coronary Artery Disease

Chapter 9: Aortic Stenosis

Chapter 10: Aortic Regurgitation

Chapter 11: Mitral Stenosis

Chapter 12: Mitral Regurgitation

Chapter 13: Tricuspid Valve

Chapter 14: Prosthetic Valves

Chapter 15: Endocarditis

Chapter 16: Right Heart Disease

Chapter 17: Aortic Disease

Chapter 18: Pericardial Disease

Chapter 19: Tumors and Masses

Chapter 20: Congenital Heart Disease

NOTES PHYSICS OF ULTRASOUND

The higher the ultrasound Ultrasound Wave

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

Frequencies between 2 – 10 MHz are used.

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

Diagnostic ultrasound Safety of Ultrasound

The higher the pulse Ultrasound Pulse

Pulse Pulse repetition period

2D Image Ultrasound is a cut-plane

Types of Probes In echocardiography we use

Image quality increases with

What determines overall resolution?

• Spatial resolution – lateral • Contrast resolution

Determinants of Spatial Resolution

Lateral resolution Axial resolution

Beam width/line density Ultrasound frequency

Ultrasound frequency Pulse repitition frequency

Harmonic imaging Harmonic Imaging

Aim for high frame Frame Rate – Influence

• Attenuation • Limited penetration (obesity, narrow

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

Attenuation may be caused by:

Types of Artefacts Imaging is difficult in patients

Highly echogenic pericardium

Side lobes Reverberation

Beam width artefact

Beam width artefacts occur

Different gain settings in the

Artefacts are When Do Artefacts Occur?

ARTEFACT IN PROSTHETIC VALVE

Shadowing and reverberations of

Tips to Avoid Artefacts

• Know the pitfalls • Be cautious of strong reflections

OPTIMIZING THE 2D IMAGE NOTES

Post-Processing Use predefined settings for

COLOR MAPS – PSAX/2D

Different 2D color maps for