Echo_Factsheets_-_Companion_Syllabus_to_the_Masterclass_Lectures_2Nd_Edition.pdf

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

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
Echo Factsheets, 2nd Edition

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

NOTES
001 // PRINCIPLES OF ECHOCARDIOGRAPHY
10
Ultrasound Wave
PHYSICS OF ULTRASOUND
Pulse Pulse repetition period
Wave propagation occurs through
compression and decompression of
tissue.
Alternating current applied to piezoelec-
tric crystals generates ultrasound waves..
Safety of Ultrasound
Physical effects of ultrasound:
• Thermal effect (depends on US intensity)
• Cavitations
The higher the US frequency, the higher the pulse repetition frequency.
Received ultrasound waves (echoes)
cause the piezoelectric crystals to
generate an electric signal which is
transformed into an image..
The velocity of ultrasound is 1540 m/s in
tissue and 1570 m/s in blood.
Medical Ultrasound
Frequencies between 2 – 10 MHz are used.
Ultrasound Pulse
SEND RECEIVE
The higher the ultrasound
frequency, the better the
resolution. However, you lose
penetration.
Diagnostic ultrasound
has no adverse effects.
The higher the pulse
repetition frequency, the
higher the frame rate and
image resolution.

11
NOTES
2D IMAGE
2D Image
Types of Probes
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
Ultrasound is a cut-plane
technique. Several elements
are used to generate a 2D
image.
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.

12
NOTES
”
Harmonic Imaging
SEND RECEIVE
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.
Frame Rate – Influence
The frame rate describes the number of frames/sec that are displayed.
Frame rate depends on:
• Sector width • Frequency
• Scan lines • Depth
Limitations of 2D Imaging
• Attenuation
• Tissue properties (fibrosis, calcification)
• Artefacts
• Limited penetration (obesity, narrow
imaging window)
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.
Harmonic imaging
uses the resonance
characteristics of
tissue. The advantage
is less artefacts,
improved spatial and
contrast resolution,
leading to better
image quality.
Aim for high frame
rates. They allow the
study of rapid motion
when using the image
review function.
2D IMAGE

13
NOTES
Side lobes usually occur at strong
reflectors (e.g. prosthetic material). Power
density is higher in the central beam than
in side lobes. This may lead to the edge
effect, which makes structures appear
wider than they actually are.
Imaging is difficult in patients
with small intercostal spaces
(bone) and in patients
with COPD (air).
Side
lobe
Main lobe
Reverberation occurs when the echo
bounces back and forth several times
– sometimes between a structure and
the surface of the transducer.
Beam width artefacts occur
when the beam width is wide
and unfocused.
US beam
Image
Wide Narrow
REVERBERATION –
apical four-chamber view/2D
Highly echogenic pericardium
leading to reverbations
ARTEFACTS
Types of Artefacts
• Near field clutter • Side lobe artefact
• Reverberation • Beam width artefacts
• Acoustic shadowing • Attenuation artefacts
• Mirror imaging/double images (caused by refraction)
Specific Forms
Side lobes Reverberation
Beam width artefact

14
NOTES ARTEFACTS
When Do Artefacts Occur?
• Good image quality (e.g. mirror artefacts)
• Poor image quality
• Strong reflectors (e.g. calcification,
prosthetic material)
• More frequent in fundamental imaging
Tips to Avoid Artefacts
• Know the pitfalls • Be cautious of strong reflections
• Know the anatomy • Use multiple views
Artefacts are
inconsistent.
ARTEFACT IN PROSTHETIC VALVE
– apical four-chamber view/2D
Shadowing and reverberations of
the left atrium caused by a me-
chanical mitral valve prosthesis.
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).

15
NOTES
OPTIMIZING THE 2D IMAGE
Important Settings
• Gain • Depth
• Time gain compensation (TGC) • Imaging frequency
• Sector width • Focus
Post-Processing
• Gray scale
• Contrast
• Compression
• Color maps
MMODE
MMode
Advantage
• High temporal resolution
• Good for certain measurements
• Allows measurement of time intervals
• Timing of events
Where is it used?
• Aorta/left atrium (measurements,
opening of the aortic valve)
• Left/right ventricle (measurements,
LV function)
• Mitral/prosthetic valve (type of valve)
• Endocarditis (motion of suspected
vegetation)
• Tricuspid annular plane systolic
excursion (TAPSE) for RV function
• Mitral valve (mitral stenosis)
• Mitral valve annular excursion (MAPSE)
for longitudinal LV function
• Display of mid-systolic notching
(flying W) of the posterior pulmonary
valve cusp
Know your echo
machine!
Use predefined settings for
specific situations (i.e. patients
who are difficult to examine)
and for specific modalities (i.e.
standard echo, contrast).
MMode has lost much of its
importance, but is still
valuable in certain situations.
Diastole Systole
RV
IVS
Post.
wall
COLOR MAPS – PSAX/2D
Different 2D color maps for
individualized 2D display.

16
NOTES
Other Forms of MMode
Anatomical MMode Freedom of axis
Color Doppler MMode Timing of flow (i.e. flow
propagation)
Tissue Doppler MMode Myocardial function,
timing of events
Curved MMode Functional information along
a variable MMode line
SPECTRAL DOPPLER
Doppler Formula
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
Doppler Aliasing
Depends on
• Depth
• Velocity
• Width of sample volume
• Doppler frequency
MMODE
Aliasing will occur when blood
flow velocity exceeds the
Nyquist limit. The Nyquist limit
is equal to a half of the pulse
repetition frequency. Use the
baseline shift to ”stretch” the
Nyquist limit.
The measured velocity
greatly depends on the angle
between blood flow and the
ultrasound beam. Always try
to be as parallel to blood
flow as possible. Use color
Doppler to visualize the
direction of flow.
Anatomical MMode
Conventional MMode
!d = 2!f0 cos"
v
c
The Doppler formula allows us
to calculate velocities (i.e.
blood and tissue), based on
the Doppler shift between the
send and the receive signal.
!d = frequency alteration between
S and E (=Doppler shift)(Hz)
f0
= transmitting frequency (Hz)
v = blood flow (m/s)
c = sound propagation
velocity (1550 m/s)
" = Doppler irradiation angle

17
NOTES
Tissue Doppler Imaging
Information
• Myocardial velocity
• Displacement
• Strain
• Strain rate
FLOW DYNAMICS
Bernoulli Equation
The simplified Bernoulli equation permits
easy estimation of pressure gradients
from velocities.
SPECTRAL DOPPLER
PW spectral tissue Doppler
measures deformation and
velocities at a specific site
(within the sample volume).
Tissue Doppler is
angle dependent.
P(mmHg)
P(mmHg)
V(m/s) P = 4xV2
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 – apical
four-chamber view
Tissue Doppler color display of
the heart during early systole.
Red indicates myocardial motion
towards the transducer.

18
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
Color Encoding
Flow towards the transducer is coded in red, and flow away
from the transducer in blue.
The manner of displaying
flow, flow velocities or
turbulant flow is determined
by the color map. Most
scanners allow you to
change the color map.
Check your machine setings.
towards + 62 m/s
- 62 m/s
away

19
NOTES
COLOR DOPPLER
Color Doppler and Aliasing
Once the Nyquist limit is reached, the color changes abruptly
(red to blue, or blue to red). The color Doppler display will show
a mosaic pattern. Some color maps also display variants of velocity
in green (high variants in velocities indicate turbulent flow).
Color Doppler Frame Rate
• Scan line density
• Emphasis (2D vs. color)
• Sector width (2D)
• Sector width (color)
• Pulse repetition frequency
• Depth
The phenomenon of
aliasing provides good
delineation of jets
(e.g. PISA).
Always aim for a high color
Doppler frame rate.
Try to use the same settings for
quantification of regurgitation in
all patients (maps, aliasing limits,
color gain).
COLOR DOPPLER ALIASING–
apical four-chamber view/
Color Doppler
Patient with mitral stenosis. The
color Doppler of mitral valve
inflow shows the typical pattern
of a high velocity jet. Red color
denotes the direction of flow
towards the transducer. The sud-
den change from yellow to blue
depicts the region where aliasing
occurs.
Flow towards the transducer
lower velocity
turbulant/high velocity
flow– green
Aliasing border
(from orange to blue)
Flow towards
the transducer higher
velocity (orange)
Flow towards the
transducer
low velocity (red)

20
NOTES

21
002//
How to Image
CONTENTS
22 How to Move the Transducer
22 Imaging Windows
22 Image View
28 Abbreviations

002 // HOW TO IMAGE
22
NOTES
NOTES
Use enough
ultrasound gel.
Use as many views as
possible, including
atypical views. Always
image so that the
pathology of interest
is seen best.
HOW TO MOVE THE TRANSDUCER
IMAGING WINDOWS
IMAGE VIEW
Parasternal Long-Axis Views
Displacement Rotation Angulation
Parasternal 2nd–4th intercostal space
left sternal border
Apical 4th – 5th intercostal space,
lateral
Subcostal Below xiphoid
Right parasternal 2nd–4th intercostal space,
right sternal border
Suprasternal Suprasternal notch
AMVL
RV
LV
LA
AV
MV
Ao
Parasternal
long-axis view
Right
parasternal long axis
RV
Right parasternal
Suprasternal
Left parasternal
R L
Apical
Subcostal
TV
Anterior
Posterior
002 // HOW TO IMAGE
22
NOTES

002 // HOW TO IMAGE
23
NOTES
23
NOTES
PM
PM
PM
Move down one intercostal
space to obtain good image
quality and a “more“ spherical
(round) configuration of the
distal parts of the left
ventricle.
IMAGE VIEW
Parasternal Short-Axis Aiews
Parasternal short
axis – base
Parasternal short axis –
mitral valve
RV
RV
LA
RA
AC
LC
PA
r-PA
RC
MV
Parasternal short axis
– mid-ventricle
PM
AL
l-PA
002 // HOW TO IMAGE
23
NOTES

24
NOTES
4-chamber view 2-chamber view 3-chamber view
Four-chamber view Two-chamber view Three-chamber view
A B
Parasternal
approach
Parasternal
approach
Parasternal
approach
Four-chamber view
Two-chamber view
Three-chamber view
Orientation of the Apical Views
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
aspects of the left and
right ventricle.
Use a medial position (A) to
visualize the lateral wall of the
LV and a lateral position (B) to
visualize the RV.
IMAGE VIEW
Apical Views Rotate counterclockwise
RV LV LV LV
RA
LA LA
LA
TV MV MV
MV
AV
Ao
RV
002 // HOW TO IMAGE
24
NOTES

Five-chamber view
25
NOTES
Coronary sinus view
Subcostal Views
The five-chamber view shows
the anterior portions of the
interventricular septum.
Avoid foreshortening; place
the transducer as lateral and
caudal as possible.
In some patients it
may be possible to see
the superior vena cava
on this view.
Abdominal gas may
obscure the apex on
the subcostal view.
IMAGE VIEW
RV
RA
LV
LVOT
LA
Ao
LV
RV
RA
LA
CS
RL – PV
RU – PV
LU – PV
LL – PV
LIVER
RV
LV
RA
LA
Subcostal four-chamber view
Inferior vena cava view (rotate counterclockwise)
LIVER
IVC
SVC
LA
RA
RV
002 // HOW TO IMAGE
25
NOTES

26
NOTES IMAGE VIEW
AO
LA
B
r
a
c
h
i
o
c
e
p
h
a
l
i
c
a
r
t
e
r
y
L
e
f
t
c
o
m
m
o
n
c
a
r
o
t
i
d
a
r
t
e
r
y
Left subclavian
artery
Suprasternal View
Suprasternal view
MMode MMode aorta/left atrium
MMode left ventricle
Measure the end-diastolic
diameter where the LV is
largest, shortly before
contraction starts (beginning
of the QRS complex).
The suprasternal view allows
you to detect coarctation, a
persistent Botalli‘s duct, or
aortic dissection, as well as
quantify retrograde flow in
the aorta (aortic
regurgitation).
MMode – LA is measured in
its largest extension at end
systole. The dimensions of
the aorta are measured at
end diastole, shortly before
the aortic valve opens.
Obtain subcostal
views in all patients.
Subcostal short-axis view (rotate clockwise)
RA
PA
Ao
RV
r-PA
Asc Ao
Desc Ao
RV
LV
IVS
Posterior Wall
002 // HOW TO IMAGE
26
NOTES

27
NOTES
IMAGE VIEW
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 you use color 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
Optimize the 2D image
before using color
Doppler.
002 // HOW TO IMAGE
27
NOTES

002 // HOW TO IMAGE
28
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

29
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

NOTES
There must be
agreement between
M-Mode and 2 D
measurements in
regard of LV size.
Normal chamber size
increases with body
surface area
(and body size).
THE LEFT VENTRICLE
Quantification of LV Diameter
PLAX MMODE Four-chamber
view
Left Ventricular End-Diastolic (LVED)
Diameter – Reference Values
Normal (mm) 42 – 59 39 – 53
Mild (mm) 60 – 63 54 – 57
Moderate (mm) 64 – 68 58 – 61
Severe (mm) ≥ 69 ≥ 62
LVED Diameter/Body Surface Area (BSA) – Reference Values
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
ESC/ASE 2005
Only use MMode values when
your line of interrogation is
perpendicular to the LV cavity
and walls.
Measure distances
between the endocardial
borders, not the
pericardium (lateral).
RV
PW
IVS
LVEDD
LEFT VENTRICULAR DIAMETER –
apical four chamber view/2D
The endiastolic diameter of the
left ventricle (LVEDD) is measured
from the lateral to the septal bor-
der of the endocardium between
the tips of the mitral valve and
the papillary muscle at end dias-
tole. If a septal bulge is present,
measure more basally.
LVEDD
Endocardial border
Epicardial border
003 // HEART CHAMBERS AND WALLS
30
NOTES

Volume measurements are
superior to diameter and
area measurements.
31
NOTES
THE LEFT VENTRICLE
LV End-Diastolic Volume (4-chamber view) –
Reference Values
Normal (mL) 67 – 155 56 – 104
Mild (mL) 156 – 178 105 – 117
Moderate (mL) 179 – 200 118 – 130
Severe (mL) ≥ 201 ≥ 131
LV Systolic Volume (4-chamber view) – Reference Values
Normal (mL) 22 – 58 19 – 49
Mild (mL) 59 – 70 50 – 59
Moderate (mL) 71 – 82 60 – 69
Severe (mL) ≥ 83 ≥ 70
Pathophysiology
Principles of LV Function:
Factors influencing ejection fraction/stroke volume
ESC/ASE 2005
ESC/ASE 2005
Do not trace the papillary
muscles. Their volumes
should be included in the
calculation.
A reduction of
longitudinal function is an
early marker of LV
dysfunction.
stroke volume
myocardial mechanics
contractility shape preload afterload
SIMPSON METHOD – apical
four-chamber view/2D
Tracing of the endocardial bor-
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 end-diastolic volume
Papillary muscle
31
NOTES

32
NOTES
Contractility, preload and
afterload influence myocardial
function. A reduction in
contractility is initially
compensated by activation of
the sympathetic nervous system
(compensatory increase in heart
rate and contractility) as well as
dilatation of the left ventricle.
Stroke volume is kept adequate
at rest, but cannot adapt to
exercise (reduced functional
reserve). In end-stage heart
failure, stroke volume is also
reduced at rest
(decompensation).
THE LEFT VENTRICLE
Pathophysiology of LV Failure:
Cascade and Compensatory Mechanisms
LEFT VENTRICULAR FUNCTION
Parameters of LV Function
• Fractional shortening
• Cardiac output/index
• ”Eyeballing” of LV function
• Deformation parameters
(strain, strain rate)
• Ejection fraction (EF) – Simpson method
• Contractility (dp/dt)
• Stroke volume
• Tei index
• TDI velocity of the myocardium
• MAPSE (mitral annular plane
systolic excursion)
Fractional Shortening – Reference Values
Normal 25 – 43% 27 – 45%
Mild 20 – 24% 22 – 26%
Moderate 15 – 19% 17 – 21%
Severe ≤ 14% ≤ 16% ESC/ASE 2005
LV function and
(longitudinal) contractility
may be reduced despite a
”normal” ejection fraction,
especially in patients with
small ventricles.
Fractional shortening is a
rough estimate of global left
ventricular function. Do not
use the Teichhholz formula
to derive the ejection
fraction from these values.
stroke
volume
(exercise)
stroke
volume
(at rest)
reduction in
contractility
increased
preload
increased
afterload
sympathicus
dilatation
compensation

33
NOTES
Fractional Shortening – Contraindications
• LBBB/dyssynchrony/pacemaker
• Abnormal septal motion
• Regional wall motion abnormalities
• Inadequate (oblique) MMode orientation
• ”Pseudo-shortening” of the
LV (very small ventricle)
ESC/ASE 2005
Ejection Fraction – Simpson Method
Normal > 55 %
Mild 45 – 54 %
Moderate 30 – 44 %
Severe < 30%
Stroke Volume, Cardiac Output, Cardiac
Index – Reference Values
Rest Exercise
Stroke volume 70 – 110mL 80 – 130mL
Cardiac output 5 – 8.5 L/min 10 – 17 L/min
Cardiac index > 2.5 L/min/m2
> 5 L/min/m2
In these settings, fractional
shortening cause
overestimation or
underestimation of left
ventricular function.
1) Ejection fractions tend
to be higher in small
ventricles. 2) Athletes often
have ejection fractions in the
low normal range.
3) Ejection fraction does not
predict exercise capacity or
functional reserve.
4) Ejection fraction is super-
normal in patients with
reduced afterload (e.g.
mitral regurgitation).
EF = x 100
EDvol – ESvol
EDvol
The calculation of these
parameters is very highly
dependent on correct
measurement of LVOT
width.
LEFT BUNDLE BRANCH BLOCK
– PLAX/Mmode
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.
MMode
AV
AMVL
LV

Measuring Contractility – dP/dt
Normal > 1200 mmHg/sec
Borderline 800 – 1200 mmHg/sec
Reduced < 800 mmHg/sec
Severely reduced < 500 mmHg/sec
Limitations: Mitral regurgitation (MR) signal needed, inexact, not completely
load independent
THE RIGHT VENTRICLE
Characteristics of the RV
• The wall is thinner (< 5 mm)
• Moderator band
• Strongly trabeculated
• ”Wrapped around” the left ventricle
PV = pulmonic valve
RAA = right atrial appendage
RVIT = right ventricular inflow tract
RVOT = right ventricular outflow tract
A rough estimate of
contractility can also be
obtained by eyeballing the
slope of the MR curve. 1m/s
3m/s
dP/dt
dP/dt
1 m/s
CW Sample
MR
3 m/s
DP/DT – apical four-chamber
view/CW Doppler mitral
regurgitation
The dP/dt is calculated by
measuring the slope of the initial
mitral regurgitation signal
between 1 m/s and 3 m/s.
PA SVC
PV
RVOT
RVIT
RAA
TV RA
IVC
The geometry of the
right ventricle is more
complex than that of
the left ventricle:
it resembles a bagpipe.
34
NOTES

THE RIGHT VENTRICLE
Measurements of the Right Ventricle
ESC/ASE 2005
Right Ventricular Systolic Function
Tricuspid annular plane systolic excursion (TAPSE) < 16 – 18 mm
TDI maximum velocity at the basal lateral wall (S‘) > 10 cm/s
PW Doppler myocardial performance index > 0.4
Tissue Doppler myocardial performance index > 0.55
RV diameters appear
larger when the
transducer is too far
cranial.
Speckle-trackingderived
longitudinal strain of the free
right ventricular wall may
provide additional information
to quantify right ventricular
function. It also reflects RV
function in the apical segments.
Reference Slightly Moderately Severely
Range Abnormal Abnormal Abnormal
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
Mid
Basal
RIGHT VENTRICULAR DIAMETER
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-
cle. The right ventricular diam-
eter will be overestimated when
the ventricle is foreshortened.
35
NOTES

36
NOTES
RV Diastolic Function
E/A ratio < 0.8 or > 2.1
E/e‘ > 6
Deceleration time (ms) < 120ms
Causes of RV Dilatation
• Dilated cardiomyopathy
• Right heart infarction
• Myocarditis
• Pulmonary embolism/hypertension
• Right ventricular dysplasia
• RV volume overload (e.g. atrium septal
defect, pulmonic/tricuspid regurgitation)
• Athletes (normal reaction to training)
THE RIGHT VENTRICLE
Assessment of RV
diastolic dysfunction is
rarely used in clinical
practice.
Always look for the
cause of RV dilatation.
TAPSE – apical four-chamber
view/Mmode RV wall
TAPSE is measured by placing
the MMode through the tricus-
pid annulus and measuring the
displacement from diastole to
systole.
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
ventricle. S’ denotes RV longitu-
dinal function.
Free RV Wall
TDI Velocity (max.)
MMode
TAPSE
S‘
E‘ A‘
RA
TDI
SAMPLE

37
NOTES
Fractional Area Change (FAC)– Reference Values
Normal 32-60 %
Mild 25 – 31 %
Moderate 18 – 24 %
Severe ≤ 17 %
THE LEFT ATRIUM
MMode Measurements of LA – Reference Values
Normal (mm) 30 – 40 27 – 38
Mild (mm) 41 – 46 39 – 42
Moderate (mm) 47 – 52 43 – 46
Severe (mm) ≥ 52 ≥ 47
LA Length (4-Chamber View)– Reference Values
LA diameter (mm) 27–38 39–42 43–46 ≥ 47
LA diameter/
BSA (mm/m2) 15–23 24–26 27–29 ≥ 30
LA diameter (mm) 30–40 41–46 47–52 ≥ 52
LA diameter/
BSA (mm/m2) 15–23 24–26 27–29 ≥ 32
Trace the RV contour in diastole and
systole in an optimized 4-chamber view
to obtain the areas. Calculate the
percentage of change.
(RV area end-diastole – RV area
end-systole)/RV area end-diastole *100
ESC/ASE 2005
Measure the length of
the left atrium parallel to
the interatrial septum.
ESC/ASE 2005
THE RIGHT VENTRICLE
Tracing of RV contours may
be difficult (trabeculations,
thin wall).
LA size and volume predict
adverse events (i.e. afib,
stroke) and constitute a
marker of disease severity.

38
NOTES
LA Area – Reference Values
Normal (cm2
) ≤ 20
Mild (cm2
) 20 – 30
Moderate (cm2
) 30 – 40
Severe (cm2
) > 40
ESC/ASE 2005
LA Length – A Practical Scale
Normal (mm) ≤ 50
Mild (mm) 51 – 60
Moderate (mm) 61 – 70
Severe (mm) > 70
THE LEFT ATRIUM
LA
LA
LEFT ATRIAL LENGTH –apical
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
provides a rough estimate of left
atrial size.
LEFT ATRIAL AREA –apical
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
LA diameter
End-Systole
Pulmonary vein
Pulmonary vein

39
NOTES
LA Volume – Reference Values
LA Volume (Area
Length Method) –
Reference Values Practical Scale
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
• Inclusion of pulmonary veins
• Tenting area of MV
• Alignment/atrial foreshortening
• Lateral resolution
• Measurement not performed at end
systole
• Oblique view of the LA
• Foreshortening of the atrium
Parameters of LA Function
• Doppler (MV inflow)
• Area changes systolic/diastolic
• Pulmonary vein flow
• TDI/2D strain
In most cases the Doppler
(MV inflow) signal is
sufficient to estimate LA
function. Functional
assessment of the LA is still a
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.
Optimize the 4-chamber
view specifically to the left
atrium to obtain best results.
THE LEFT ATRIUM
V = X
8! A4c x A2c
3 L
LA volume measurements
are superior to MMode
and 2D diameter
measurements. LA
volumes > 200 ml denote
very severe atrial
dilatation (LA volumes
may even exceed 1 liter).

40
NOTES
Causes of LA Dilatation
• Diastolic dysfunction
• Mitral stenosis/regurgitation
• Aortic stenosis
• Restrictive/hypertrophic cardiomyopathy
• Atrial fibrillation
• Impaired LV function
THE RIGHT ATRIUM
Causes of RA Dilatation
• Pulmonary hypertension
• Tricuspid valve disease
• Right ventricular failure
RA Length – Reference Values (4 chamber view)
RA minor axis
diameter (mm) 29–45 46–49 50–54 ≥ 55
RA minor axis
diameter/BSA
(mm/m2
) 17–25 26–28 29–31 ≥ 32
ESC/ASE 2005
The right atrium can be
stretched in length when
the left atrium expands.
expands ands.
The RA is generally
smaller than the LA.
However, for
practical reasons you
may also apply the
simple grading scale
shown for the left
atrium.
The most frequent
cause of LA dilatation
in the adult is
hypertension.
THE LEFT ATRIUM
RA
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
Vena cava

41
NOTES
THE RIGHT ATRIUM
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
Size < 17 mm, Inspiratory collapse ≥ 50%
IVC size varies greatly, depending on fluid status and central venous pressure
Causes of IVC dilatation:
• Tricuspid regurgitation
• Pericardial tamponade constriction
• Restrictive cardiomyopathy
• Right heart failure
• Scimitar syndrome (anomalous pulmonary venous return into the IVC)
LEFT VENTRICULAR HYPERTROPHY
Forms of Left Ventricular Hypertrophy
LVMI (left ventricular mass index) = LV mass/BSA
Reference adapted from Ganau et al. JACC 1992
Relative Wall Thickness (RWT)
Normal values 22 – 42 %
IVC allows estimation of RA
pressure. Dilated IVC without
respiratory changes indicates
elevated RA pressure (> 15
mmHg).
A large inferior vena cava does
not always indicate a medical
condition. Some patients simply
have a large inferior vena cava
(even in the absence of elevated
RA pressure).
Most patients with
hypertension have
concentric LVH.
2 x PWT
LVID
RWT =
RWT
0.43
LVMI
Concentric
remodelling
Normal
Concentric
hypertrophy
Eccentric
hypertrophy
Left ventricular geometry

42
NOTES
Quantification of LVH – Severity of Septal Thickness
Normal (mm) 6 – 10 6 – 9
Mild (mm) 11 – 13 10 – 12
Moderate (mm) 14 – 16 13 – 15
Severe (mm) ≥ 17 ≥ 16
2D measurements: end-diastole, mid-septum, 4 chamber view ESC/ASE 2005
Sigmoid Septum
• Septal buldge – less than
3 cm in length
• Associated with hypertension
• Not associated with
hypertrophic cardiomyopathy
Potential problems: the
measurements were not
performed at end diastole
(2D), RV structures interfere
with the measurement, the
shape of the IVS (basal septal
bulge), incorrect image
orientation (non-
perpendicular).
May cause obstruction
and SAM, especially
under certain clinical
conditions
(hypovolemia,
hyperkinesia,
catecholamines).
Buldge
INTERVENTRICULAR
SEPTUM – apical four-chamber
view/2D
The interventricular septum is a
prominent structure. The center
of the septum is highly echoge
nic. A septal bulge is frequently
observed, especially in hyper-
tensive patients. The thickness
of the bulge should be reported
separately.
IVS diameter
Interventricular septum

43
NOTES
Quantification of LV Mass (ESC/ASE 2005)
Measurments obtained from 2D-targeted M-mode or 2D linear LV measure-
ments: LV internal dimensions and wall thicknesses should be measured at the
level of the LV minor dimension, at the mitral chordae level.
Abbreviations:
LVIDd= left ventricular internal diameter at end diastole
PWTd= posterior wall thickness at end diastole
SWTd= septal wall thickness at end diastole
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
• Left atrial enlargement
• Right ventricular hypertrophy
• Dilated aorta
• Aortic valve sclerosis
• Mitral annular calcification
Athlete‘s Heart
• Left ventricular hypertrophy (RWT
≤ 45 and septum rarely > 13mm)
• Normal or supranormal
diastolic function
• Left and right ventricular dilatation
• Supranormal left atrial booster pump
function
• Changes occur only after intensive
and prolonged training
for several years
In a patient with these
findings, left ventricular
hypertrophy is likely to be a
consequence of
hypertension.
Endurance training/
isotonic exercise (such as
marathon running)
causes an eccentric form
of hypertrophy. Isometric
exercise (such as weight
lifting) causes a more
concentric form.
Deconditioning reverses
left ventricular
hypertrophy.
LV mass better reflects the
extent of LVH than the
measurement of septal
thickness. Even small
measurement errors are
magnified. Therefore, LV mass
measurement should only be
performed in patients with
good image quality.
This formula is appropriate for
evaluating patients without
major distortions of LV
geometry.
LV mass = 0.8 x {1.04[(LVIDd + PWTd + SWTd)3
– (LVIDd)3
]} + 0.6 g

44
NOTES

45
004//
Diastolic Function
CONTENTS
46 Basics of Diastolic Dysfunction
51 Specific Situations

NOTES
Any patient with systolic
dysfunction also has diastolic
dysfunction.
Patients with diastolic
dysfunction usually have a
dilated left atrium.
Diastole beginns with aortic
valve closure, which can be
assessed with PW Doppler
sample volume in the LVOT
(end of signal).
BASICS OF DIASTOLIC DYSFUNCTION
Causes
• Aging
• Sytolic dysfunction
• Heart failure with preserved ejection fraction
• Left ventricular hypertrophy
• Restrictive cardiomyopathy/infiltrative disease
• Coronary artery disease
• Hypertrophic cardiomyopathy
• Heart transplantation
Diastole Duration
Timing of Diastole
Components
• IVRT – isovolumetric relaxation (AV
closure to MV opening)
• E= rapid early (passive) LV filling
• Diastasis
• A= late LV filling – atrial contraction
Diastole
T
R R
P
Fusion of the E- and
the A- wave may occur in
tachycardia. The duration of
diastasis decreases with
heart rate and PQ duration.
IVRT
E A
Diastasis
Physiology of Diastolic Function
Echo assessment of
diastolic function
primarily reflects left
atrial filling pressure.
Geometry
dyssynchrony
Preload
Active myocardial
relaxation Percardium
LA compliance/
function
Heart rate
Diastolic
function
Filling pressure
LV compliance
004 // DIASTOLIC FUNCTION
46
NOTES

47
NOTES
Mitral Inflow Signal
E A
Early filling Atrial contraction
Mitral Inflow – Reference Values
16–20 years 21–40 years 41–60 years > 60 years
IVRT (ms) 50 ± 9 67 ± 8 74 ± 7 87 ± 7
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
PW Doppler sample volume
should be at the tip of the
MV leaflets.
In some situations the
parameters of diastolic
function may be
inconsistent and difficult to
interpret.
Diastolic filling
D
T
EAE/ASE 2009
The deceleration time (DT)
shows the pressure decay of
early filling. In general the
shorter the DT, the higher
the filling pressure.
Diastolic filling
Atrial contraction
Early filling
A-wave
E-wave
MITRAL INFLOW SIGNAL –
PW Doppler MV
The mitral inflow signal allows
assessment of diastolic function
as well as the timing of events
(such as diastolic filling time).
The E-wave represents early
diastolic filling while the A-wave
represents atrial contraction. It is
advisible to always use an ECG.
47
NOTES

48
NOTES
TDI Mitral Annulus – Reference Values
16–20 years 21–40 years 41–60 years > 60 years
Septal e‘ (cm/s) 14.9 ± 2.4 15.5 ± 2.7 12.2 ± 2.3 10.4 ± 2.1
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
Situations in Which TDI at the Mitral Annulus
Should Not Be Used
• Annular calcification
• Mitral valve prosthesis
• Myocardial infarction
• Moderate to severe mitral regurgitation
Pulmonary Venous Flow
• Peak systolic PV flow velocity (S)
• Peak diastolic PV flow velocity (D)
• Peak reverse atrial flow velocity (AR)
• AR duration
Signs of impaired diastolic function:
Decrease in systolic component, increase
in peak AR, increase in AR duration
Use right upper PV to record
the PW signal. Remember to
reduce PRF.
An E/e’ ratio ≤ 8 (septal or
lateral) indicates normal left
atrial pressure; a septal E/e’
≥ 15 or a lateral E/e’ ≥ 12
indicates elevated left atrial
pressure.
S
AR
AR duration
Isovolumic relaxation
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.
e´
a´

49
NOTES
Pulmonary Veins – Reference Values
16 – 20 years 21 – 40 years 41 – 60 years > 60 years
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
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)
Pulmonary vein flow has many
limitations and is rarely used in
clinical practice.
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
? ?
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
deceleration of the E-wave is
prolonged.
A-wave
E-wave

50
NOTES
Algorithm for the estimation of filling pressures in patients with
normal left ventricular function (EF >55%) according to
the ASE/EAE guidelines (2009)
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)
Normal LAP Normal LAP Elevated LAP
E/e’ < 8
E/Vp < 1.4
S/D > 1
Ar-A < 0 ms
Valsalva ! E/A < 0.5
PAS < 30 mmHg
E/e’ > 15
E/Vp ≥ 2.5
S/D < 1
Ar-A ≥ 30 ms
Valsalva ! E/A ≥ 0.5
PAS > 35 mmHg
Elevated LAP
E/A < 1 and E ≤ 50 cm/s
E/A > 1 – < 2 or
E/A < 1 and E ≤ 50 cm/s
Mitral E/A
E/A ≥ 2 , DT <150 ms
Normal LAP Normal LAP Elevated LAP
LA vol. < 34 ml/m2
Ar-A < 30 ms
Valsalva ! E/A < 0.5
sPAP < 30 mmHg
LA vol. < 34 ml/m2
Ar-A ≥ 30 ms
Valsalva ! E/A ≥ 0.5
sPAP > 35 mmHg
Elevated LAP
E/e’< 8
(sep., lat. or av.)
E/e’ 9 – 14
E/e’
E/e’ sep. ≥ 15 or
E/e’ lat. ≥ 12 or
E/e’ av. ≥ 13 or

51
NOTES
A Simple Approach to Diastolic Function/Rules
• Supernormal diastolic function:
When the echo is normal and the
patient is young
• Normal diastolic function:
When the echo is normal, the patient is
< 45 years of age, and E>A
• Impaired relaxation:
When A is higher than E (E/A ratio is < 1),
filling pressure is normal or slightly
elevated
• Pseudonormal diastolic function:
When echo is abnormal (LVH, red LVF,
etc) or the patient is > 65 years of age
and E is higher than A (E/A ratio > 1)
• DD normal vs pseudonormal:
Look at deceleration time,
LA enlargement, and E/e‘ (≥ 8 – 12)
• Restrictive filling:
When E is twice of A (E/A ratio is >2),
then filling pressure elevated
• Perform TDI:
When E/e´is > 12 – 15 then filling
pressure is elevated (PCWP > 12 mmHg)
• Perform valsalva:
Unloading of the atrium, LA pressure
(LAP) drops, unmasking of pseudonor-
mal filling (discrimination between
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
A-wave
E-wave
Carotid artery maneuver
E/A fusion
EA FUSION – apical four-
chamber view/PW Doppler MV
E/A fusion can be abolished by
slowing down the heart rate – in
this example by performing a
carotid artery maneuver.

L-Wave
• Mid-diastolic filling of the LV
• Elevated filling pressure?
• Bradycardia
• Can also occur in atrial fibrillation
(difficult to detect, no A wave)
Atrial Fibrillation/Flutter in Diastolic Dysfunction
• Often associated with
diastolic dysfunction
• Pulmonary venous flow is difficult to
assess
• No A-wave, therefore the E/A ratio
cannot be obtained
• Use E/e‘ and deceleration time
(average several beats)
Left Atrial Pressure in Mitral Valve Disease
• Left atrial size does not necessarily
reflect elevated filling pressures
• Left atrial size may also be enlarged
due to volume overload + atrial
fibrillation
• E-wave velocity also reflects
increased stroke volume
• E‘ is reduced in mitral stenosis and
elevated in mitral regurgitation
SPECIFIC SITUATIONS
The presence of an L-wave
indicates elevated filling
pressure.
Diastolic dysfunction/LV filling
pressure should not be
assessed in the setting of
mitral regurgitation > grade II.
Estimate filling pressure to
determine the severity of
disease and how the LV can
cope with the problem
(e.g. AS, AR, cardiomyopathy).
L WAVE – apical four-chamber
view/PW Doppler MV
The L-wave occurs between the
E- and the A-wave, and denotes
mid-diastolic filling of the LV.
It is indicative of eleva-
ted LV filling pressure.
A-wave
E-wave
L-wave
E L A
52
NOTES

53
005//
Dilated Cardiomyopathy
CONTENTS
54 Background
54 Echo Features
55 Specific Forms

NOTES BACKGROUND
Definition
• Myocardial disease (primarily)
• Impaired systolic function
• Left ventricular dilatation
• In the absence of coronary artery disease
and significant primary valvular disease
Causes
• Genetic
• Congential
• Infections
• Drug and alcohol abuse
• Certain cancer medications
• Exposure to toxins
Associated Problems
• Left heart failure
• Atrial fibrillation, ventricular arrythmias
• Mitral regurgitation
• Dyssynchrony
• Thromboembolism
ECHO FEATURES
Diagnosis
• Reduced left ventricular function
• Dilated left ventricle
• Reduced right ventricular function
• Exclude other causes (coronary artery
disease, valvular)
Signs of Advanced Dilated Cardiomyopathy
• Low cardiac output (LVOT velocity
< 0.5 m/sec)
• Very low ejection fraction
• Atrial size (large atria in more
advanced forms)
• Significant mitral regurgitation
• Diastolic function/filling pressure
(restrictive pattern)
• Severe pulmonary hypertension and
tricuspid regurgitation
• Poor right ventricular function
• Pleural effusion
Right ventricular function
correlates better with
prognosis than LVF (it
denotes end-stage heart
failure).
Ischemic cardiomyopathy is
similar to dilated
cardiomyopathy but is, by
definition, NOT a form of dilated
cardiomyopathy.
The etiology remains unidentified
in many cases because a biopsy is
not performed.
About 30% of patients with
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.
End-stage ischemic
cardiomyopathy
and dilated
cardiomyopathy look
very similar.
005 // DILATED CARDIOMYOPATHY
54
NOTES

55
NOTES
55
NOTES
Mechanisms of Mitral Regurgitation in Cardiomyopathy
• Annular dilatation geometry
• Bileaflet restriction
• Atrial enlargement
• Dyssynchrony
The degree of mitral regurgitation may change rapidly and is related to factors
such as increased afterload, preload, and volume status.
SPECIFIC FORMS
Ischemic Cardiomyopathy
• Not really a form of dilated cardi-
omyopathy but shares several
features
• Most common cause of heart failure
• Occurs in large infarctions, leads to
ventricular remodeling and
global dysfunction
• Thin scarred walls, ventricular
distortion and clearly segmental
myocardial dysfunction suggests
ischemic cardiomyopathy
MR increases mortality.
(additional volume
overload of LV).
Rule out a structural cause for
mitral regurgitation. It could
point to the presence of a
primary valvular cause of
systolic dysfunction.
It may be difficult or even
impossible to distinguish
between dilated and ischemic
cardiomyopathy on
echocardiography.
ECHO FEATURES
ECHOFEATURES OF DILATED
CARDIOMYOPATHY –
Color Doppler
Dilated left ventricle with re-
duced left ventricular function,
mitral regurgitation with a central
jet caused by annular dilatation,
Dilated LV
Enlarged LA
MR central jet
(annular dilitation)

56
NOTES SPECIFIC FORMS
Taktsubo Cardiomyopathy
• Stress–induced cardiomyopathy is
more common in women
• Echo features include segmental wall
motion abnormalities (in particular
apical ballooning), hyperdynamic
basal segments which may cause
LVOT obstruction, and right ventricular
involvement
• Normal coronary angiogram
• Abnormalities are reversible
Peripartum Cardiomyopathy
• A non-familial, non-genetic form of
dilated cardiomyopathy associated
with pregnancy
• Clinical presentation in the last month
of pregnancy or 5 months
post partal
• Recovery rate > 40%
• Often presents as acute heart failure
• May involve both ventricles
• Has no specific echo features
Tachycardia/Arrythmia-Mediated Cardiomyopathy
• Prolonged periods of tachycardia in
atrial fibrillation or ventricular
tachycardia
• In arrhythmia-mediated
cardiomyopathy, frequent ectopic
beats (> 17,000/24h)
• Cardiac function returns in most cases
after heart rate control, but may take
several weeks or months
• Assessment of left ventricular function
is difficult and is underestimated in
tachycardia. Always repeat the
echocardiogram after heart rate
control
The duration of, and the
heart rate needed for, the
induction of tachycardiomy-
opathy are highly
variable and depend on nu-
merous factors.
Abortive forms of Takot-
subo cardiomyopathy
with more subtle wall
motion abnormalities
have been reported.
TAKOTSUBO
CARDIOMYOPATHY – apical
A typical feature of Takotsubo
cardiomyopathy is apical bal-
looning. The basal segments tend
to be hyperdynamic.
Apical
ballooning

57
NOTES
SPECIFIC FORMS
HIV-Mediated Cardiomyopathy
• Focal myocarditis
• Most common form of cardiomyopathy in African countries (e.g. Burkina Faso)
Causes
• Myocarditis
• Autoimmune cardiomyopathy
• Nutritional deficiency
• 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
• Characterized by prominent
trabeculae and intertrabecular
recesses (sinus)
• Associated with other cardiac
abnormalities
• Genetic disease, risk of
cardiomyopathy, family screening
is important
• Associated with neuromuscular
disorders
• Congenital cardiomyopathy
characterized by prominent
trabeculae and intertrabecular
recesses (spongy myocardium)
• May present at any age
• May be associated with normal or
reduced left ventricular function
• Echocardiography is the most
important diagnostic tool
(alternative: MRI)
SPECIFIC FORMS
There is a genetic link
between non–compaction
and hypertrophic
cardiomyopathy.
LV NON-COMPACTION –
The apical portion of the left
ventricle is strongly trabeculated
and appears spongy. Look care-
fully and visualize all portions of
the myocardium to find hyper-
trabe culated areas. Use contrast
and color Doppler when in doubt.
Hypertrabeculation
Sinus

58
Echo Evaluation
• The involved segments are mid
ventricular (especially inferior and
lateral) and apical. Is usually seen best
on atypical views
• Right ventricular involvement may be
present but is difficult to differentiate
from normal trabeculae
• Use color Doppler with low PRF and
contrast to visualize blood flow
between the trabeculae
• Use deformation imaging to detect
myocardial dysfunction (i.e. speck-
le-tracking echocardiography) at the
regions of hypertrabeculation
Chagas Disease
• Trypanosoma cruzi
• Megaesophagus
• Cardiac disease
• Megacolon
• Most common form of
cardiomyopathy in Latin America
• Right heart failure is dominant
(regional + global dysfunction)
• Caused by infection with Trypanosoma
cruzi (present in feces of reducidae e.g.
triatoma infestand = kissing bug)
• Most common form of cardiomyopa-
thy in Latin America
• Associated with megaesophagus,
megacolon induced by neural
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

59
006//
Hypertrophic Cardiomyopathy
CONTENTS
60 Basics
61 Echocardiographic Evaluation

BASICS
Epidemiology
• Prevalence: 1 in 500
• Annual mortality: Adults 2%
Childhood 4 – 6%
• Most common cause of sudden
cardiac death in athletes
Cause
• Genetic disease (sarcomere)
• Autosomal dominant
• Associated syndromes (Noonan‘s, Friedreich ataxia, LEOPARD)
Symptoms
• Asymptomatic
• Chest pain
• ECG abnormalities
• Syncope
• Arrhythmias
• Sudden death
• Dyspnea
• Palpitations
When to Consider Hypertrophic Cardiomyopathy?
• Unexplained left ventricular
hypertrophy (> 15 mm)
• LVOT/LV gradient
• ”Spade-shaped” left ventricular cavity
• Speckled appearance of
the myocardium
• Asymmetric left ventricular hypertrophy
• Turbulent flow in the LV/LVOT
Cardiomyopathy may
differ markedly in terms of
morphology, clinical
presentation and
prognosis.
The onset of disease may
vary: childhood,
adolescence, or sometimes
late in life.
Perform family screening.
Other causes of left
ventricular hypertrophy
include hypertension,
aortic stenosis, athlete‘s
heart, and infiltrative
heart disease.
Mid-ventricular
turbulences
Turbulent flow LVOT
Posterior
MR jet
PMVL
OBSTRUCTIVE HYPERTROPHIC
CARDIOMYOPATHY –apical
four-chamber view/Color
Doppler
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
acceleration is also present in the
mid-ventricular portion (addi-
tional mid-ventricular obstruc-
tion).
006 // HYPERTROPHIC CARDIOMYOPATHY
60
NOTES

BASICS
Obstructive Forms Non-Obstructive Forms
LVOT obstruction Asymmetric
Mid-ventricular obstruction Apical
ECHOCARDIOGRAPHIC EVALUATION
Non-Obstructive Cardiomyopathy (Apical Type)
• More common in the Asian population
• Associated with a favorable prognosis
• ECG tends to show giant negative T-waves
• A typical echocardiographic finding: spade-
shaped left ventricle
Views to Display SAM = Systolic Anterior Motion
(of the Anterior Mitral Valve Leaflet)
• Parasternal long-axis view
• Parasternal short-axis view at MV
• Apical long-axis view
• Mmode/Color MMode
• Five-chamber view
Apical hypertrophy may
be difficult to detect. Use
contrast for LV cavity
opacification.
There is an overlap
between obstructive and
non-obstructive forms;
the gradients may be
inconsistent.
APICAL HYPERTROPHIC
CARDIOMYOPATHY – apical
Pronounced hypertrophy of
the apex with a spade-shaped
ventricular cavity. Atrial enlarge-
ment is also a common feature of
hypertrophic cardiomyopathy.
Spade sign
Apical
hypertrophy
61
NOTES
61
NOTES

62
NOTES
62
NOTES ECHOCARDIOGRAPHIC EVALUATION
SAM (Systolic Anterior Motion) Increases With
• Hypovolemia
• Exercise
• Medication (i.e. nitroglycerin, diuretics)
• Dobutamine
• Valsalva
• Post-extrasystolic
Quantification of Obstruction
• Measure maximal LVOT velocity
(CW Doppler)
• The Doppler signal is typically
dagger-shaped
• A late peak generally indicates obstruc-
tion more towards the mid/apical parts
of the ventricle
• Early obstruction is hemodynamically
more relevant
• It may be difficult to discern the signal
of LVOT obstruction from that of aortic
stenosis or mitral regrgitation. Use color
Doppler for guidance
Use Valsalva or exercise
to provoke a gradient
during the exam.
It may ”unmask”
obstructive
cardiomyopathy.
Find the site of
obstruction with 2D and
color Doppler (SAM), put
CW through this site. The
CW Doppler focus point
should be postioned at
the site of obstruction.
SAM
PMVL
AV
LVOT
AM
VL
SYSTOLE
Hypertrophy
SYSTOLIC ANTERIOR MOTION
OF THE MV – apical three-cham-
ber view/2D
Dynamic left ventricular out-
flow tract (LVOT) obstruction is
caused by anterior motion of the
mitral valve during systole.
LVOT FLOW ACCELERATION –
apical five-chamber view/CW
Doppler
Dagger-shaped spectrum in a
patient with obstructive hyper-
trophic cardiomyopathy. In this
example maximum obstruction
occurs rather late in systole (late
peak).
Systole
start
SYSTOLE
Vmax

63
NOTES
Mitral Regurgitation in Obstructive Cardiomyopathy
• Distortion of mitral valve geometry due to SAM)
• The jet is directed posteriorly
• The severity correlates with the degree of obstruction
Other Causes of LVOT Obstruction
• Hypertensive heart disease caused by a
sigmoidal septum
• Following surgery for aortic stenosis
due to the presence of left ventricular
hypertrophy and a sudden decrease in
afterload or increase in contractility
• Post-mitral valve repair when
the anterior mitral valve leaflet is
left too long
• Hypovolemia
• Hypercontractile state (e.g. hypothyroi-
dism, fever, catecholamines)
Mid-Ventricular Cardiomyopathy
• Least common type of
hypertrophic cardiomyopathy
• Often combined with LVOT
obstruction
• Rather late peak of maximum
gradient velocity
• Gradients are rarely very high
Echocardiographic Assessment in
Hypertropic Cardiomyopathy
• Myocardial thickness and location of
hypertrophy
• Systolic/Diastolic function
• Doppler measurement of maximal
gradients
• Degree of mitral regurgitation/SAM
• Atrial size
• (Deformation imaging)
SAM may also occur in
diseases and conditions
other than hypertrophic
cardiomyopathy.
Mid-ventricular and LVOT
obstruction may be
combined.
Septal thickness > 30mm =
increased risk for sudden
cardiac death.
Because the left ventricle
cavity is usually small, left
ventricular function appears
better than it is. In addition,
most patients have reduced
longitudinal function, especially
in those segments which are
very hypertrophic or fibrotic.
Mitral regurgitation may
also increase with
provocation and a rise in
gradients.

Also consider surgical
myectomy, especially in
patients who are candidates
for surgery (e.g. aortic
stenosis with LVOT
obstruction).
Patient history, distribution of
left ventricular hypertrophy,
other echo findings and speckle
tracking may be helpful in
establishing the correct
diagnosis.
Differential Diagnosis
• Hypertensive heart disease
• Aortic stenosis
• Amyloid heart disease
• Sarcoid heart disease
• Athlete‘s heart
• Fabry‘s disease
Alcohol Septal Ablation – Recommendations
• Severe heart failure symptoms
(NYHA classes III or IV) refractory to medication
• Subaortic Doppler gradient > 50 mmHg at rest
or with provocation (i.e. exercise)
• Adequate coronary anatomy/echo morphology
ESC 2003
64
NOTES

65
007//
Restrictive Cardiomyopathy
CONTENTS
66 Basics
67 Specific Forms

007 // RESTRICTIVE CARDIOMYOPATHY
66
NOTES
1) Restrictive cardiomyopathy is
NOT the same as a restrictive
filling pattern. A restrictive filling
pattern may also be present in
other forms of cardiomyopathy.
2) Subclinical systolic dysfunction
(despite normal ejection fraction)
may be present in early stages of
disease.
BASICS
Definition
• Idiopathic, systemic or
infiltrative disorder.
• May involve the left and/or right
ventricle.
• Primarily a ”diastolic disease”
of the ventricles
• Normal or slightly reduced systolic
function (in the early stages).
Most Common Causes
• Amyloidosis
• Idiopathic
• Endomyocardial fibrosis
• Radiation
• Chemotherapy
• Carcinoid
• Hemochromatosis
Pathophysiology
• Elevated filling pressure
• Stiff ventricle
• Hepatomegaly
• Peripheral edema
Echo Features
• Bi-atrial enlargement
• Normal left ventricular volume (in the
early stage)
• Normal left ventricular ejection
function (in the early stage)
• Expanded left atrial appendage
• Dilated inferior vena cava and pulmo-
nic veins
How to Distinguish Restriction from Constriction
(Doppler MV Inflow and TDI MV Annulus)
Patients typically present with
signs of right heart failure.
Clinical and echocardiographic
features may be similar to those
of constrictive pericarditis.
Restrictive cardiomyopathy is
the least common form of
cardiomyopathy (5% of all cases
of primary heart muscle
disease).
Suspect restrictive CMP in
patients with normal left
ventricular function and
unexplained significant
bi-atrial enlargement.
Normal Restrictive Constrictive
E A
E´
E´
E´
E
A
E
A
Progressive decline of
the E‘ wave in restrictive
CMP
DD: The E‘ wave is
preserved/exaggerated
in constrictive pericardi-
tis.

67
NOTES
67
NOTES
SPECIFIC FORMS
Amyloid Heart Disease – Echo Features
• Ground glass pattern
• Thickened interatrial septum
• Thickened valves frequently with mild
regurgitations
• Advanced diastolic dysfunction
• Pericardial/Pleural effusion
• ”Apical sparing pattern” of
longitudinal strain
• Systolic dysfunction (endstage)
• Right heart involvement
Hypereosinophilia/Endomyocardial Fibrosis (EMF) –
Echo Features
• Fibrous thickening of the endocardium
• Echogenic eosinophilic infiltrates in the
left and right ventricular apex
• Different stages (necrotic/thrombotic/
fibrotic)
• Late-stage restrictive filling pattern
Sarcoid Heart Disease – Echo Features
• Cardiac involvement in sarcoidosis is
associated with a poor prognosis
• Left ventricular aneurysms
• Wall motion abnormalities (not related to
coronary perfusion territories)
• Hypertrophy (segmental)
• Edema/Fibrosis
• End-stage: left ventricular dilatation,
wall thinning and impaired left
ventricular function
The echocardiogram is often
so typical that it leads to the
diagnosis of amyloidosis.
Eosinophilic thombi are
found in endomyocardial
fibrosis even in the absence
of regional wall motion
abnormalities or global LV
dysfunction.
20 – 30 % of patients with
proven sarcoidosis have
cardiac involvement. MRI is
more sensitive than echo in
the detection of sarcoid
heart disease.
LVH
Speckled
myocardium
AMYLOIDOSIS – apical
Typical features of amyloidosis,
including echogenic/hourglass
appearance of the myocardium,
thickened valves, and enlarged
atria. This patient also received a
pacemaker.
TV
PM
leads
MV
Thickened
valves
Thickened
IAS
SARCOIDOSIS – apical
Abnormal cardiac geometry with
segmental wall motion abnormal-
ities, thickening, and increased
echogenicity in the region of the
mid- and distal anterior septum.
Wall Motion
abnormality
Enlarged
atria
Segmental
hypertrophy
Fibrosis

68
Fabry‘s Disease: Manifestation
• Rare multisystemic disease
• X-linked genetic disease
• Alpha–galactosidase deficiency
• Renal failure
• Angiokeratoma
Fabry‘s Disease: Echo Features
• Myocardial fibrosis
• Diastolic dysfunction/enlarged left atria
Some authors suggest that the
binary sign, defined as binary
appearance of the left ventricular
endocardial border, aids in the
diagnosis of Fabry‘s disease.
However, the sensitivity and
specificity of this sign is rather low.
Speckled
myocardaum
LV hypertrophy
RV hypertrophy
FABRY’S DISEASE – apical
Pronounced bi-ventricular hy-
pertrophy and rather speckled
appearance of the myocardium.

69
008//
Coronary Artery Disease
CONTENTS
70 Segmental Approach
72 Wall Motion Abnormalities
76 Patterns of Myocardial Infarction
77 Complications

SEGMENTAL APPROACH
Segmentation (16-Segment Model)
The left ventricle is divided
into basal (6), mid (6) and
apical (4) segments.
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).
IS= inferoseptal, AS=anteroseptal , A = anterior,
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.
Apical four-chamber view
Apex
Mid ventricle
Base
The inferolateral segment is
also referred to as the
posterolateral or posterior
segment.
In echocardiographic
nomenclature there is no
diaphragmatic segment.
as = apical septum
(a/i)ms= mid inferoseptum
(i)bs = basal inferoseptum
al = apical lateral
ml = mid anterolateral
bl = basal anterolateral
ai = apical inferior
mi= mid inferior
bi = basal inferior
aa = apical anterior
ma = mid anterior
bal = basal anterior
al/pl = apical lateral
mpl= mid inferolateral (posterior)
bpl = basal inferolateral (posterior)
as = apical anteriorl
m(a)s = mid anteroseptum
b(a)s = basal anteroseptum
as al
(a/i)ms ml
(i)bs bl
bi ba
mi ma
ai aa al/pl as
mpl
bpl
b(a)s
m(a)s
008 // CORONARY ARTERY DISEASE
70
NOTES
( )

71
SEGMENTAL APPROACH
Bull’s Eye Representation
16-Segment model 17-Segment model (supra-apical cap)
Coronary Supply
Ant Ant
Inf Inf
Sept (ant) Sept (ant)
Lat Lat
Sept (inf) Sept (inf)
Inf.lat/
post
Inf.lat/
post
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
What Are We Looking For?
• Lack of wall/myocardial thickening
• Wall motion
• Hinge points
• Ventricular geometry
• Echogenicity/scar
Wall Motion Abnormalties
LV contrast study improves
endocardial border detection.
Try your best to obtain the
best possible image quality.
This is what counts most
when you are looking for
regional wall motion
abnormalities.
If possible, compare
wall motion with a
reference segment.
Aneurysm
Mitral
valve
Anterior
wall
Left atrial
appendage
Inferior
wall
Akinetic
myocardium
Coronary
sinus
INFERIOR WALL ANEURYSM –
apical two-chamber view/2D
Inferior myocardial infarction
leading to distortion of ventric-
ular geometry (aneurysm) and
regional wall thinning in the basal
and mid inferior segments.
Hyperkinesia Normokinesia Hypokinesia Akinesia Dyskinesia
72
NOTES

Wall Motion in Ischemic Conditions
Coronary artery Myocardial wall: thickness
and motion at rest
Remodeling
• Progressive LV dilatation
• Eccentric LV hypertrophy
• Distortion of geometry
• Hypokinesia of normally perfused segments
• further increase of mitral regurgitation
Ischemia, hibernation
and stunning are all
marked by hypo/akinesia
AND preserved wall
thickness.
Predisposing factors for
remodeling are large
infarctions ( anterior >
inferior), mitral
regurgitation, and
elevated afterload
(hypertension, AS).
Normal
Exercise-
induced
ischemia
Ischemia
Necrosis
”Hibernation”
”Stunning”
73
NOTES

Aneurysm
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
Myocardial Tissue After Acute Coronary Syndrome
Transmural scar: akinesia, dyskinesia,
aneurysm, thinning, bright echo
Subendocardial scar: hypokinesia,
thickness is normal/mildly thinned
Transmural scar + viability: akinesia +
hypokinesia of neighboring segments
Viable myocardium (Acute ischemia/
hibernation/stunning): hypokinesia,
akinesia, wall thickness preserved
Normal Viable ischemia/stunning/hibernation Scar/fibrosis
The degree of wall motion
abnormalities depends on
the transmurality of the
infarction. Various different
wall motion abnormalities
may exist simultaneously
(akinesia, hypokinesia,
aneurysm, scars).
Look for edema (myocardial
thickening, bright echoes) in
patients with myocardial
infarction after reperfusion.
There is no risk of rupture in
chronic aneurysms.
END-SYSTOLE
LV Aneurysm
APICAL ANEURYSM – apical
Very large apical aneurysm after
anterior myocardial infarction.
The apical region is dilated and
dys-/akinetic.
74
NOTES

Quantification of Left Ventricular Function in
Coronary Artery Disease
• Simpson method
• Visual assessment
• Wall motion scoring
• Center line
• 3D methods (e.g. regional
ejection fractions)
• Endocardial contour
enhancement (contrast)
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
branch block)
• Pacemaker
(e.g. postoperative, right ventricle
pressure/volume load)
• Myocarditis
• Cardiomyopathy (e.g. Takotsubo)
The Simpson method DOES
NOT account for regional
wall motion abnormalities
in the posterior and all
anterior septal segments
(segments seen on the
apical long-axis view).
75
NOTES

PATTERNS OF MYOCARDIAL INFARCTION
Supra-Apical Infarction Distal Septum Infarction
LAD (distal, mid., prox.), small supra-
apical aneurysm, low remodeling risk
LAD (distal,mid., prox.),
low remodeling risk
Proximal LAD Type Infarction Small Basal Inferior
Infarction
LAD (before 1st septal branch, left main),
always remodeling, poor prognosis RCA
Difficult region to interpret, low remode-
ling risk
Inferior Infarction Infero-Posterior
Infarction
RCA, low-moderate remodeling risk RCA (dominant) or Cx (large, prox.),
moderate remodeling risk
Inferior/posterior/postero-
lateral infarctions pose an
elevated risk for restrictive
mitral regurgitation
(tethering of the posterior
leaflet) .
Supra-apical and distal septal
infarctions may also occur in
proximal LAD occlusion
when rapid reperfusion is
achieved and only the distal
portions of the ventricle are
damaged.
Patients with left main
myocardial infarction rarely
survive.
76
NOTES

When assessing the patterns
of myocardial infarction,
always consider the possibility
of multiple/sequential
infarcts!
PATTERNS OF MYOCARDIAL INFARCTION
Posterolateral Infarction Infero-Posterior-Lateral
Infarction
CX, RCA, moderate remodeling risk Dominant RCA, CX (large, prox.), high
remodeling risk
Lateral Infarction
CX, LAD (diagonal branch), difficult to interpret, low remodeling risk
COMPLICATIONS
Overview
Acute/subacute
• Cardiogenic shock
• Thrombus formation (acute)
• Myocardial rupture
• Right ventricular infarction
• Papillary muscle rupture
• Ischemic ventricular septal defect
Chronic
• ”Remodeling” chronic heart failure
• Thrombus formation (late)
• Mitral regurgitation
Pseudoaneurysm
• Short, narrow neck (diameter < 50% of
the fundus diameter)
• Hematoma
• Outer walls formed by pericardium
and mural thrombus
• Often pericardial effusion
Perform serial echo
exams after infarction. It
will help you to detect
potential complications
earlier and assess the
patient‘s prognosis and
risk of further
complications.
High risk of secondary
perforation/rupture.
77
NOTES

78
NOTES COMPLICATIONS
Myocardial Rupture
• Mortality 95%
• Also small infarctions
• Hematopericardium
• True incidence unknown
• Tamponade
• Urgent surgery required
Ischemic Ventricular Septal Defect
• Incidence 0.5 – 1% • 50% Mortality
• Within 4–5 days • Risk factors (hypertension, 1st MCI)
Echo Features
• Left ventricular volume overload
• Disrupted/spliced interventricular
septum
• Turbulent flow/jet on color Doppler
• CW Doppler jet velocity depends on
the size of the VSD and pressure
relation between the left and right
ventricle
• Elevated flow velocity across the
pulmonic valve
• Acute pulmonary hypertension
Papillary Muscle Rupture
• Incidence 1%
• Rupture of the posteromedial papillary
muscle is more common than the
anterolateral one (which has dual
blood supply)
• 5% of deaths due to myocardial
infarction
• Mortality 70%
• Also in small infarctions
The most common site of
rupture is the distal anterior
septum (anterior myocardial
infarction), followed by the
basal inferior septum (inferior
myocardial infarction).
Basal VSD jets may be difficult
to discern from a tricuspid
regurgitation signal in the
Color Doppler.
Ischemic VSDs are rarely a
simple hole in the septum, but
rather the result of splicing of
the interventricular septum.
VSD color Doppler
VSD 2D
VSD
IVS
ISCHEMIC VENTRICULAR
SEPUTM DEFECT (VSD) – apical
four-chamber view
Rupture of the interventricular
septum is visible on the 2D image
(left). Turbulent flow across the
defect is seen with color Doppler
(right).

79
NOTES
COMPLICATIONS
Echo Features
• Severe mitral regurgitation
• Flail papillary muscle
• Left ventricular volume overload (LV
dilatation/hyperdynamic function)
• Low-velocity mitral regurgitation signal
• Triangular shape of the mitral regurgitati-
on spectrum (low systolic blood
pressure in shock and pressure
equilibration between the left ventricle
and the left atrium)
• Dilated pulmonary veins
Right Ventricular Infarction
• 30 – 50% of inferior myocardial infarction • Poorer prognosis
• Posterior wall, posterior septum affected • Usually in proximal RCA (Cx possible)
• Recovery of right ventricular function is
common after acute myocardial infarction
Echo Features
• Dilated right ventricle
• Wall motion abnormalities (inferior)
• Global/regional reduced right
ventricular function
• Tricuspid regurgitation (common)
• Dilated inferior vena cava
Mural Thrombus
• Thrombogenicity of the infarct tissue
• Low flow state in the infarcted area
• More common in large anterior
myocardial infarction
• Usually apex (aneurysm)
• Systemic embolism 2%
• Small thrombi are difficult to detect
Echo Evaluation
• Visible in > 1 plane.
• Assess mobility to estimate the risk of
embolism.
• Assess echogenicily (fresh/old thrombus).
• Measure size to monitor treatment
effects.
Transthoracic echo assessment
may be difficult (due to
tachycardia, pulmonary edema,
lack of a distinct mitral
regurgitation jet due to a large
regurgitant orifice and low flow
velocity, mitral regurgitation) –
perform a transesophageal exam.
Look at regional and global
RV function in EVERY patient
with inferior myocardial
infarction. When asssessing
the right ventricle, rotate
around its axis to visualize the
entire right ventricular
myocardium.
Thrombi may be difficult to
distinguish from prominent
apical trabecula. Use LV contrast.
Move the focus zone to the apex
(near field) to increase your
sensitivity.
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
to the mitral valve.
Chordae
ṔM head
PMVL
AM
VL

80
NOTES
Mitral Regurgitation in CAD – Mechanism
• Annular dilatation
• Leaflet restriction
• Rupture of papillary muscle (acute)
• Aggravation of mitral regurgitation in
pre-existing MR caused by ventricular
distortion (combined mechanisms)
Diagnosis of Posterior Leaflet Restriction
• Increase in tenting area
• ”Y” position of anterior to
posterior leaflet
• Jet origin further within the ventricle
• Immobility of the posterior
leaflet (tethering)
• Posterior jet direction
• Increase in tenting area (increase
of coaptation depth)
Restriction of the posterior
leaflets is a frequent finding
in patients with inferior
infarctions (regional
remodeling of the inferior
wall). Restriction of both
leaflets is a consequence of
global remodeling (and
usually combined with
annular dilatation).
Apical
thrombus
APICAL THROMBUS – zoomed
The thrombus has a slightly
different echogenicity than the
myocardium. Older thrombi ap-
pear more echodense.
COMPLICATIONS

81
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

BASICS
Natural History of Aortic Stenosis
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).
Left Ventricular Failure in Aortic Stenosis
Persistent pressure overload leads to deterioration of left
ventricular function and eventually heart failure.
100
75
50
25
10 20 30
YEARS
Heart failure
Syncope
Angina
Asymptomic stage
Onset of symptoms With aortic valve
replacement
Without aortic
valve
replacement
PERCENT
SURVIVAL
Afterload
LV pressure overload
Filling pressure LVH
Severe asymptomatic aortic
stenosis is generally associated
with a favorable prognosis. The
risk increases dramatically once
symptoms occur.
LVF
Low output Filling pressure
Heart failure
009 // AORTIC STENOSIS
82
NOTES

BASICS
Causes of Aortic Stenosis
Congenital abnormalities of the aortic valve are a frequent cause of aortic stenosis.
In some patients a stenosis is present at birth; in others congenital abnormal valves
predispose the individual to aortic stenosis later in life (accelerated aging/calcifica-
tion of the valve).
< 70 Years > 70 Years
Adapted from Passik et al. Mayo Clinic Proc 1987
Rheumatic Aortic Stenosis
• Usually mild to moderate stenosis
• May progress to severe aortic stensos
(accelerated valve aging)
• Often combined with aortic
regurgitation
• Thickened leaflets/focal calcification
• Often multivalvular disease
Congenital Abnormalities of the Aortic Valve
• Unicuspid, bicuspid, quadricuspid
• Syndromes (e.g. Down‘s, Heyde‘s)
• May be associated with genetic
syndromes (such as Down‘s, Heyde‘s)
Morphology of the Aortic Valve
Normal valve (tricuspid) Functional bicuspid
(tricuspid with raphe) – congenital
A raphe may be small and
subtle. In this setting the
valve may appear
tricuspid, especially on a
still frame.
In the Western world,
the cause of severe
aortic stenosis in
patients <50 years is
almost always
congenital.
The aortic valve is the
second most common
valve involved in
rheumatic heart disease.
To establish the diagnosis of a
bicuspid valve, use the short-
axis view and observe the
opening motion of the valve.
Degenerative Bicuspid Postinflammatory
Unicommissural Hypoplastic Indeterminate
27%
25%
23%
50%
3%
48%
18%
2%
2% 2%
83
NOTES

BASICS
Bicuspid – congenital Unicuspid – congenital
Echocardiographic Assessment of Aortic Valve
2D
• Valve morphology (cusps)
• Visual assessment of aortic valve
opening and motion
• Degree of calcification
• Left ventricular function
• Exclude subvalvular membrane
• Measurement of the aortic annulus (for
valve sizing in TAVR)
MMode
• Eccentric AV closure
• ”Box” seperation of cusps
A dilated ascending aorta
in a young patient may
point to a congenital
aortic valve abnormality.
Coronary artery disease is
frequent in calcified
aortic stenosis.
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.
PV
Calcification
Cusp
Aortic valve area
TRICUSPID AORTIC VALVE –
zoomed PSAX AV
Calcified aortic valve with re-
duced opening (aortic valve area=
AVA) in a patient with severe
aortic stenose.
84
NOTES

BASICS
Doppler Assessment of the Aortic Valve
Color Doppler
• Color Doppler aliasing caused by high
velocity jet (stenotic turbulences)
• Look for the origin of aortic stenosis jet
to exclude LVOT obstruction (SAM/
membrane)?
CW/PW Doppler
• Measurement of maximum and mean
velocity gradient across the aortic valve
(CW Doppler)
• Measurment of LVOT velocity (PW
Doppler)
• Diastolic dysfunction (filling pressure,
indirect sign of severity, correlation
with symptoms (PW Doppler)
• Elevated pulmonary pressure is a sign
of left heart failure (CW Doppler)
QUANTIFICATION OF AORTIC STENOSIS
Methods
• Planimetry (TEE)
• Pressure gradients
• Aortic valve area using
continuity equation
Evaluation of Gradients
• Gradient = 4 x Vmax2
(simplified Bernoulli equation)
• Gradients are influenced by
heart rate and stroke volume
• Jet velocity is elevated (> 2m/s)
when AVA < 2 – 2.5 cm2
Check were aliasing (flow
acceleration) occurs: at
the valve (valvular AS),
below the valve
(subvalvular stenosis)
or above the valve
(supravalvular aortic
stenosis).
Planimetry (TTE) is usually
not possible because the
valves in AS are too
heavily calcified (tracing
the aortic valve orifice
will be difficult).
A late peak of the
Doppler signal
indicates severe aortic
stenosis.
220 mmHg 120 mmHg
! 100 mmHg
time
velocity
(m/s)
peak velocity
Stenosis results in a pressure gradient.
The pressure gradient is high before the
obstruction and low behind the stenosis.
AV
trace
Peak velocity
LVOT
velocity
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
(8 m/s). Additionally, the LVOT
velocity can be seen within the
AS spectrum, indicating good
Doppler alignment.
85
NOTES

Practical Considerations
• Try to be parallel to the stenotic jet and
optimize the angle.
• Evaluate gradients from multiple
windows (apical, suprasternal and right
parasternal).
• Set the focus point of the CW Doppler
in the aortic valve.
• Use the pencil probe.
• In the setting of atrial fibrillation,
average the gradients of several beats
and the PW-LVOT velocity.
Calculation of Aortic Valve Area (Continuity Equation)
LVOT width is measured in the PLAX, slightly proximal to the aortic valve, exactly
where you should also place the PW Doppler sample (5-chamber view).
Patients with bicuspid stenosis
and those with severe AS
generally have eccentric AS jets.
In these patients you will usually
obtain the highest gradient from
a right parasternal approach.
High cardiac output (young or
anxious patients, hyperthyroi-
dism, fever, dialysis shunts, etc.)
may cause flow velocities >2 m/s
and thus mimic AS.
LV
LA
Ao
A1
x V1
A2
= V1
x A1
/V2
A2
x V2
LVOT diam = A1
LV=Tvel = V1
AVvel = V2
Measurement of LVOT width
is most critical for
the calculation of the
aortic valve area. Small
measurement errors result in
large differences.
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.
86
NOTES

Limitations of Continuity Equation
• Measurement of LV may be difficult.
• The true geometry of LVOT (round,
oval) is not appreciated by
the measurement of distances
• PW sample volume position plays an
important role
• Underestimation of AV peak velocity in
suboptimal Doppler alignment
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
Valvulo-Arterial Impedance
Zva = (SAP + MG)/SVI
• Z(va) = measure of global LV load
• SAP = systolic arterial pressure
• MG = mean transvalvular
pressure gradient
• SVI = stroke volume index.
ESC 2012
To find the optimal location
of the PW Doppler sample
volume, place it first in the
AS jet and slowly move the
sample volume proximally
until there is a sudden
velocity drop.
Valvuloarterial
impedance <3.5
increases the mortality
risk 2.3 to 3 fold.
IVS
Aorta
AV
LVOT
diameter
AMVL
LVOT DIAMETER – PLAX/2D
The LVOT diameter is measured
on a parasternal long-axis view,
closely below the aortic valve. It
is advisable to slightly over-
measure the LVOT diameter and
thus compensate the oval shape
of the LVOT.
87
NOTES

SPECIAL CIRCUMSTANCES
Low Gradient Aortic Stenosis
• Mean gradient
< 30 mmHg – 40mmHg
• EF < 40%
• AVA < 1.0 cm2
Factors in Favor of True Severe
”Low-Flow Low-Gradient” Aortic Stenosis
• Heavily calcified valve
• Late peak of AS signal
• LVH (in the absence of hypertension)
• Previous exams with higher gradients
”Paradoxical” Low-Flow Low-Gradient Aortic Stenosis
Patients with aortic stenosis and very small ventricles/cardiac output may also have
low gradients in the setting of severe aortic stenosis.
Low gradients in severe AS/
normal EF
• AVA < 1.0 cm2
• EF > 50 %
• Mean gradient < 40mmHg
Low stroke volume (<35ml/m2
)
• Concentric LVH ?
• Small, restrictive LV
• Calcified valve
• (Hypertension)
Aortic Stenosis and Aortic Regurgitation
• Tend to occur simultaneously
• Common in bicuspid valves
• Significant aortic regurgitation leads to higher
gradients (overestimation of the severity of aortic stenosis)
Correct classification makes
a difference. Patients with
true aortic stenosis are
potential candidates for valve
replacement.
Patients with paradoxical
low-flow low-gradient AS
tend to have a higher level of
LV global afterload, which is
reflected by a higher valvulo-
arterial impedance.
The gradients
overestimate AS severity
only when aortic
regurgitation is moderate
or in excess of moderate.
To differentiate between
true severe and pseudo-
severe AS, you should
perform a dobutamine
stress echo.
Features of AS
+
red. LVF
Pseudo-severe AS True severe AS Severe AS
Gradient < 30–40 mmHg Gradient > 40 mmHg
88
NOTES

SPECIAL CIRCUMSTANCES
Pressure Recovery
Increase of pressure downstream from the stenosis caused by reconversion of
kinetic energy to potential energy
Where is it relevant?
• Small aorta < 30mm
• Moderate aortic stenosis
• High flow rate
• Bileaflet prosthesis
• 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
Other Findings in Subvalvular Aortic Stenosis
• Abnormal mitral valve chords
• Associated defects (50%) (e.g. PDA, VSD, bicuspid AV, pulmonic stenosis)
Echo Features
• Color flow aliasing at the site of
obstruction
• Elevated CW velocity despite normal
AV morphology
• Membrane of varying thickness within
the LVOT, often with a small muscular
ridge. Best visualized on atypical PLAX
views
Pressure recovery
may lead to
overestimation of
gradients.
Subvalvular obstruction
leads to aortic valve
destruction (jet lesion)
and aortic regurgitation.
Subvalvular
Membrane
AMVL
AV
SUBVALVULAR AORTIC
STENOSIS – PLAX/2D
A muscular ridge with a mem-
brane causing obstruction is seen
in the LVOT. In some patients
you will need to scan through
the entire LVOT to detect the
membrane.
89
NOTES

When the patient does not
fulfill the criteria/indications for
surgery, annual follow-up
should be performed. Shorter
intervals are necessary when AS
is severe, heavily calcified or
when symptoms are uncertain.
Use other imaging modalities
(CT/MRI) and look for other
congenital abnormalities
(Williams syndrome).
The indication for aortic
valve surgery must be
established individually.
Consider age, co-
morbidities, the risk of
myocardial fibrosis in
LVH, longitudinal
dysfunction, the degree
of calcification, the
patient‘s preference and
expectations, the rate of
progression, etc.
SUB- AND SUPRAVALVULAR AORTIC STENOSIS
Types of Supravalvular Aortic Stenosis
INDICATIONS FOR AORTIC STENOSIS
SURGERY/INTERVENTION
Indications for Surgery in Severe AS (Class I/ESC 2012)
• Symptomatic patients with severe AS
(dyspnea, syncope, angina)
• Symptomatic patients with severe AS
and reduced LV function (<50% EF)
• Asymptomatic patients with severe AS
and abnormal exercise test
• When other cardiac surgery
is being performed (e.g. CABG;
ascending aorta)
Other Things to Consider in Asymptomatic Severe AS
• Valve morphology (bicuspid)
• Severity of AS (very severe AS)
• Degree of calcification
• Subclinical myocardial dysfunction (longitudinal function)
• Rapid progression
Hourglass type
(most common)
Membranous type Tubular type
90
NOTES

INDICATIONS FOR AORTIC
STENOSIS SURGERY/INTERVENTION
Transcatheter Aortic Valve Replacement (TAVR)
Consider interventional valve replacement in:
• Symptomatic/severe aortic stenosis
• High-risk patients
• Suitable anatomy (AV annulus diameter)
• Appropriate anatomical access for valve implantation (transfemoral/transapical)
Echo Assessment for TAVR
• Establish the presence of
severe aortic stenosi.
• Assess annular dimension during
systole in a zoomed PLAX for valve
sizing Undersizing may lead to device
migration or significant paravalvular
aortic regurgitation. Oversizing increases
the risk of underexpansion, reduces
durability, and increases vascular
access complications
• Assess the extent and
distribution of calcification
• Exclude patients with bicuspid valves
(an ellipitical orifice may predispose to
incomplete valve deployment)
• Exclude patients with basal septal
hypertrophy and dynamic LVOT
obstruction
Consider alternatives for the
measurment of the aortic
valve annulus (2D/3D TEE,
CT), as these methods are
more accurate than 2D
echocardiography.
The indications for TAVR may
change with improvements in
methodology.
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
91
NOTES

92
NOTES

93
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

010 // AORTIC REGURGITATION
94
NOTES
Study the morphology
of the aortic valve on a
PSAX view at the base.
Elevated left ventricular filling
pressure (diastolic dysfunction)
usually denotes LV deterioration
(and symptoms).
LV dilatation is usually less when
AS and LVH are additionally
present.
In our experience the ventricle
compensates more by dilatation
than with an increase in ejection
fraction.
Look at the vena contracta and
PISA. Use an integrative
approach for quantification.
BASICS
Cause of Chronic Aortic Regurgitation
• Degenerative/Sclerosis/Aging
• Aortic dilatation
• Congenital
• Postendocarditis
• Rheumatic
• Aortic valve prolapse/rupture
Hemodynamics in Aortic Regurgitation
• Left ventricle volume overload
• Filling pressure elevated
• Afterload increased
Quantification of Aortic Regurgitation
Should be Based on
• Aortic regurgitation jet (Vena contrac-
ta, width, flow convergence)
• Deceleration time or aortic regurgitation
spectrum (PHT)
• Retrograde flow in the aorta
• Indirect findings
Indirect Findings in Aortic Regurgitation
• Hyperdynamic function
• Eccentric left ventricular hypertrophy
• Slightly enlarged left atrium
• Mitral regurgitation (annular dilatation)
Imaging of Aortic Regurgitation Jet
• PLAX
• PSAX (visualize origin of jet)
• Five-chamber view/
three-chamber view
• Suprasternal (to determine
retrograde flow)

95
NOTES
1) AR may be difficult to quantify
in tachycardia and higher heart
rates. 2) Retrograde flow is very
important. 3) Use both color
Doppler and PW Doppler to study
retrograde flow.
To detect retrograde flow in
the descending aorta, place
the sample volume
(PW-Doppler) at the inner
curvature of the cranial
portion of the descending
aorta.
Holodiastolic retrograde flow in
the aorta = severe AR.
BASICS
Aortic Regurgitation – Reference Values
Vena contracta < 3mm 3 – 6mm > 6mm
Jet width (% of LVOT) < 25 25 – 65 > 65
Flow convergence not visible small large
Pressure half-time (PHT)
aortic regurgitation (msec) > 500 200 – 500 < 200
ESC 2013
RETROGRADE FLOW IN AR –
suprasternal view/Color Doppler
Severe retrograde flow during
diastole. The red color Doppler
signal denotes flow towards the
transducer from the descending
aorta towards the the arch. Color
Doppler may be used to guide
positioning of the PW Doppler
spectrum.
Left carotid artery
Left subclavian artery
Retrograde flow
Aortic arch
Pulmonary
artery
RETROGRADE FLOW IN AR –
Suprasternal view/PW Doppler
Holodiastolic flow with a
maximum velocity of 0.7 m/s,
indicating severe aortic
regurgitation.
Holodiastolic
retrograde
flow
Forward flow
PW sample

96
NOTES BASICS
Pitfalls
• Complex, eccentric, or multiple jets.
• Poor alignment of CW Doppler with
the aortic regurgitation jet
• Calcified valves (it will be difficult to see
the proximal flow convergence zone)
• Machine settings (PRF)
Aortic Regurgitation and Other Forms of
Valvular Heart Disease
• Aortic regurgitation increases gradients
in aortic stenosis.
• Aortic regurgitation shortens the PHT
of mitral inflow in mitral stenosis.
• Volume overload of aortic regurgitati-
on and mitral regurgitation add up (two
halves make a whole).
The AR signal should have a
velocity above 4.5 m/second.
Otherwise the signal quality
will be inadequate for
assessment of pressure half
time (non-parallel jet
alignment) .
VENA CONTRACTA –
apical three-chamber view
Severe aortic regurgitation with
a large flow convergence zone, a
vena contracta >6 mm, and a jet
width of 70% of the LVOT. Vena contracta
Flow
convergence
AMVL
Jet
width
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
by a very steep slope.
AR signal AR PHT

97
NOTES
The PISA method for AR
quantification is rarely used,
but you can use flow
convergence (PISA zone) for
semiquantitative assessment.
Hemodynamic calculations of
AR are rarely used. Their main
limitation is the inaccuracy of
calculating the MV cross-
sectional area.
HEMODYNAMIC CALCULATION OF
REGURGITANT VOLUME AND FRACTION
SVMV
= CSAMV
x VTIMV
SVLVOT
= CSALVOT
x VTILVOT
CSA= d2
x 0.785
CSA = cross-sectional area SV = stroke volume d=diameter (MV/LVOT)
Reference Values
Regurgitant volume (ml/beat) < 30 30 – 59 ≥ 60
Regurgitant fraction (%) < 30 30 – 49 ≥ 50
PROXIMAL ISOVELOCITY
SURFACE AREA (PISA) METHOD
Aortic regurgitationflow
= 2! x r2
x Vr
r = radius of flow convergence,
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
No one ever uses this
calculation, but you
can impress your
friends with it!
ERO (PISA) = =
AR Flow – SV MV
AR vel
RF (%) = =
SV LVOT – SV MV AR vol
SV LVOT SV LVOT

ACUTE AORTIC REGURGITATION
Causes
• Endocarditis
• Cusp rupture
• Aortic dissection
• Iatrogenic (trauma)
Echo Features of Acute Aortic Regurgitation
• Small/slightly dilated left ventricle
• Tachycardia
• ”Initially” hyperdynamic left ventricle
• Holodiastolic retrograde flow in the
descending aorta
• 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 reduced
resting LVF (LVEF < 50%)
• In patietnts undergoing CABG or
surgery of the ascending aorta, or
another valve.
• In asymptomatic patients with severe
LV dilatation: (left venricular enddiasto-
lic diameter=LVEDD > 70 mm, LV
endsystolic diameter=LVESD > 50 mm
or LVESD/BSA >25 mm/m2
))
• If EF is too poor (< 30 – 35%)
!
Candidates for heart transplantation
LV size = normal or slightly
dilated and hyperdynamic
(the ventricle has not had
time to dilate/adapt).
98
NOTES

99
011//
Mitral Stenosis
CONTENTS
100 Introduction
102 Quantification
103 Mitral Valve Pressure Half-Time
104 Valvuloplasty

LV
LA
Ao
RV
Doming
011 // MITRAL STENOSIS
100
NOTES INTRODUCTION
Causes
• Rheumatic (most common)
• Stenotic annular calcification
• Congenital
Congenital Mitral Stenosis
• Rare (0.6% of CHD)
• Combined with other congenital defects
• Forms: MV annulus hypoplasia, parachute MV, double-orifice MV
Effects of Mitral Stenosis
• LA-LV gradient
• Elevated pressure in LA
• Elevated pressure pulm. capillaries
• Pulmonary congestion/edema
• Right ventricular dilatation
Echo Characteristics of Mitral Stenosis
Valve features:
• Doming (diastolic bulging) of the
anterior mitral valve leaflet
• Reduced valve opening
• Commissural fusion
• Leaflet tip thickening
• Subvalvular involvement
(thickened and fused tendinae)
• Secondary calcification
Doppler Features
• Color Doppler is indicative of mitral
stenosis (candle flame appearance)
• CW Doppler is used to quantify mitral
stenosis (gradients/pressure half-time)
Vavular involvement is
present in 2/3 of patients with
rheumatic fever.
Rheumatic heart disease is very
common in developing countries.
The Shone complex is characterized
by a combination of congenital
mitral stenosis and other forms of
left-sided inflow and outflow
obstructions (coarctation, valvular/
subvalvular aortic stenosis).
In mitral stenosis there is
no ”burden” on the left
ventricle (no pressure or
volume overload).
The MMode is no
longer used to
diagnose or quantify
mitral stenosis.
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.

Thickened
aortic valve
DIASTOLE
Doming
AMVL
Tip
thickening
Reduced opening
MITRAL STENOSIS – PLAX/2D
Typical features of mitral ste-
nosis: Doming of the anterior
leaflet, thickening of leaflet tips,
thickened aortic valve (aortic
valve involvement), and enlarged
left atrium.
Calcified
AV
Mitral
stenosis
Shadow
Thrombus
THROMBUS IN MITRAL STENOSIS
– PLAX/2D
Severe mitral stenosis with
large left atrial thrombus (partly
shadowed by the calcified aortic
valve).
101
NOTES
INTRODUCTION
Other features of mitral stenosis/rheumatic heart disease
• Thickened aortic valve
(high risk of atrial fibrillation)
• Enlarged left atrium, atrial fibrillation
• Aortic regurgitation
• Tricuspid stenosis
• Left atrial thrombuss
Risk of Thrombus Formation
• Systemic embolism in 20% of all MS patients
• 80% of patients with severe MS are in atrial fibrillation
• 45% have left atrial spontaneous echo contrast
Many of these features
develop and progress over
time. Also consider these
problems in your
management strategy.
Most thrombi are seen in the
left atrial appendage. Thus,
you will miss them on
transthoracic echo.

The funnular form is usually
seen when there is strong
involvement of the
subvalvular apparatus.
Planimetry is the most direct
method to quantify MS.
It does not rely on
hemodynamic assumptions.
However, it is also technically
the most challenging method.
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
Problems of Mitral Valve Planimetry
Mitral valve area is measured on an optimized parasternal short-axis view at the
smallest mitral valve orifice.
• Image quality
• Alignment
• Timing
• Calcification
• Incomplete commissural fusion
• Operator experience
Forms of Mitral Stenosis
Classic form Funnular form
LV LV
LA LA
Ao Ao
RV RV
RV
IVS
MVA
Calcified MV
MITRAL VALVE PLANIMETRY –
PSAX MV/2D
The mitral valve was investi-
gated at the tip of the leaflets,
where the mitral valve opening is
smallest. The image is frozen in
diastole at the time when mitral
valve opening is largest. Tracing-
may be difficult when the valve is
calcified.
102
NOTES

Transvalvular gradients are
higher in the setting of
additional mitral
regurgitation.
The pressure half-time method is
based on hemodynamic
assumptions and was initially
tested in young patients with
rheumatic heart disease. It
works less well in elderly and
multimorbid patients with
additional valvular lesions, left
ventricular dysfunction and left
ventricular hypertrophy.
QUANTIFICATION
Mitral Stenosis Mean Gradient – Reference Value
Mild (mmHg) < 5
Moderate (mmHg) 5 – 10
Severe (mmHg) > 10
MITRAL VALVE PRESSURE HALF-TIME
The rate at which the gradient between the left atrium and the left ventricle
diminishes corresponds to the size of the mitral valve orifice. The smaller the
orifice, the longer is the pressure half-time.
PHT – pitfalls
• Diastolic dysfunction leads to overesti-
mation of mitral stenosis
• Aortic regurgitation leads to underesti-
mation of mitral stenosis
• PHT is unreliable after valvuloplasty.
• Heavily calcified valves make PHT
unreliable
• Concave shape of tracing
Color Doppler, PISA and Continuity Equation
• Candle flame appearance of mitral valve
inflow with color Doppler
• PISA for quantification (rarely used)
• 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)
MVA =
D2
LVOT VTIAortic
4 VTIMitral
x
MV PHT
MITRAL STENOSIS SPECTRUM –
apical view/CW Doppler
Mean gradients are obtained by
tracing of the CW Doppler mitral
valve inflow spectrum. The decel-
eration time (pressure half-time)
is used to calculate mitral valve
area.
MV trace
MV Area =
220
PHT
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
Clinically significant MS (valve
area less than 1..5 cm2
( 1.8 cm2
in
unusually large patients)
Results
Good immediate results (valve area
> 1.5 cm2
without regurgitation)
can be obtained in over 80%
Suitability of Valve Morphology
• Mobility • Subvalvular thickening
• Valve thickening • Valve calcification
• Thrombus • Mitral regurgitation
AV
Artefact
Balloon
PMVL
A
M
V
L
BALLOONVALVULOPLASTY
IN MITRAL STENOSIS – TEE
long-axis view
The balloon is positioned within
the mitral valve and expanded to
enlarge the mitral valve orifice.
104
NOTES

VALVULOPLASTY
Wilkins Score
Patients with a Wilkins score > 8 – 10 are not ideal for mitral valve valvuloplasty.
Grade Mobility Thickening Calcification Subvalvular
thickening
1 Highly mobile
valve with only
leaflet tips
restricted
Leaflets near
normal in
thickness (4-5
mm)
A single area of
increased echo
brightness
Minimal
thickening just
below the mitral
leaflets
2 Leaflet mid and
base portions
have normal
mobility.
Mid-leaflets
normal,
considerable
thickening of
margins (5-8
mm)
Scattered areas
of brightness
confined to
leaflet margins
Thickening of
chordal
structures
extending to
one third of the
chordal length
3 Valve continues
to move
forward in
diastole, mainly
from the base.
Thickening
extending
through the
entire leaflet
(5-8 mm)
Brightness
extending into
the mid
portions of the
leaflets
Thickening
extended to
distal third of
the chords
4 No or minimal
forward
movement of
the leaflets
occurs in
diastole.
Considerable
thickening of all
leaflet tissue
(>8–10 mm)
Extensive
brightness
throughout
much of leaflet
tissue
Extensive
thickening and
shortening of all
chordal
structures
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
For the suitability of mitral
valve valvuloplasty also look
at the commissural region.
Patients with calcification of
the commissures are not ideal
candidates.
105
NOTES

106
NOTES

107
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

Severe mitral
regurgitation is no
benign condition.
In the setting of
significant mitral
regurgitation, an ejection
fraction of 55% to 60%
(which is otherwise
considered normal)
already denotes left
ventricular failure. EF 68%
Normal Acute MR
Even when mitral
regurgitation is severe,
the patient may remain
asymptomatic for a
long period of time.
Echocardiography
provides important clues
as to the cause of mitral
regurgitation.
Combinations of several
etiologies are not
uncommon (e.g. annular
dilatation and restrictive
leaflets).
BASICS
Natural History of Severe Mitral Regurgitation
• 10-year survival rate of 57%
• The 5-year all-cause mortality in patients
with asymptomatic mitral regurgitation
patients is 22%
• The 5-year risk for cardiac events in
asymptomatic mitral regurgitation
patients is 33%
Hemodynamics of Mitral Regurgitation
In acute mitral regurgitation (MR), the ejection fraction is high and the size of the
left ventricle is normal or slightly enlarged (unadapted). In chronic mitral regurgita-
tion the ejection fraction is ”supranormal” and the left ventricle is dilated (adapted).
In decompensated mitral regurgitation the left ventricle is significantly enlarged
and the ejection fraction starts to drop.
Consequences of Mitral Regurgitation
• Elevated left ventricular filling pressure
• Reduced systolic wall stress
• Reduced afterload
Causes
Primary (structural) causes
• Mitral valve prolapse, myxomatous
mitral valve disease
• Flail leaflet
• Valve fibrosis and calcification
• Rheumatic heart disease
• Congenital
• Papillary muscle rupture
• Endocarditis
• Drugs
• Systemic diseases
Secondary (functional) causes
• Annular dilatation
• Restrictive leaflets
• Systolic anterior motion
Chronic MR Decompensated MR
EF 77% EF 30%
EF 83%
012 // MITRAL REGURGITATION
108
NOTES

QUANTIFICATION OF MITRAL REGURGITATION
Integrative Approach
Color Doppler Jet (flow convergence, vena contracta)
2D Imaging Indirect signs
Quantification Based on Color Doppler
Vena contracta (mm) < 3 3 – 6.9 ≥ 7
Jet area (%) Small, central jet
(<20% of LA area)
Variable Large, central jet
(> 40% of LA area)
ESC 2013
Color Doppler Confounders
• Geometry of regurgitant orifice
• Multiple jets
• Coanda effect (”wall hugging” jets)
• Driving force (systolic pressure)
• LA compliance
Your ability to image jets
is more important than
quantitative parameters.
Use multiple views.
The proximal portions of the
jet (the vena contracta and the
flow convergence zone) are
more important for the
quantification of mitral
regurgitation than jet area,
length or width.
Do not base the quantification
of mitral regurgitation on a
single parameter.
The PRF setting greatly
influences the size of the jet.
Always use the same PRF. If
not, you will be unable to
make comparisons.
The maximal mitral
regurgitation velocity (CW
Doppler) represents systolic
blood pressure and does not
correlate with the severity of
mitral regurgitation.
Flow convergence
PMVL
AMVL
TV
Vena contracta
Jet area
QUANTIFICATION OF MITRAL
REGURGITATION – apical
four-chamber view/Color
Doppler
Typical color Doppler features
of mitral regurgitation with a
prominent flow convergence
zone (PISA), a vena contracta ≥
7mm, and a jet area > 40%
of LA area.
109
NOTES

110
NOTES QUANTIFICATION OF MITRAL REGURGITATION
Indirect Signs
• Hyperdynamic left ventricular function
• Left atrial enlargement
• Interatrial septum bulging (towards RA)
Retrograde Flow in Pulmonic Veins
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.
Proximal Isovelocity Surface Area (PISA) Method
The PISA method allows calculation of: 1) regurgitant flow 2)
regurgitant fraction 3) effective regurgitant orifice area
• Flow through hemispheric surface =
flow through the orifice
• Shift aliasing limit to lower velocity
20 – 40cm/s (larger hemisphere)
• Effective regurgitant orifice area
(EROA) = [(2r2
x Vpisa)/Vmr]
• r= PISA radius, Vpisa= aliasing velocity,
Vmr= peak MR velocity
Regurgitant volume= EROA x MR VTI
Regurgitant flow = Q = 2 x r2
x! x Nyquist vel.
Limitations of PISA
• The geometry of orifice is not truly
hemispheric.
• Multiple or excentric jets
• Difficulties in delineation of PISA
• Dynamic mitral regurgitation (flow
changes throughout the cardiac cylce
Use magnifications
(zoom/RES) to enhance
the accuracy of your
measurement.
To calculate the
regurgitant volume, you
need to trace the mitral
regurgitation spectrum
obtained with CW
Doppler.
There is much controversy as
to whether PISA should be
used. New 3D echo techniques
are likely to make PISA more
reliable (better approximation
of PISA geometry).
The size of the left atrium
does not permit
quantification of mitral
regurgitation.
In most instances you will
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.
Distal
Isovelocity
shells
Proximal
Orifice
Aliasing

The severity of mitral
regurgitation may differ
markedly in one and the same
patient, especially in cases of
functional mitral
regurgitation.
111
NOTES
QUANTIFICATION OF MITRAL REGURGITATION
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
• Blood pressure (afterload)
• Volume status
• Dyssynchrony
• Anesthesia
• Exercise
Echo Signs of Acute Mitral Regurgitation
• Hyperdynamic left ventricle
with a normal size
• Tachycardia
• Abnormal valve morphology (e.g.
papillary muscle rupture, flail leaflet)
• Low velocity of the MR signal (shock)
• Triangular shaped MR spectrum
• Elevated MV inflow velocity
MECHANISMS OF MITRAL REGURGITATION
Why Is the Mechanism Important?
• Etiology
• Prognosis (reversible)
• Management
• Repair?
What Should Be Examined?
• Valve morphology (thickened, myxo-
matous)
• Extent of involvement (which parts of
the valve are involved?)
• Origin of regurgitant defect
• Mechanism of mitral regurgitation
Patients with acute MR are
difficult to image and
interpret. These patients
usually have low MR
velocity jets (shock),
tachycardia, and
tachypnea.
Usually transthoracic echo is
sufficient to determine the
mechanism. If not, use
transesophageal echo.
The extent of morphologic
abnormalities of the mitral
valve does not necessarily
correlate with the severity of
mitral regurgitation.

112
NOTES
Do not forget to image
the commissural regions.
It is easy to miss mitral
regurgitation.
How to Visualize Mitral Valve Segments
CS = coronary sinus LC = lateral commissure MC = medial commissure
Mitral Valve Prolapse
Anterior leaflet prolapse
(jet direction posterior + lateral)
Posterior leaflet prolapse
(jet direction anterior + medial)
Bileaflet prolapse (central jet) Commissural prolapse/defect
(jet at the origin of the commissure)
As a general rule in MV
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).
4-Chamber
view
Commissural view 2-Chamber
view
3-Chamber
view
LC
MC
CS
A1 P1
P2
P3
A2
A3

113
NOTES
Flail Mitral Leaflet
Anterior flail leaflet
(jet direction posterior + lateral)
Anterior flail leaflet
(jet direction anterior + medial)
The direction of the jet may
vary throughout systole
(like a loose garden hose).
AMVL
Prolapse
PMVL
PMVL PROLAPS – apical four-
chamber view/2D
Severe prolapse of the posterior
mitral valve leaflet (medial scal-
lop – P2). The valve is thickened
(myxomatous) and the left atri-
um/ventricle are enlarged.
Excentric jet
ant./med. direction
PMVL PROLAPSE – apical four-
chamber view/Color Doppler
The jet direction is typically
anterior and medial (towards the
interatrial septum).
Flail
AMVL
PMVL
PMVL FLAIL – apical four-
chamber view/2D
Flail posterior leaflet; the pos-
terior leaflet protrudes behind
the anterior leaflet into the left
atrium. Small chordal structures
are seen attached to the tip of
the posterior leaflet.
AMVL

114
NOTES MECHANISMS OF MITRAL REGURGITATION
Mitral Valve Leaflet Restriction
Restriction of both leaflets
(central jet direction)
Posterior leaflet restriction
((jet direction lateral, posterior)
It is not uncommon to see a
combination of mechanisms
(e.g. annular dilatation and
leaflet restriction)
PMVL
AMVL
Flow convergence
Anterior
jet
PMVL FLAIL – apical four-
chamber view/Color Doppler
Chordal ruputure of the posteri-
or leaflet directs the jet towards
the interatrial septal and anterior
(seen best on an apical long-axis
view).
AMVL
AV
Restricted
PMVL
RESTRICTED PMVL – apical
three-chamber view/2D
Inferior infarction and change
of LV geometry restricts the
motion of the PMVL. The leaflet
is drawn towards the apex. This
results in incomplete closure of
the mitral valve.
RESTRICTED PMVL – apical
three-chamber view/Color
Doppler
The jet in restricted posterior
leaflet motion is typically direc
ted posteriorly. It aligns with the
position of the posterior leaflet.
AMVL
PMVL
AV
Posterior
jet

115
NOTES
Other Causes
Annular dilatation
(central jet direction)
MR in hypertrophic CMP
(posterior jet direction)
Valve perforation
(jet through leaflet)
Other mechanisms of mitral
regurgitation include:
annular calcification, leaflet
retraction, and leaflet
shrinkage (drugs/toxins).
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.
AMVL
PMVL
Perforation
Perforation
Jet through
AMVL
AMVL Perforation – apical
The anterior leaflet is thickened
and destroyed. A small gap can
be seen in the anterior leaflet.
This patient has a perforated
mitral valve after endocarditis.
AMVL PERFORATION – apical
four-chamber view/
color Doppler.
The color jet clearly traverses the
basal anterior leaflet through the
perforation. The most frequent
site of perforation is the anterior
leaflet.

116
NOTES MECHANISMS OF MITRAL REGURGITATION
Unfavorable Factors for Repair
• Extensive involvement (more than two segments)
• Repair of the anterior leaflet is more difficult than the posterior one
• Commissural defects
• Calcification
MITRAL VALVE PROLAPSE
Forms of Mitral Valve Prolapse
• Barlow‘s syndrome (classic mitral valve
prolapse, myxomatous)
• Fibroelastic deficiency
• Pseudoprolapse (small ventricles,
MV enlargement)
• Connective tissue disease
(e.g. Marfan, Ehlers-Danlos)
Myxomatous Mitral Valve
(Floppy Valve, Barlow’s Syndrome)
• Prevalence = 2 – 3%
• Rapid multiplication of cells
• Rocking motion of the annulus
• Involvement of the entire subvalvular
apparatus
• Billowing
• Excessive tissue
• Segmental involvement
• Elongated chords
Repair techniques include
quadrangular resection with
sliding plasty, chordal transfer,
and the use of artificial chords.
Mitral valve repair usually
includes implantation of an
annuloplasty ring.
The success of mitral valve
repair strongly depends on the
surgeon‘s experience.
The normal mitral valve plane is
shaped like a saddle. Do not
base your diagnosis solely on
the four-chamber view since the
non-planer shape of the MV
mimics a prolapse in this view.
Barlow‘s syndrome is a
structural disease of the
mitral valve. It has many
features. Do not base
your diagnosis on the
presence of a prolapsing
valve alone.
MITRAL VALVE PROLAPSE –
TEE 3D surgical view
A myxomatous mitral valve with
a prolapse of the posterior leaflet
(P3/P2). Chordal rupture is also
present. 3D may be helpfu l in
localizing a prolapse or defect.
Prolapse
Fail

FLAIL LEAFLET
Etiology of the Flail Leaflet
• Myxomatous mitral valve
• Endocarditis
• Degenerative
• Rheumatic
Echo Criteria – Flail Leaflet
• Chordal structures in the LA
• Concave position of leaflet
• Double contour (parallel sign)
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
Ruptured chordae may be
found in more than 50% of
myxomatous valves.
A flail leaflet can be very
subtle, especially when
secondary chords are involved.
The degree of mitral
regurgitation depends on the
location and type of chord that
is ruptured. A flail leaflet does
not always imply severe MR.
concave
Parallel
sign
PARALLEL SIGN – zoomed apical
The ruptured leaflet always
extends behind the non-ruptured
leaflet to which it frequently lies
parallel (as seen in the example
with a ruptured AMVL). This sign
may be helpful in cases of subtle
chordal rupture.
PMVL
AMVL
117
NOTES

118
NOTES OTHER CAUSES OF MITRAL REGURGITATION
Congenital Abnormalities of the Mitral Valve
• Chordal abnormalities
• Papillary muscle abnormalities
• Cleft MV, parachute MV
• Abnormal leaflet shape/length
INDICATIONS
Indications for Mitral Valve Surgery (ESC Class I)
• Surgery is indicated in symptomatic
patients with LVEF > 30% and LVESD
<55 mm
• Surgery is indicated in asymptomatic
patients with left ventricular dysfuntion
(left ventricular end systolic diameter
[LVESD]≥ 45 mm and/or left ventricular
ejection fraction ≤ 60%)
• Mitral valve repair should be the
preferred technique when it is inten-
ded to last for a long time
LVF < 30%: no surgery (conservative, HTX or MitraClip procedure)
ESC 2012
MitraClip Procedure
Cleft mitral valve is almost
always present in primum
septal defects (ASD I).
Repair is better than
replacement. Chordae
should be preserved
whenever possible.
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
anulus
Mitral valve
orifice
MitraClip

119
NOTES
The MitraClip procedure is
an interventional therapy by
which a clip is used to attach
the anterior leaflet to the
posterior one. It is similar to
the surgical procedure know
as the ”Alfieri” stitch. Studies
have shown that this
technique is able to reduce
mitral regurgitation and
improve symptoms in both
functional and structural MR.
INDICATIONS
Suitability for the MitraClip procedure
(german society of cardiology)
OPTIMAL POSSIBLE
• Central pathology (segment 2),
• No calcification
• MVA > 4 cm2
• Mobile length of post leaflet > 10 mm ,
• Coaptation depth <11 mm,
• Normal leaflet thickness + mobility,
• Flail leaflet width <15 mm,
gap <10 mm
• Pathology in segment 1 or 3,
• Calcification (mild) outside
the clip zone,
• Post annulopasty/ring
• MVA > 3cm2
, good mobility of leaflets,
• Mobile length of the posterior leaflet
7-10 mm
• Coaptation defect > 11 mm
• Leaflet constriction during systole, flail
leaflet >15 mm (only with large MV
annulus and multiple clips)
Unsuitable valve morphology for MitraClip:
• Perforated mitral leaflet/
cleft mitral valve
• Severe calcification in
the clip zone
• Significant mV stenosis
(mean gradient ≥ 5 mmHg)
• Mobile length of the posterior
leaflet < 7 mm
• Rheumatic thickening of the leaflets
and restriction in systole and diastole,
• Barlow‘s syndrome with extensive
involvement
Echocardiographic Approach in Asymptomatic Patients
• Monitor left ventricular function
and size.
• Check for pulmonary hypertension.
• Atrial size correlates with the risk of
atrial fibrillation.
• Consider stress tests.
• Early surgery when repair is likely.
The prognosis depends on
preoperative LVF.
The indication and suitability for
the MitraClip procedure are still
evolving. They depend on
operator/center experience and
the improvments of the
technique.

120
NOTES

121
013//
Tricuspid Valve Disease
CONTENTS
122 Basics
122 Causes of Tricuspid Regurgitation
124 Quantification of Tricuspid Regurgitation
125 Tricuspid Stenosis

013 // TRICUSPID VALVE DISEASE
122
NOTES BASICS
Morphology
• Three leaflets
• Larger than mitral valve (3.2 – 6.4 cm2
)
• More apical and thinner
leaflets than mitral valve
How to Image the Tricuspid Valve
RV PLAX ant. + post. leaflet
RV inflow-outflow view ant./sept. +post leaflet
RV optimized
4-chamber view sept. + ant. leaflet
RV inflow E/A wave lower than MV inflow,
velocity varies with respiration
CAUSES OF TRICUSPID REGURGITATION
Prognosis of TR
Survival depends on:
• Severity of tricuspid regurgitation
• Presence and degree of
pulmonary hypertension
• Reduced left/right ventricular
function
Causes of Functional Tricuspid Regurgitation
• Left heart disease
• Mitral valve disease
• RV dilatation (e.g. atrium septal
defect/left-right shunt)
The posterior leaflet is
usually rather small!
The location and size of
the papillary muscles is
highly variable.
The tricuspid valve is more
difficult to image than the
mitral valve. Use a more
cranial four-chamber view
(1 intercostal space higher).
Trivial (physiologic) TR is
common! (70% of adults).
TR severity is a good marker
of disease progression. This is
true for many conditions
(cardiomyopathy, valvular
heart disease, pulmonary
hypertension etc.)
Functional (secondary)
tricuspid regurgitation is
much more common than
structural (primary) TR!
RV-PLAX
ANTERIOR
SEPTAL
POSTERIOR
4 Chamber
Annular dilatation
POSTERIOR
SEPTAL ANTERIOR

123
NOTES
CAUSES OF TRICUSPID REGURGITATION
Causes of Primary Tricuspid Regurgitation
• Rheumatic (TR combined with TS)
• Trauma (blunt trauma, flail/rupture)
• Pacemaker lead associated
• Endocarditis
• Congenital (e.g. dysplasia, Ebstein‘s
anomaly)
Heart Disease and Carcinoid Tricuspid Regurgitation
Release of vasoactive substances (such as serotonin) leads to:
• Endocardial fibrosis
• Tricuspid leaflet restriction
• Wide coaptation defect
• May be associated with pulmonary
valve stenosis/regurgitation
Morbus Ebstein
• Variable morphology
• Large anterior leaflet
• Leaflet tethering
• Apical displacement (atrialized RV)
Associated with
• Atrium septal defect (> 1/3 of patients)
• Ventricular septal defect
• Patent ductus arteriosus
• Aortic coarctation
• RVOT obstruction,
• Arrhythmia (e.g. WPW syndrome)
Consider a rudimentary form
of Ebstein‘s anomaly or
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).
The origin of the tricuspid
regurgitation jet is far in the
right ventricle, caused by
apical displacement of the
tricuspid valve.
Left heart/valve involvement
may be found in the presence
of ASD or PFO.
Apical
displacement
Atrialized
RV
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.

124
NOTES
QUANTIFICATION OF
TRICUSPID REGURGITATION
Quantification
• Flow convergence • Vena contracta
• Jet area • Jet length
• Eye-balling
Tricuspid Regurgitation – Reference Values
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
Echo Findings in Severe Tricuspid Regurgitation
• Dilated right ventricle/atrium
• Dilated inferior vena cava without
respiratory variations
• Systolic flow reversal in hepatic veins
• Flattened interventricular septum in diastole
• Visible coaptation defect
The degree of tricuspid
regurgitation may
increase with inspiration.
Therefore, observe
several beats with echo.
One overestimates right
ventricular function in the
presence of tricuspid
regurgitation (reduced
afterload).
Right ventricular function
is hyperdynamic in the
initial phase, but may
deteriorate in later stages.
Dilated
RA
Dilated
RV
TR
jet
SEVERE TRICUSPID REGURGITA-
TION – apical four-chamber view
RV optimized/color Doppler
Tricuspid regurgitation with a
large flow convergence zone and
a wide vena contracta. The right
ventricle and atrium are severely
dilated (volume overload).
flow convergence (PISA) vena contracta

125
NOTES
QUANTIFICATION OF
TRICUSPID REGURGITATION
Indications for Tricuspid Valve Surgery (ESC Class I)
• In patients with severe primary or
secondary TR undergoing left-sided
valve surgery
• In symptomatic patients with severe
isolated primary TR without severe
right ventricular dysfunction
ESC 2012
TRICUSPID STENOSIS
Overview
• In 9 % of rheumatic heart disease
• Congenital tricuspid stenosis (very rare)
• Functional tricuspid stenosis due to
intracardiac (obstruction) or extracar-
diac (compression) masses
• Endocarditis (very rare)
• After repair/replacement.
When patients with severe TR
develop signs of right heart
failure (pleural effusion,
peripheral edema, ascites), it
may be too late for surgery
(irreversible RV dysfunction).
Look for doming of the tricuspid
valve in 2D and turbulent flow on
color Doppler.
Tricuspid stenosis may also occur
after tricuspid valve repair (under-
sizing of the annuloplasty ring).
Adding tricuspid repair, if
indicated, during left-sided
surgery does not increase the
risk of surgery.
Enlarged RV
DIASTOLE
LV
Pericardial effusion
Flattened IVS
FEATURES OF SEVERE TR –
PSAX/2D
D-shaped ventricle with a
flattened interventricular septum,
both in systole and diastole – in
severe TR and pulmonary
hypertension.
TRICUSPID VALVE STENOSIS –
apical four-chamber view/CW
Doppler
Elevated flow velocity across
the tricuspid valve with a mean
gradient >5 mmHg. Fluctuations
in inflow velocity, which increase
during inspiration.
Inspiration
TR
PHT

TRICUSPID STENOSIS
Hemodynamics
• Diastolic RA-RV gradient
• Dilatation and elevated pressure in the right atrium
Quantification of Tricuspid Stenosis
• Pressure half time: Tricuspid valve
area (TVA)= 190/PHT – A TVA < 1 cm2
indicates severe TS (not validated).
• Mean gradient: Mean gradient
> 5 mmHg indicates significant
tricuspid regurgitation.
Symptoms of tricuspid valve
may mimic those of right heart
failure.
You will find a significant
increase in gradients during
inspiration. Therefore, average
several beats.
Look for turbulent flow on color
Doppler across the tricuspid
valve in all patients with
rheumatic mitral stenosis.
Doming of the tricuspid valve
may be difficult to visualize.
Thus, you will not miss
associated tricuspid stenosis.
126
NOTES

127
014//
Prosthetic Valves
CONTENTS
128 Types of Valves
129 Echo Assessment of Prosthetic Valves
133 Complications
137 Mitral Valve Repair
Alles_EchoFacts_140821_KD.indd 127 28.08.14 21:13

014 // PROSTHETIC VALVE
128
NOTES TYPE OF VALVES
Mechanical Valves
• Metal case/occluders
• Types: ball cage, tilting disc, bileaflet
• Anticoagulation necessary
• High durability
• Composite graft (prosthesis + aortic
tube graft – Bentall procedure)
Types of Mechanical Valves – Few Examples
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
• Ring (struts)/stentless valves
• No anticoagulation
• Less durable than mechanical valves
• Homograft (cadaver)
• Autograft (pulmonic valve) – Ross
operation
• New implantation systems for rapid
deployment (e.g. Edwards Intuity)
Types of Biological Valves (examples)
Manufacturer Model
Carpentier- Edwards Perimount
Carpentier- Edwards Magna
Medtronic Hancock
Medtronic Mosaic
Sorin Group Mitroflow
Consider mechanical valves in
younger patients.
The risk of mechanical
failure of a prosthesis
is very low.
Newer models include Open
Pivot (Medtronic) and the OnX
mechanical valve (OnX).
Biological valves for the
elderly (but not exclusively).
Biological valves also include
prosthetic material (struts,
sewing ring). These can be
seen on the echo.

129
NOTES
ECHO ASSESSMENT OF PROSTHETIC VALVES
Assessment of Valve Prosthesis
2D Assessment
• Occluder/cusp motion,
• Rocking motion of the prosthesis
• Cusp thickening/calcification
(biological valve)
• Annulus (cavities, pseudoaneurysms,
thrombi/vegetation)
Doppler Assessment
• Maximum and mean gradients across the valve using CW Doppler
• Valvular and paravalvular regurgitation using Color Doppler
Do not forget to look at the
ventricle and systolic pulmonary
artery pressure in mitral valve
prosthesis.
Obtain an early postoperative
baseline study for comparison
later on.
Struts
Valve tissue
FLOW PATTERN IN MECHANICAL
VALVE PROSTHESIS – zoomed
apical five-chamber view
Typical flow pattern of a mecha
nical bileaflet aortic prosthesis.
The regurtitant jets originate
within the frame of the prosthesis
(central) and the jet direction is
”V-shaped”.
BIOLOGICAL MITRAL VALVE –
The struts (2 of 3 visible) protrude
into the left ventricle. The tissue
component of the valve cusps are
seen between the struts.
V-shaped jet

130
NOTES ECHO ASSESSMENT OF PROSTHETIC VALVES
Flow Patterns in Mechanical Valve Prosthesis
Forward flow Physiologic regurgitation
Bileaflet prosthesis
Tilting disc
Medtronic Hall
Common Findings
• Residues of the subvalvular apparatus
• Cavitations
• Suture material + normal regurgitations
Imaging Problems in Patients With Mechanical Valves
• Artefacts
• Shadowing
• Limited visibility of LA
• Limited visibility of the left atrium in
patients with mitral valve prosthesis
• Limited visibility of the regurgitant jet
• Endocarditis is difficult to diagnose
• Visualization of a thrombus is difficult
• Difficult to see leaflet motion
• Difficult to assess flow convergence
Search for a view that displays
the opening/closing motion of
the occluders (mitral valve
prosthesis).
The inflow and regurgitation
pattern varies, depending on the
type of prosthesis.
The motion of mechanical
valves in the aortic position is
difficult to assess.
Use atypical views.
TEE allows visualization of the
atrial side of the prosthesis. TTE
shows the ventricular side.
Combine TTE and TEE if you are
in doubt.

131
NOTES
Consider prosthetic aortic
valve dysfunction when the
maximal velocity is > 3 m/s
and the mean gradient
> 20 mmHg.
Reference Values for Prosthetic Aortic Valves
Bioprosthesis Vmax (m/s) Max. gradient Mean gradient
(mmHg) (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
Mechanical
leaflet
Shadow
MECHANICAL MITRAL VALVE –
The two mechanical leaflets are
almost parallel during diastole.
The prosthesis causes shadowing
of the left atrium.

Reference Values for Prosthetic Mitral Valves
Bioprosthesis Vmax (m/s) Max. gradient Mean gradient PHT
(mmHg) (mmHg) (ms)
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
Pressure Recovery
• Leads to overestimation of
gradients by Doppler
• Relevant in a small aortic
root (< 30 mm)
• Common in small bileaflet valves
• Especially when high flow present
Prosthesis Patient Mismatch (Aortic Valve)
• A calcified aortic annulus can make it
difficult to implant adequately large
valves
• Associated with increased late
mortality
• Think of mismatch in the setting of left
ventricular dysfunction
Prosthetic Effective Orifice Area (EOA)
in Aortic Valve Prosthesis
VTI of AV velocity Stroke volume LVOT
Consider prosthesis-patient mismatch when the indexed prosthetic
effective orfice area < 0.85 cm2/m2
Consider prosthetic mitral
valve dysfunction if the
maximal velocity is
! 2 m/s and the mean
gradient is ! 8 mmHg.
The geometric orifice
area is not the effective
orifice area.
Nobody understands
pressure recovery
anyway! Just remember
these key issues.
Prosthesis–patient mismatch
leads to high transvalvular
gradients through normal
functioning valves. This
influences the resolution of left
ventricular hypertrophy and may
also influence prognosis and
exercise capacity.
EOA =
Stroke volume
VTI
132
NOTES

Left ventricular dysfunction may
occur after valve surgey due to
intraoperative ischemia, residual
valvular defects, or ventricular
dysfunction at the time of
surgery (too late). It may occur
several years after surgery.
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.
Compare with previous studies
and initial postoperative
gradients.
COMPLICATIONS
Prosthetic Valve Complications
• Paravalvular leaks
• Valve obstruction (thrombus/pannus)
• Endocarditis
• Mechanical failure (mechanical valves)
• Degenerative changes (biological valves)
• Pseudoaneurysm/fistula
Predisposing Factors for Structural Failure in Bioprosthesis
• Renal failure
• Hemodialysis
• Hypercalcemia
• Adolescence (growing)
• Porcine > pericardia
• Autoimmune disease
Bioprosthesis Obstruction – Echo Findings
• Thickened calcified leaflets
• Reduced mobility
• Elevated gradients
• Prolonged pressure half-time (mitral
prosthesis)
• Turbulent flow
• Dilated left atrium with spontaneous
contrast (mitral prosthesis)
• LV dysfunction (eventually)
Structural failure (obstruction)
is unlikely when the prosthesis
is < 2 years old and the patient
does not have endocarditis.
PROSTHETIC VALVE ENDOCAR-
DITIS – TEE short-axis view/2D
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.
Ring abscess
Mechanical leaflet
Shadow
Shadow
133
NOTES

COMPLICATIONS
Mechanical Valve Obstruction – Echo Findings
• Impaired/stuck leaflet
• Echogenicity in valve region
(thrombus?)
• Pathologic flow pattern on color
Doppler
• Elevated gradients
• Pressure half time (MV)
Mechanical Valve Obstruction – Pannus vs. Thrombus
Pannus Thrombus
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
Quantification of Obstruction
Aortic Valve Prosthesis Mitral Valve Prosthesis
Morphologic findings Morphologic findings
Symptoms Symptoms
Velocity > 3.0 m/sec Mean gradients (>6–8 mmHg)
Doppler Vel. Index < 0.3 PHT > 130 ms
(Doppler Velocity Index = VLVOT
/VProsth valve
)
Use fluoroscopy to detect
mechanical valve
obstruction.
Quite often only the
surgeon can give the
answer if a thrombus or a
pannus is present
Use color Doppler to
guide the position of the
CW Doppler (mitral valve).
Use several windows to
quantify prosthetic aortic
valve obstruction.
THROMBUS OF MITRAL PROS-
THESIS – TEE/2D
Mechanical obstruction of a
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-
thoracic exam.
Thrombus
Mech
leaflet
134
NOTES

Some degree of
paravalvular regurgitation
is always present.
Patients with relevant
paravalvular regurgitation
often have hemolysis.
Paravalvular regurgitation of
the aortic valve is best seen
on the parasternal short-axis
view (color Doppler).
COMPLICATIONS
Regurgitation in Valve Prosthesis
• Normal/physiologic
• Pathologic (paravalvular)
• Valvular/structural failure (bio)
• Valvular/mechanical failure (mech)
Mitral Regurgitation and Type of Prosthesis
Type Valvular Paravalvular Normal/physiologic
Mechanical X (mech. failure) X X
Biological X X ----
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
• More common in aortic than in mitral
valve prosthesis
• Predisposing factors: calcified annulus,
endocarditis, suture technique
• Small atria
Echo Evaluation of Regurgitation
• Multiple/atypical views
• Eccentric jets
• Parasternal short axis (aortic valve)
• CW Doppler + gradients
PARAVAVULAR LEAK – TEE/3D
surgical view
Paravavular leak in a patient with
a bileaflet mechanical mitral
valve.
Mech bileaflet
prosthesis
Sutures
Paravalvular
orifice
135
NOTES

COMPLICATIONS
Elevated Gradients – Considerations
• Compare with baseline/
reference values
• Likelihood of obstruction (anticoagu-
lation within the therapeutic range/
symptoms)
• Presence of regurgitation (increase
gradients per se or as a secondary sign
of prosthetic dysfunction)
• Prosthesis mismatch?
• Presence of mobile structures
(thrombi/vegetations)
• High flow state (dialysis shunt, high
cardiac output, heart rate)
Other Complications
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
Pseudoaneurysm
• Often caused by endocarditis (before and after surgery).
• Occurs in native and prosthetic valves.
• May lead to the formation of fistulas.
Prosthetic Valve Endocarditis (see Chapter 15)
In the setting of elevated
gradients in mitral valve
prosthesis, measure the
pressure half-time. If the
pressure half-time is high,
prosthesis obstruction is likely.
If the pressure half-time is
normal, consider significant
mitral regurgitation or high
flow states.
Tricuspid regurgitation tends to
increase after left heart valve
surgery.
If you suspect an aortic valve
pseudoaneurysm, look for a
pulsatile cavity with oscillating
flow in (systole) and out
(diastole) of the cavity.
136
NOTES

Mitral valve repair is always
combined with ring
implantation.
Measure the mean gradient and
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
Mitral Valve Repair – Ring Implantation (Annuloplasty)
• Different types of rings (flexible, open,
closed)
• Prevents annular dilatation
• May resemble annular
calcification on echo
• The posterior leaflet may appear rather
short after ring implantation
Common Techniques of Mitral Valve Repair
• Annuloplasty (see above)
• Quadrangular/triangular resection
(with/without sliding plasty)
• Chordal transfer
• Artificial chords
Complications of Mitral Valve Repair
• Residual regurgitation
• Obstructed left ventricular inflow
(undersizing of the ring)
• Ring dehiscence (partial dehiscence,
the origin and path of regurgitation are
outside the ring)
• LVOT obstruction/SAM caused by
redundant leaflets in the setting of
small hyperdynamic left ventricles
Patients with unsuccessful
repair (if not corrected)
have a poor prognosis.
MITRAL VALVE REPAIR –
Artifical chords and annuloplasty
ring after mitral valve repair.
Papillary
muscle
Artificial
chords
Annuloplasty
ring
Thickened
AMVL
Thickened
PMVL
137
NOTES

138
NOTES

139
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

PRINCIPLES OF ENDOCARDITIS
Definition
Endovascular microbial infection of cardiovascular structures
Location
• Valves
• Large intrathoracic vessels
• Ventricular and atrial endocardium
• Prosthetic material
• Polymere associated structures (lines)
• Eustachian valve
Pathophysiology of Endocarditis
The prevalence of
endocarditis associated
with prothetic valves and
pacemaker leads is on the
increase.
Embolism
Active infection
Post endocarditis
Non-significant
endocardial lesion/
fibrosis
Healing with
calcification/
fibrosis/thickening
Perforation
Endocardial defect
Thickened
leaflets
TRICUSPID VALVE
ENDOCARDITIS – apical four-
chamber view RV optimized/2D
Endocarditis with a large
vegetation attached to the native
tricuspid valve.
TV vegetation
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.
Vegetation is an infected
mass attached to
endocardial structures,
such as valves or implanted
intracardiac material. On 2D
echo they frequently
appear as oscillating
structures of variable size
and morphology.
015 // ENDOCARDITIS
140
NOTES

Staph. aureus infection
predisposes to abscess
formation and
complications of
endocarditis!
PRINCIPLES OF ENDOCARDITIS
Microbiology
Epidemiologic Facts on Endocarditis
• Large geographical variations in the
incidence of endocarditis (3–10
episodes/100.,000 person-years)
• Increase in the elderly population
• Sclerosis and aging also predispose to
endocarditis
NATIVE VALVE ENDOCARDITIS
Diagnosis, Symptoms and Findings
• Fever/night sweat
• Predisposing factors
• Conjunctival petechiae
• Janeway lesions
• Roth spots
• Splinter hemorrhages
• Vegetations
• Regurgitations
• Complications of endocarditis
(abscessive destruction)
Echo Culture
Clinics
Endocarditis may be manifested
in many ways, many of which
may be atypical
In the setting of infection, heart
murmur or atypical symptoms,
think of endocarditis. Early
diagnosis saves lives.
Blood culture and other signs of
infection (CRP, leukocytes, etc.)
are equally important. A negative
blood culture does NOT rule out
endocarditis.
Staph. aureus 25%
Staph. epidermidis 13%
Strept. bovis 20%
Enterococcus 11%
Culture negative 17%
Other 14%
AMVL
Vegetation
LA
MITRAL VALVE ENDOCARDITIS
– PLAX zoomed/2D
A vegetation is attached to the
tip of the anterior mitral valve
leaflet.
015 // ENDOCARDITIS
141
NOTES

015 // ENDOCARDITIS
142
NOTES NATIVE VALVE ENDOCARDITIS
• Fibrosis/calcification
• Myxomatous degeneration (e.g. mitral
valve prolapse)
• Lambl‘s excrescence/strands
• Tangential imaging of structures
• Old vegetations
• Tumors/thrombi
Indication for Transthoracic Echo in
Suspected Endocarditis
Follow-up studies help to make
an accurate diagnosis
(progression?).
Transesophageal
echocardiography is not
mandatory in isolated
right-sided native valve
endocarditis with good
transthoracic quality.
TTE
Prosthetic
valve,
intercardiac
device
Poor quality
TTE
TEE
If the initial TEE is negative but endocarditis is still suspected,
repeat TEE within 7–10 days
TEE Stop
Low
High
Positive Negative
Persistent clinical suspicion
Clinical Suspicion of Endocarditis
MITRAL VALVE ENDOCARDITIS –
TEE surgical view/3D
Large vegetation on the posterior
leaflet prolapsing into the left
atrium
ESC guidelines 2009
Vegetation
Posterior leaflet
Anterior leaflet

015 // ENDOCARDITIS
143
NOTES
”Healing” usually leads to some
degree of fibrosis or calcification
of the affected valve.
Embolization is the primary
manifestation of endocarditis in
28–47% of all patients. The risk
of embolization depends on the
size (>10 mm) and mobility of
the vegetation.
Exclude endocarditis in the
setting of stroke and fever.
MV perforation Fistula
NATIVE VALVE ENDOCARDITIS
What Else to Look For?
• Involvment of other valves
• Regurgitations and resulting
volume overload
• Myocardial function (right + left)
• Pericardial/pleural effusion
• Valve obstruction (large
vegetations, rare)
• Coronary embolization of
vegetation leading to wall motion
abnormalites (rare)
COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS
Complications
• Embolism
• Valve destruction
• Regurgitation/heart failure
• Abscess
• Pseudoaneurysm
• Perforation
• Fistula
• Mycotic aneurysm
Types of Valve Destruction
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).
Pulsatile perivalvular (echo-free) cavity communicating
with the cardiovascular lumen.
Pseudoaneurysm –
intervalvular
fibrosa
MV pseudo-
aneurysm

COMPLICATIONS OF NATIVE VALVE ENDOCARDITIS
Types of Valve Destruction
Perivalvular cavity filled with infectious material which has a non-homogeneous
(echodense/echolucent) appearance
Tear in the aortic cusp or chordal rupture, which usually
leads to excentric regurgitation jets.
MV flail leaflet
AV cusp
rupture
AV ring abscess MV annular
abscess
PSEUDOANEURYSM IN
AV ENDOCARDITIS –
TEE long-axis view/2D
A pulsating cavity surounds the
aortic valve (pseudoaneurysm).
Numerous vegetations are pre-
sent at the aortic cusps.
AV
Vegetation
Pseudoaneurysm
Communication
to the left ventricle
015 // ENDOCARDITIS
144
NOTES

Tricuspid valve endocardits is
very likely in patients with
pulmonic abscess + drug abuse
+ new heart murmur.
Use atypical views to image
tricuspid valve endocarditis
and also look for pleural
effusion (secondary to
pulmonary infection).
Tricuspid valve vegetations
may become very large.
RIGHT HEART ENDOCARDITIS
Causes of TV Endocarditis
• Intravenous drug abuse
• Immunocompromised
• Indwelling catheters
• Pacemaker
Tricuspid Valve Endocarditis – Facts
• The most common organisms are
Staphylococcus aureus (60–80%)
and Pseudomonas.
• Pulmonary hypertension, pulmonary
embolism or tricuspid regurgitation
may result in right heart failure.
• The prognosis is relatively good (10%
inhospital mortality), but is poor in
fungal infection.
• High recurrence rates.
• Endocarditis frequently causes a flail
tricuspid valve leaflet..
• Tricuspid valve endocarditis may
also occur in patients without
predisposing factors.
Complications
• Valve destruction
• Involvement of neighbouring cardiac
structures
• Septic pulmonary embolism
• Lung abscess
PROSTHETIC VALVE ENDOCARDITIS
Risk Factors
• Heart failure
• Wound complications
• Direct contamination during cardiac
surgery
• Valve degeneration
• Prior history of endocarditis
• Prosthesis thrombi (super-infection)
• Artefacts
• Subvalvular residuals
• Surgical materials
• Strands
• Thrombus
• Hematoma
Compare your findings with previous studies.
Prosthetic valve endocarditis is
difficult to detect.
Transesophageal echo is
recommended in case of
suspicion.
Find out which operation was
performed, talk to the surgeon.
Surgical material such as suture
material or patches may mimic
endocarditis.
015 // ENDOCARDITIS
145
NOTES

015 // ENDOCARDITIS
146
NOTES
Complications
• Periannular abscess
• Pseudoaneurysms
• Paravalvular leaks
• Valve dehiscence
• Valve obstruction
• Fistula
PACEMAKER/POLYMER-ASSOCIATED
ENDOCARDITIS
Predisposing Factors
• Pouch/Pocket infection
• Impaired immunity
• Systemic infection
• Temporary pacing before implantation
• Diabetes
• The surgeon‘s experience
• Advanced age
Clinical Presentation
• Fever, subfebrile (recurrent)
• Pulmonary embolism
• Local complications
• Septic shock (acute)
• Poor general condition
Typical Sites of Infection
• Vena cava superior
• Right atrium
• Tricuspid valve
• Tricuspid annulus
PROSTHETIC VALVE ENDOCARDITIS
Lead infection usually
occurs at sites where
the leads are in contact
with the endothelium.
Prosthetic valve endocarditis
is a life-threatening
condition and is associated
with a poor prognosis.
Pacemaker lead infection is
difficult to diagnose. A negative
study does not rule out
endocarditis. Combine
transthoracic and
transesophageal echo to
visualize as many portions of
the leads as possible.
PERIANNULAR PROSTHETIC
VALVE ABSCESS – TEE short-
axis/2D
The echodense area surounding
the prosthesis corresponds to a
periannular abscess. Additionally,
a large vegetation is seen on the
rim of the cusps.
AV
vegetation
Abscess

015 // ENDOCARDITIS
147
NOTES
PACEMAKER/POLYMER-ASSOCIATED
ENDOCARDITIS
NON-INFECTIVE/ABACTERIAL ENDOCARDITIS
Types
• Marantic endocarditis
• Hypercoagulable state
• Libman-Sacks endocarditis
• Antiphospholipid syndrome
Echo Characteristics
• Valve thickening
• Mild or moderate regurgitation
• Small vegetations
Cardiac Manifestations of Libman-Sacks Endocarditis
• Valve thickening and vegetations
• Mural thrombus
• Spontaneous contrast
• Left + right ventricular dysfunction
Thickened
valve
LIBMAN-SACKS ENDOCARDITIS –
apical three-chamber view/2D
Patient with lupus and antiphos-
pholipid syndrome. Several small
vegetations are seen on the
mitral valve.
Vegetations
CENTRAL LINE ENDOCARDITIS
&TEE bicaval view/2D
Central line with its tip in the
right atrium. Mobile vegeta-
tion attached to the catheter
(thickened tip) on transthoracic
echo (left) and the adjacent wall
(right) seen in TEE.
Mobile
structure
Left atrium
Vegetation
Sup, vena cava
Inf.
vena cava
Catheter
Thickened
catheter

015 // ENDOCARDITIS
148
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

149
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

BASICS OF PULMONARY HYPERTENSION
Definition and Classification of Pulmonary Hypertension
Definition: mPAP ≥ 25 mmHg at rest
• Pulmonary arterial hypertension (PAH)
• Pulmonary hypertension owing to left
heart disease (CTEPH)
• Pulmonary hypertension owing to lung
disease and/or hypoxia
• Chronic thromboembolic pulmonary
hypertension
• Pulmonary hypertension with unclear
multifactorial mechanisms
Causes of Pulmonary Hypertension
Hemodynamic Definition of Pulmonary Hypertension
Definition Characteristics Clinical groups
Pulmonary hypertension Mean PAP ≥ 25 mmHg All
Pre-capillary pulmonary Mean PAP ≥ 25 mmHg PAH
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
By definition, the diagnosis of
pulmonary hypertension can only
be made by introducing a right
heart catheter.
Left heart disease
(postcapillary) is the most common
cause of pulmonary hypertension.
Patients with chronic
obstructive pulmonary disease
rarely develop severe forms of
pulmonary hypertension.
Look at the left heart.
Does it explain pulmonary
hypertension? Is LV filling
pressure elevated? The
echo can provide clues as
to whether pre- or
post-capillary pulmonary
hypertension is present.
Left heart disease 78%
Lung disease 10%
PAH 4%
CTEPH 1%
Others 7%
016 // RIGHT HEART DISEASE
150
NOTES

BASICS OF PULMONARY HYPERTENSION
Prognosis of Pulmonary Hypertension
Echocardiographic Screening for Pulmonary Hypertension
Class Level
PH unlikely Tricuspid regurgitation
velocity ≤ 2.8 m/s, sPAP ≤ 36
mmHg and no additional
echocardiographic variables
suggestive of PH
I B
PH possible Tricuspid regurgitation
velocity ≤ 2.8 m/s, sPAP ≤ 36
mmHg, but the presence of
additional echocardiographic
variables suggest PH
IIa C
Tricuspid regurgitation
velocity 2.9–3.4 m/s, sPAP
37–50 mmHg with/without
variables suggestive of PH
IIa C
PH likely Tricuspid regurgitation
velocity > 3.4 m/s, sPAP > 50
mmHg, with/without
variables suggestive of PH
I B
Additional echo variables suggestive of pulmonary
hypertension = IVS flattening, short PVAT, PA- dilatation
ESC 2009
Pulmonary hypertension is
a disease with a poor
prognosis, especially in
advanced stages. Early
diagnosis is important.
Exercise Doppler
echocardiography is
currently not
recommended for
screening patients for
pulmonary hypertension.
151
NOTES

ECHO ASSESSMENT OF
PULMONARY HYPERTENSION
systolic PAP (sPAP) =
= 4 TR Vmax2
+ Right Atrial Pressure (RAP)
Quantification of sPAP and Pulmonary Hypertension
• Normal TR velocity is 1.7– 2.3 m/s
• Elevated when TR velocity > 2.8–3.0 m/s
• 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
Factors That Influence TR velocity/sPAP
• Severity of tricuspid regurgitation
• Doppler/image quality
• Alignment of the TR jet to CW Doppler
• Right ventricular function
• Inspiration (higher with inspiration)
Normal tricuspid
regurgitation velocity is
age dependent. The
severity of TR tends to
increase with age.
Pulmonary hypertension
does not imply severe
and severe TR does not
imply severe pulmonary
hypertension.
Peak velocity
MEASUREMENT OF SYSTOLIC
PULMONARY ARTERIAL PRES-
SURE – apical four-chamber
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).
CW sample
TR signal
152
NOTES

In very severe tricuspid
regurgitation, the TR
spectrum is triangular. In this
case RAP and thus
pulmonary artery pressure
cannot be estimated (no
gradient between RA and
RV).
Elevated RA pressure may
lead to significant shunts
across a patent foramen
ovale, or ASD causing
undersaturation.
153
NOTES
ECHO ASSESSMENT OF
Estimation of Right Atrial Pressure
RA pressure IVC (diameter) Inspiration
0 – 5 mmHg small (< 1.5 cm) collapsing
5 – 10 mmHg normal (1.5 – 2.5 cm) > 50% diameter reduction
10 – 15 mmHg dilated (>2.5 cm) < 50% diameter reduction
> 20 mmHG IVC + liver veins dilated no diameter change
RA pressure estimation based on this scale is not always reliable.
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)
• Shortened in elevated pulmonary artery pressure
• May be normal in elevated right-sided cardiac output
Should only be applied for heart rates between 60 – 100
Normal > 130 ms
Borderline 100 – 130 ms
Mild 80 – 100 ms
Severe < 80 ms
PVAT can be very valuable in
situations where sPAP cannot
be measured due to
insufficient TR signal.
RA
Dilated hepatic vein
Dilated IVC
DILATED INFERIOR VENA CAVA –
subcostal IVC view/2D
Severely dilated inferior vena
cava without respiratory fluctu-
ations in diameter and dilated
hepatic veins in a patient with
pulmonary hypertension. These
findings suggest right atrial pres-
sures > 20 mmHg.

154
NOTES
ECHO ASSESSMENT OF
Echo Findings in Pulmonary Hypertension
• Dilated right ventricle
• Septal flattening (systolic) = D-shaped
ventricle
• Dilated pulmonary artery
• Pulmonary regurgitation
• Enlarged right atrium
• Pleura effusion
• Low cardiac output
The normal pulmonary artery
is a) smaller than the
ascending aorta b) <27 mm in
women and <29 mm in men.
Patients with pericardial
effusion have a poor prognosis.
Septal flattening can be very
subtle, especially when systolic
pressure is high.
SYSTOLE
RV hypertrophy
Dilated RV
Flattened
IVS
TV
LV
ECHO FINDINGS IN PULMONARY
HYPERTENSION – PSAX/2D
Echo features of severe pulmo-
nary hypertension: D-shaped
left ventricle with a flattened
interventricular septum in systo-
le, a dilated right ventricle, right
ventricular hypertrophy, and peri-
cardial effusion.
PULMONARY ACCELERATION
TIME (PVAT) – PSAX/PW PV
PVAT is measured from the onset
to the peak of the RVOT/PV
outflow signal. In the abscence
of pulmonary hypertension, the
peak is rather late and the curve
symmetrical.
Sample volume
Signal onset PVAT
Peak velocity
PA

155
NOTES
The McConnell sign is
marked by akinesia of the
mid-free wall but normal
motion of the apex. It is
also present in right
ventricular infarction. The
60/60 sign is a PVAT
below 60 ms in the
presence of a TR
maximum gradient above
30 but below 60 mmHg.
DISEASE OF THE RIGHT VENTRICLE
Echocardiographic Signs of Acute
Pulmonary Embolism
• The sensitivity of echo for the
detection of pulmonary embolism is
low. In cases of typical echo findings
(especially dilated RV with reduced
RV function), the patients are usually
very symptomatic (large PE)
• McConnel sign: Characterized by
akinesia of the mid-free wall but
normal motion in the apex (poor
positive predictive value)
• 60/60 sign: Characterized by a PVAT
below 6 0ms in the presence of a
tricuspid regurgitation maximum
gradient above 30 mmHg but
below 60mmHg
• Right ventricular pressure overload:
Characterized by a D-shaped right
ventricle
DD: Pulmonary Embolism and RV Infarction
• Similar symptoms
• Similar ECG
• Similar echo findings
• Look for regional wall motion abnormalities (inferior infarction)
RIGHT VENTRICULAR INFARCTION
Right Ventricular Infarction
• Associated with inferior myocardial infarction (30–50%)
• Poor prognosis
• Hypotension/shock
• Arrhythmia
Echo Findings
• Global and regional reduction in
right ventricular function
• Low cardiac output
• Low annular velocity (Ttssue
Doppler) and decreased longitudinal
strain (speckle-tracking)
The untrained right ventricle is
unable to cope with acute
pressure overload. Therefore,
very high sPAP measurements
are uncommon in acute
pulmonary embolism
(exceptions are patients with
recurrent pulmonary
embolism/CTEPH with
preexisting pulmonary
hypertension).
The majority of patients
with RV infarction
recover in a period of
weeks or months.
Look at the right
ventricular wall motion in
all patients with inferior
infarcts.

156
NOTES RIGHT VENTRICULAR HYPERTROPHY
• Right ventricle free wall ≥ 6mm
• Use a subcostal 4-chamber view to
image the free right ventricle wall
• Consequence of pressure overload on
the right ventricle
• Concentric right ventricular hypertro-
phy in pulmonary stenosis
• Measurement may be difficult;
also use visual assessment
• Right ventricle hypertrophy may also
lead to right ventricular outflow tract
obstruction (narrow right ventricular
outflow tract)
Causes of Right Ventricular Hypertrophy
• Chronic pulmonary hypertension
• Pulmonic valve stenosis (including
congenital abnormalities,
e.g. tetralogy of Fallot)
• Tetralogy of Fallot
• High altitude
• Athlete‘s heart syndrome
• Hypertrophic cardiomyopathy
(with right heart involvement)
ARRHYTHMOGENIC RIGHT VENTRICULAR
DYSPLASIA (ARVD)
• Usually autosomal dominant
• Fatty and fibrous replacement of
myocardium, especially in the right
ventricular outflow tract
• 5–10% of sudden cardiac deaths
(<65 years)
• Its prevalence is 3-fold higher in males
Echo Findings in ARVD
• Aneurysmal dilatation, usually in the
diaphragmatic, apical and infundibular
regions (triangle of dysplasia)
• Regional wall motion
abnormalities + thin wall
• Right ventricular dyssynchrony
Carcinoid Heart Disease
• Characterized by plaque-like deposits
of fibrous tissue, which most com-
monly occur on the endocardium of
valvular cusps and the leaflet.
• Occurs in 50% of patients with
carcinoid syndrome
• High circulating concentrations of
serotonin in the heart is the underlying
substrate of carconoid heart disease.
• The right heart is most commonly
affected because serotonin is inactiva-
ted by the lung and therefore protects
the left heart
ARVD may affect both
ventricles. Echo has rather
low sensitivity and specificity
in subtle forms of ARVD ->
MRI will be needed.
Echocardiographic assessment
should always include the RVOT
(aneurysm?). Use atypical views.
Use atypical views of the
RV (2-chamber RV view,
inflow/outflow RV view).

If you suspect carcinoid
heart disease, tilt the
transducer to the abdomen
and image the liver. The
majority of patients with
carcinoid heart disease have
hepatic metastases.
ARRYTHMOGENIC RIGHT VENTRICULAR
DYSPLASIA (ARVD)
Echo Findings in Carcinoid Heart Disease
• Right ventricular enlargement
• Tricuspid valve, pulmonic valve leaflets
and the subvalvular apparatus are
thickened and rigid
• Usually significant tricuspid
regurgitation with restricted motion
of the leaflets, causing a wide
coaptation defect.
• Abnormal motion of the interventricu-
lar septum (volume overload caused
by tricuspid regurgitation).
• Triangular CW spectrum indicative of
severe tricuspid regurgitation.
• Associated with pulmonic stenosis
(and regurgitation).
CARCINOID HEART DISEASE –
apical four-chamber view RV
optimized/2D
Restricted motion/position of the
tricuspid leaflets, leaving a wide
coaptation defect. The leaflets
are thickened (from the base) and
rigid. The endocardium
is bright. These findings are high-
ly indicative of carcinoid heart
disease.
SYSTOLE
Prominent
Moderator band
Dilated RV
Rigid
leaflets
+
Coaptation
defect
157
NOTES

158
NOTES

159
017//
Aortic Disease
CONTENTS
160 Imaging of the Aorta
161 Basics
161 Aortic Aneuryms
164 Aortic Dissection
167 Aortic Coarctation (CoA)

017 // AORTIC DISEASE
160
NOTES IMAGING OF THE AORTA
How to Visualize the Aorta with
Transthoracic Echocardiography
Transoesophageal Echo (TEE)
BETTER RESOLUTION MORE SEGMENTS
The esophagus is close to the
aorta. We may therefore use higher
transducer frequencies, which
translate into better resolution.
TEE is much better for the
assessment of the descen-
ding thoracic aorta
Where and How to Measure
Use a modified parasternal long-
axis view (one intercostal space
cranial) to see more of the
ascending aorta.
Every echo report should
include a description
of the ascending aorta
(normal/dilated)
with corresponding
measurements.
Even with TEE it may be
difficult to see cranial
segments of the
ascending aorta.
The aortic diameter is
slightly larger in systole
than in diastole.
The aorta can be measured on a long- and/or
short-axis view. Most reference values were
obtained with the leading edge method.
However, to correlate measurments better
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
these measurements methods is minimal
and insignificant, thanks to improved image
resolution.
By using several measurements (in
the setting of aortic dilatation), it is
also possible to determine the shape
and extension of aortic aneurysms.
Three-chamber
view
PLAX
Four-chamber view
(descending aorta)
Suprasternal win-
dow (aortic arch)
Two-chamber
view
(descending
aorta)
Axial view
Longitudinal view
Leading
edge
Inner
edge
Leading
edge
Inner
edge
Sinus of
valsalva
Descending
aorta
Aortic arch
Sinotubular
junction
Ascending
aorta
Aortic
annulus

161
NOTES
BASICS
Size of the Aorta
Diameter Diameter/BSA
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
The size of the aortic is
strongly related to body
surface area (in particular
hight) and age.
VISUALIZATION OF
THE ASCENDING AORTA –
modified PLAX/2D
The more cranial portions of the
ascending aorta can be better vi-
sualized by moving the transduc-
er up one intercostal space and
more laterally.
Ascending aorta

AORTIC ANEURYMS
Incidence – Facts
• Death – aneurysm =
0.7/100,000 per year
• Death – dissection =
1.5/100,000 per year
• No difference between prevalence
in men and women
• Thoracic aneurysms >6 cm are subject
to a rupture and dissection risk
of 6.9% per year.
Forms of Aneurysms
Pure ascendens type ”Sausage” type Bulbus type (Marfan)
In the setting of aneurysms the aorta changes its orientation
(to the right); it may even be elongated.
Bicuspid Aortic Valve and Aneurysm
• Dilatation of the aorta may be present in patients with
congenital abnormal valves (e.g. bicuspid).
• 9-fold higher risk of dissection in the presence
of bicuspid valves.
• 6–10% of all dissections occur in the setting
of bicuspid valves.
To quantify aneurysms of the
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.
Look at the shape of the
ascending aorta: something is
wrong when there is no
narrowing at the sinotubular
junction.
Progressive dilatation of the
aorta continues even after
aortic valve replacement in
patients with bicuspid valves.
Follow such patients closely.
Any increase in the diameter
of the aorta is related to
(blood) pressure, the size of
the aorta, and the thickness
of the wall (law of Laplace).
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
the sinotubular junction.
Aortic
aneurysm
Calcified
aortic valve
162
NOTES

Inherited disorders
also include so called
”overlap syndromes”.
AORTIC ANEURYMS
Inherited Disorders Affecting the Aorta
• Marfan
• Ehlers Danlos (type IV)
• Familial forms of connective tissue
disorders
• Annulo-aortic ectasia
• Loeys-Dietz syndrome
Marfan Syndrome – Cardiac Manifestations
• Aortic dilatation
• Aortic dissection
• Aortic regurgitation (annular dilatation)
• Mitral valve prolapse
• Pulmonary artery dilatation
• Large aortic valve cusps
Inflammatory Diseases of the Aorta
• Syphilis
• Staph. aureus infection
• Kawasaki disease
• Giant cell arteritis
• Takayasu arteritis
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)
• Asymptomatic patients with an
ascending aortic diameter or an aortic
sinus diameter ≥ 55mm
• Patients with Marfan syndrome with an
aortic diameter between 40-50 mm
• Patients with a growth rate of more
than 0.5 cm/year in an aorta
less than 5.5 cm in size
• Patients undergoing aortic
valve repair, with an aortic
aneurysm ≥ 4.5 cm in size
ACC 2010
Aortic disease/dissection
is the main cause of
morbidity and mortality in
Marfan syndrome.
Infections may trigger
non-infectious vasculitis by
generating immune complexes
or by cross-reactivity.
Inflammation may result in
aortic dilatation and ostial
stenosis of major branches.
Use other imaging
modalities (mitral
regurgitationI and CT)
for precise
measurements and for
decision-making. Use
the technique you are
most familiar with.
163
NOTES

164
NOTES AORTIC DISSECTION
Aortic Dissection
Characteristics:
• Intima (media) disruption/
intimal flap – true + false
lumen
• Spiral-shaped dissections may
occur, sometimes involving
branches (coronaries!!,
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.
The false lumen is usually
larger than the true lumen,
with slower flow, and often
with thrombi.
Intimal flaps may prolapse
through the aortic valve.
Also look for intimal flaps
in the aortic arch (using a
suprasternal window).
Tear
Flap
Thrombus
True lumen
False lumen

165
NOTES
AORTIC DISSECTION
Risk Factors for Dissection
• Aortic aneurysm
• Marfan + other connective tissue
disorders
• Atherosclerosis
• Iatrogenic (e.g. left heart catheter, heart
surgery cannulation)
Aortic Dissection
Classic dissection Complications of dissection
• Aortic rupture
• Branch vessel dissection (coronaries)
• Expansion
• Intramural hematoma
• Aortic regurgitation
• Rupture with pericardial tamponade
• Leriche syndrome
TTE in Aortic Dissection
• Sensitivity = 77–80%
• Specificity = 93–96%
Always confirm dissection by using other imaging modalities.
Aortic regurgitation
in dissection
• Dilatation of the root
• Bicuspid valves
• Prolapse of the intimal flap
Untreated dissection of the
ascending aorta is associated
with a mortality rate of 90%
within 1 year (rupture into the
pericardium, mediastinum, or
left pleural cavity).
The intima/media is
detached (flap), and
divides the aorta into a
true and a false lumen.
Beware of reverberations of
the aortic wall or adjacent
structures. They may mimic
an intimal flap. A true intimal
flap is marked by motion
independent of the aortic
wall.
true
false
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

166
Aortic Syndromes
Intramural hematoma Rupture
Bleeding into the aortic wall (such as
after plaque rupture) causes an intramu-
ral hematoma.
Plaque rupture, penetrating ulcers,
and intramural hematoma may lead to
aortic rupture.
Localized dissection ”Healed” dissection
Localized dissection is usually a result
of atherosclerosis. Dissection is limited
to a circumscript region.
The false lumen of dissection may
thrombose and eventually heal.
Penetrating ulcer Intraluminal thrombus
Rupture of an atherosclerotic plaque
results in a penetrating ulcer.
Regional thickening of the aorta > 7 mm
(circular shape) (DD: thrombus in false
lumen, intramural hematoma)
Aortic syndromes are no benign
condition. The bear a high risk
of rupture. Further evaluation
with CT/mitral regurgitation is
mandatory.

167
NOTES
AORTIC DISSECTION
Aortic Plaque
• Patients with artherosclerotic plaques
in the aorta are subject to a high risk of
coronary artery disease and
myocardial infarction.
• Increased risk of embolism/stroke
(plaque in the ascending aorta/aortic
arch).
• Increased risk of aortic dissection.
• Increased risk of aortic syndromes.
Typical Locations of Plaques in the Aorta
• Aortic arch
• Cranial segments of the
descending aorta
AORTIC COARCTATION (COA)
Facts
• 5–10% of all congenital defects
• Predominantly men
• Higher blood pressure at the upper extremities
compared to the lower extremities
• Located distal to the subclavian artery
• Increased risk of intracranial hemorrhage
Echo Features
• Narrowing of the aorta
• Turbulent flow is visible on color Doppler
• Elevated CW Doppler gradient in the aorta
• The presence of a systolic and an additional diastolic gradient
denotes hemodynamic significance of obstruction
Plaque size is important
for risk stratification.
When the plaque size is >
4 mm, the risk of stroke is
significantly increased.
(OR=9.1)
TTE is also Capable of
demonstrating plaques /especially
in the ascending aorta). Capable of
demonstrating plaques/especially
in the ascending aorta).
Kinking may lead to flow
turbulence (seen in color
Doppler), thereby
mimicking CoA =
pseudocoarctation
The suprasternal view is the
most valuable window to
identify coarctation.
Quantification is based on the
maximal velocity/gradients
(measured with CW Doppler)
and the presence of a systolic
AND diastolic gradient.
Doppler measurments usually
overestimate gradients in
comparison to hemodynamic
assessment.

168
Coarctation – Associated Abnormalities
• Bicuspid aortic valve
• Persistent ductus arteriosus/ventricular septal defect
• Hypoplasia of the aortic arch
• Left ventricular outflow tract obstruction
Patients with hemodynamically
relevant forms of CoA also
have left ventricular
hypertrophy.
AORTIC COARCTATION –
suprasternal view/Color
and CW Doppler
Turbulent flow in the descending
aorta (left) denotes the location
of coarctation. The Doppler
spectrum (right) shows a systolic
and diastolic gradient (>4 m/s),
suggesting severe coarctation.
CW sample volume
Jet
Aortic
coarctation
Brachiocephalic artery
Left common carotid artery
Left subclavian artery
Systolic + diastolic
gradient

169
018//
Pericardial Disease
CONTENTS
170 The Pericardium
170 Pericardial Effusion
173 Pericardial Tamponade
175 Pericardial Constriction
176 Other Diseases of the Pericardium

THE PERICARDIUM
The Pericardium – Importance
• Limits distension
• Facilitates interaction and coupling
of the ventricles/atria
• Facilitates twist and torsion
• Normal quantity of
pericardial fluid < 50ml
PERICARDIAL EFFUSION
Forms of Pericardial Effusion
Transudative
Congestive heart failure, myxedema,
nephrotic syndrome
Exudative
Tuberculosis, spread from empyema
Hemorrhagic
Trauma, rupture of aneurysms, malig-
nant effusion, iatrogenic
Malignant
Often hemorrhagic
Causes of Pericardial Effusion
• Idiopathic: no cause is found despite
full diagnostic investigation
• Infectious: common in viral infection
(direct + immune response)
• Iatrogenic: pacemaker, catheter
procedures, biopsy, cardiac surgery
• Neoplastic: often hemorrhagic,
denotes poor prognosis
• Myocardial infarction: myocardial
rupture, epistenocardic (early) +
Dressler syndrome (late)
• Renal failure: uremia- or dialysis-
associated
• Autoimmune disease: particularly:
systemic lupus erythematodes,
rheumatoid. arthritis., systemic
sclerosis
• Radiation: 20% develop constriction
• Rheumatic: usually small
pericardial effusion
• Traumatic: contusio cordis or heart/
aortic rupture
• Endocrine disorder: e.g. myxedema
• Pulmonary hypertension: the
mechanism is unclear (poor prognosis)
• Post cardiac surgery: usually hemat-
oma, often localized
• Aortic rupture: hemorrhagic
effusion, pericardial effusion in 45%
of dissections.
The pericardium consists of a
visceral and a parietal layer.
Patients with an open
pericardium or chest (cardiac
surgery) have an abnormal
contractile pattern.
Bacterial infection
(especially tuberculosis)
predisposes to
constriction.
Exudative effusion is
characterized by fibrous
strands.
The cause of pericardial effusion
depends on the setting of your lab
and the part of the world you practice
in (e.g. tuberculosis in developing
countries, iatrogenic when
interventions and cardiovascular
surgery are performed at your
center).
The cause of effusion may remain
unclear because the diagnosis would
require peri-and/or myocardial
biopsy as well as cytological,
histoimmunological, and
microbiological analysis of the fluid.
Myocardium
Endocardium
Fibrous layer
Parietal layer
Visceral layer
Pericardial cavity
018 // PERICARDIAL DISEASE
170
NOTES

Echo Diagnosos of Pericardial Effusion
• Echo-free space measured in end-diastole.
• Use multiple views, especially
subcostal views.
• Use atypical views; specifically visualize
the surroundings of the right ventricle.
Facts
Large effusion Regional effusion
Neoplastic Postoperative
Uremic Trauma
Tuberculosis Purulent
Myxedema
• Epicardial fat
• Pericardial cyst
• Ascites
Epicardial Fat
• Follows the normal motion
of the pericardium
• Is related to the presence of abdominal fat
• Is not completely echo-free (low-
intensity echos)
• Absent above the right atrium and
usually very prominent in the atriovent-
ricular groove as well as around the
atrial appendages
The pericardium is
highly reflective in
echocardiography.
Talk to the patient.
Thorough history-taking
often helps to clarify the
cause of effusion.
Pericardial effusions are
anterior to the descending aorta
while pleural effusions are
posterior to it.
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 is common in
obese patients, diabetes, atrial
fibrillation and coronary artery
disease. Epicardial fat is seen
better in the presence of a
pericardial effusion.
PERICARDIAL EFFUSION –
subcostal four-chamber view/2D
Large circumferential pericardial
effusion with fibrin strands. The
image loop shows swinging heart
motion.
Liver
RV
LV
Fibrin strand
171
NOTES

172
NOTES PERICARDIAL EFFUSION
Location of Pericardial Effusion
Large circumferent Localized
Small circumferent
Localized
Quantification of Circumferential Pericardial Effusion
Small < 1 mm 300 ml
Moderate 10–20 mm 500–700 ml
Large > 20 mm > 700 ml
Very large > 30 mm + compression
Localized effusions occur
in the setting of fibrinous
and iatrogenic
(hemorrhagic) pericardial
effusion.
The separation of
pericardial layers can be
detected on echocardiography,
when pericardial fluid exceeds
15–35 ml.
Follow-up of pericardial
effusion requires using the
same views. Always measure in
the same region and also assess
pericardial efussion visually.
EPICARDIAL FAT – subcostal
A patient with a small pericardial
effusion and pronounced epicar-
dial fat. Epicardial fat is promi-
nent in the AV groove and absent
in the region of the right atrium.
Epicardial fat
Epicardial border

173
NOTES
Quantification of Volume
Subtract the volume derived by tracing the cardiac contour from
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
• Establish the diagnosis
• Help to find its cause?
• Hemodynamic importance
• Direct pericardiocentesis
PERICARDIAL TAMPONADE
Definitions
Tamponade: Intrapericardial fluid
Constriction: ”Stiff” pericardial sac
Effusive constricitive: ”Stiff” pericardial sac + fluid
Volume quantification is
best performed from a
subcostal view.
Always look for other echo
features which may reveal the
cause of effusion (e.g.
myocardial infarction,
pulmonary hypertension,
endo-myocarditis).
Tamponade, constriction and
effusive constriction share many
common features.
Tamponade is a medical
emergency, and occurs when
fluid accumulates rapidly.
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.

Pathophysiology of Tamponade –
Interventricular Interdependence
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.
Hallmarks of Tamponade
• Systemic venous return shifted to inspiration
• 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
Echocardiography is
important for the diagnosis of
tamponade, but a tamponade
is also a clinical diagnosis.
Use a respiratory curve
while imaging the patient
to determine the phase of
inspiration and expiration.
LV LV
RV
RV
RA RA
LA LA
174
NOTES

Use multiple views to
assess septal shift and
use respiratory curves.
Tamponade is often a
”stagewise” process. It
may occur gradually.
Echo Signs of Tamponade
• Right atrial collapse (early sign, alone
usually does not denote relevant
tamponade)
• Dilated inferior vena cava and
hepatic veins
• Right ventricular collapse (difficult to
assess in swinging heart due to out of
plane motion of the right ventricle, but
if present usually associated with
symptoms)
• Left ventricular collapse (severe
tamponade, emergent pericardiocenti-
sis required)
• Swinging heart phenomenon (usually
associated with some degree of
hemodynamic relevance of effusion)
• Septal shift towards the left ventricle
during inspiration (indicator of hemo-
dynamic significance)
• Respiratory changes in PW Doppler
mitral valve inflow (Changes > 30% are
indicative for hemodynamic significan-
ce), Apply with caution in atrial
fibrillation
• Exaggerated respiratory changes in
tricuspid valve inflow (PW Doppler)
• PW Doppler flow reversal in hepatic
veins
.
PERICARDIAL CONSTRICTION
Pericardial Constriction – Characteristics
• Pericardial calcification/fibrosis/
scarring
• Subacute/chronic disease
• Normal systolic function
• Impaired filling
• Venous distention
• Edema
• Hepatomegaly
• Ascites
Causes of Pericardial Constriction
• Inflammation (bacterial/tuberculosis)
• Radiation
• After cardiac surgery
• Connective tissue disease
• Idiopathic
Patients with radiation-
associated constriction
have a poor prognosis.
Constriction may be local,
but in most cases it
causes impairment of
biventricular filling.
VARIATIONS OF MITRAL VALVE
INFLOW– apical four-chamber
view/PW Doppler
Respiratory variations (>25%) of
the mitral inflow in pericardial
tamponade. Inflow velocities are
less during the first beat follow-
ing inspiration.
Expiration Inspiration
Max.
Min.
175
NOTES

176
NOTES PERICARDIAL CONSTRICTION
Types of Constriction
• Annular form
• Left-sided form
• Right-sided form
• Global form + myocardial atrophy
• Global form + perimyocardial fibrosis
• Restrictive cardiomyopathy
Echo Features of Pericardial Constriction
• Dilated inferior vena cava and
hepatic veins
• Predominant forward flow in early
diastole (pronounced E-wave)
(PW Doppler)
• Exaggerated trans-tricuspid flow
during inspiration (PW Doppler)
• Expiratory flow reversal in hepatic
veins (PW Doppler)
• Septal bounce (oscillating septum)
• Septal shift (pronounced shift of the
intervenricular septum towards the left
ventricle during inspiration)
• Distorted heart contour, especially in
regional forms of constriction
• Echogenic pericardium
• Rather small ventricle/atria
OTHER DISEASES OF THE PERICARDIUM
Pericardial Cyst
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
To confirm constriction, it is
sometimes necessary to use
hemodynamic catheter studies
(dip and plateau pressure drop
between the left ventricle and
right ventricle during
inspiration).
The size of the right ventricle
increases in the phase of septal
shift.
In our experience, the easiest
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.
Pericardial cysts may be
quite large and are often first
suspected on a chest X-ray.

177
NOTES
Symptomatic pericardial
effusion in malignancy
has a poor prognosis
(median survival,
4 months).
Even in patients with a
malignancy and
pericardial effusion, the
former is not always
related to the latter.
Consider the absence of
the pericardium in
patients with unusually
shaped ventricles with
abnormal contractile
motion.
Use MRI or CT to confirm
the diagnosis.
OTHER DISEASES OF THE PERICARDIUM
Differential Diagnosis: Pericardial Cyst
• Localized pericardial effusion
• Hepatic/renal/mediastinal cyst
• Echinococcal cyst
• Diaphragmatic hernia
• Atrial diverticula
• Aneurysmatic vessels
Malignant Disease of the Pericardium
• Primary malignancy
• Metastasis
• Pericardial carcinosis
• Pericardial involvment is associated
with pericardial effusion (hallmark)
Congenital Absence of the Pericardium
• 1/10.000 autopsies
• Various forms (total/left/right absence
of the pericardium)
• Often asymptomatic or chest pain
• Higher risk of traumatic dissection
• Potential complications include
herniation or entrapment of cardiac
chambers (e.g. left atrial appendages)
Echo Features of Congenital Absence of the Pericardium
• Displacement of the heart
• Excessive cardiac motion
• Enlargement of the left atrial
appendage
PERICARDIAL CYST –
apical four- chamber view/2D
Incidental finding of a large peri-
cardial cyst located in the right
cardiophrenic angle.
RV
RA
Pericardial
cyst

178
NOTES

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

019 // TUMORS AND MASSES
180
NOTES
If you have the
opportunity, attend an
autopsy and see what
these structures really
look like.
PSEUDOTUMOURS (STRUCTURES THAT MIMIC A MASS)
Pseudotumors of the Right Atrium
• Pectinate muscles
• Eustachian valve
• Chiari network
• Crista terminalis
• Lipomatous hypertrophy of interatrial
septum (dumbbell sign)
• Prominent (lipomatous) tricuspid valve
annulus
• Catheters/pacemakers
• PFO/ASD occluders
Structures of the Left Atrium
• Pectinate muscles
• Lipomatous hypertrophy of interatrial
septum
• PFO/ASD occluders
• Calcified mitral annulus
• Ridge between the left superior
pulmonary vein and the left atrial
appendage
Eustachian
valve
EUSTACHIAN VALVE – zoomed
Very prominent and long Eusta-
chiian valve in the right atrium.
The Eustachian valve typically
arises from the inferior vena cava.
LIPOMATOUS INTERATRIAL
SEPTUM – TEE bicaval view/2D
A lipomatous interatrial septum
is best seen with TEE. The fossa
ovalis is typically spared, resulting
in a ”dumbbell”.
TV
Left atrium
Right atrium
Lipomatous
interatrial
septum
Superior vena cava
Septum
secundum
Septum
secundum

These structures can also
be visualized from
subcostal views – use
them.
Elongation of chords may be
mistaken for vegetations. They
may also mimic systolic anterior
motion and falsely suggest the
presence of hypertrophic
obstructive cardiomyopyopathy.
PSEUDOTUMOURS
Pseudotumors of the Right Ventricle
• Catheters (ICU)
• Pacemakers
• Muscle bundles
• Trabeculations
• Moderator band
Pseudotumors of the Left Ventricle
• Abberant/artifical chords
• Trabeculations
• Papillary muscles
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.
Aberrant
chord
ABBERANT CHORD –
Abberant chord that traverses the
left ventricle from the septum to
the lateral wall.
181
NOTES

182
NOTES MASSES
Risk Factors for Thrombus Formation
Atria
• Mitral valve replacement
• Mitral stenosis
Left ventricle
• Aneurysm (apex)
• Acute myocardial infarction
• First week after STEMI
Echocardiographic Aspects of Thrombus
• Size
• Echogenicity (fresh vs. old)
• Mobility
• Location
Always describe these aspects of a thrombus for better comparison over time.
Tumors of the Heart
Common Sources of Metastatic Lesions
• Melanoma
• Soft tissue sarcoma
• Thyroid cancer
• Lung cancer
• Breast cancer
• Esophageal cancer
• Renal carcinoma
• Hepatocellular carcinoma
• Secondary involvement with leukemia
and lymphoma
Mural thrombi have an
overall incidence of 20%. In
large infarctions with
aneurysms the incidence is
as high as 60%. The risk of
systemic embolization is 2%.
The appearance of thrombi
may vary greatly, ranging
from fibrotic/solid/high
echogenicity to soft/jelly-
like/low echogenicity.
Metastatic lesions of the
heart are almost 20 times
more common than
primary cardiac tumors.
LV
LA
LAA
PV
Thrombus
THROMBUS IN LEFT
ATRIAL APPENDAGE/atypical api-
cal four-/two-chamber view/2D
This rare example shows that it
may be possible to detect left
atrial appendage thrombi with
transthoracic echo, especially
when using atypical views.

183
NOTES
About 75% of all primary
cardiac tumors are benign.
Given a typical
presentation, the echo
study is virtually
diagnostic. If uncertain
perform TEE or MRI.
MASSES
Benign Primary Cardiac Tumors
Myxoma Lipoma Fibroelastoma Rhabdomyoma
Fibroma Hemangioma Teratoma
Myxoma – Echo Facts
• More common in the left atrium than
the right atrium (typically located at the
fossa ovalis of the interatrial septum)
• Less common in other heart chambers
or on valves
• Myxomas are typically pedunculated
(often short stalk), either round/oval
with a smooth surface, or villous in
appearance
• Large myoxomas may cause
valvular obstruction
• Systemic embolism or microembolism
may occur
Adult Child
46 %
15 %
46 %
15 %
5 %
21 %
16 %
2 %
3 % 5 % 1 % 13 %
MV
Myxoma
LA
IAS
MYXOMA – zoomed
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-
mogeneous.

MASSES
Lipoma
• Second most common benign
cardiac tumor
• Common locations: LV, RA, IAS
• May be found in the intramyocardial
region
• CT & MRI: high specificity for fat
Papillary Fibroelastoma
• Most frequently located on the aortic
valve, followed by the mitral valve
• Its mobility predicts the risk of
embolism
• May cause coronary occlusion (rare)
• Rarely causes valvular dysfunction
(DD: endocarditis)
• Usually located on the downstream
side of the valve
Malignant Cardiac Tumors
Do not confuse a lipoma
with lipomatous
hypertrophy of the
interatrial septum.
When valvular
dysfunction is present,
think of endocarditis
rather than papillary
fibroelastoma.
Various percentages have been
reported. Some authors claim
that up to 95% of malignant
primary cardiac tumors are
sarcomas. Irrespective of the
true underlying number,
sarcomas are certainly the most
common malignant primary
neoplasms in adults.
If a tumor involves the wall of
more than one chamber, it is
usually malignant (invasive
growth). Malignant tumors are
frequently associated with
pericardial effusion.
33 %
33 %
21%
16 %
11 %
6 %
44 %
11 %
Adult Child
Angiosarcoma Rhabdomyosarcoma Mesothelioma
Fibrosarcoma Lymphoma Osteosarcoma
Malignant teratoma
AV
FIBROELASTOMA (AORTIC
VALVE) – apical three-cham-
ber view/2D
Small mass on the ventricular
aspect of the aortic valve,
which was histologically
proven to be a fibroelasto-
ma. Fibroelastomas may also
appear as pedunculated or
berry-like structures.
Fibroelastoma
AMVL
184
NOTES

Malignant tumors of the right
atrium tend to grow along the
interatrial septum. Look closely
at this structure when you see a
mass in the right atrium.
To determine changes in size of
a tumour/mass or thrombus
compare images side by side.
This is often more reliable than
comparing measurements.
MASSES
Imaging Tips for the Evaluation of Masses
• Use atypical views focusing on the
mass
• Do not be too focused on the tumor
– perform a complete exam
• Use different gain settings. In-
tramyocardial tumors are sometimes
difficult to see.
• Use color Doppler. It may help to tell
whether the tumor is vascularized and
whether there is flow within the tumor.
• Use echo contrast. It helps to delineate
the tumor and determine whether the
tumor is vascularized.
• Do not forget to point the transducer
to the liver, the inferior vena cava, and
the pleura.
Complications of Malignant Tumors
• Local compression
• Obstruction
• Pericardial effusion with tamponade
• Spread to surrounding structures
• Arrhythmias
• Valvular dysfunction
Consequences/Therapeutic Options
• If you are not certain whether it is a
tumor, perform other imaging modali-
ties (i.e. TEE, MRI, CT) and perform
follow-up exams.
• In benign tumors, consider surgical
removal when the tumor is in the left
heart. LV tumors are subject to a high
risk of embolization (e.g.
fibroelastoma).
• If it is a thrombus., anticoagulate and
repeat study. It should become smaller.
• If it is a malignant tumor, determine
what it is (biopsy of primary tumor,
pericardial tap, lab., etc.) Some tumors
respond well to treatment with
radiation or chemotherapy (such as
lymphoma).
Small and very mobile masses
are difficult to see on MRI.
Echo is superior because its
frame rate is much higher.
AMVL
Left atrium
Tumor
MALIGNANT MASS (RHABDO-
MYOSARCOMA) – atypical apical
Tumor masses in the left atrium.
The structure of the tumor is
inhomogeneous and it is causing
inflow obstruction into the left
ventricle.
185
NOTES

186
NOTES

187
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

020 // CONGENITAL HEART DISEASE
188
NOTES BASICS
Prevalence (Adults)
• Complex jet lesions:
418 per million
ATRIAL SEPTAL DEFECTS (ASD)
Hemodynamics of Atrial Septal Defects
• Right ventricular volume overload
• Potential for paradoxical embolism
• Reduced compliance of the left
ventricle
Types of Atrial Septal Defects
Associated Lesions
ASD I (primum defect)
• Cleft mitral valve (always)
• Inlet ventricular septal defect
• Septal aneurysms
ASD II (secundum defect)
• Mitral valve prolaps
• Pulmonic stenosis
• Partial anomalous venous return
Sinus venosus defect
• Partial anomalous venous return
• Overriding superior vena cava
Coronary sinus septal defect
• Unroofed coronary sinus
• Left superior vena cava persistence
• Partial/total anomalous venous return
20% of all congenital
defects are atrial septal
defects.
Severe pulmonary
hypertension is rare in the
setting of isolated atrial
septal defects.
75% of all atrial septal
defects are secundum
defects.
Patients with a primum ASD tend to
have left axis deviation and a long PQ
interval on the ECG, whereas patients
with a secundum ASD have right axis
deviation and RBBB.
A patent foramen ovale and a
secundum ASD (ASD II) are not the
same entitiy. A patent foramen ovale is
a shunt across a ”channel” (between a
septum primum and secundum) while
an ASD II is a hole in the septum.
It is possible to have both, an
ASD and a PFO.
45% have a left-to-right shunt
35% have no shunt
20% have a
right-to-left shunt
Secundum defect
Atrial appendage
Primum defect
Sinus venosus
defect (inf.)
Coronary sinus defect
Sinus venosus
defect (sup.)

189
NOTES
ATRIAL SEPTAL DEFECT (ASD)
Views to Detect an ASD
• Slanted four-chamber view
• Parasternal SAX view
• Subcostal views
• Not all ASD‘s can be detected with TTE
Difficulties in Detecting Shunts
• Suboptimal angle to shunt flow
• Low flow velocity
• Inferior vena cava inflow
may mimic ASD
• Tricuspid regurgitation may obscure the
ASD signal during systole
• Shunt flow depends on left and right
ventricular compliance
• Elevated right heart pressure may
reduce left-to-right shunt
Transesophageal
echocardiography (TEE) is
superior in quantifying the size
and morphology of an ASD (two
orthogonal planes). TEE is also
required to diagnose a sinus
venosus defect.
The intertrial septum may show
dropouts that mimic an ASD.
IVS
TV
MV
LA
RA
VSD
ASD I
COMPLETE ATRIOVENTRICULAR
CANAL DEFECT – apical four-
chamber view/2D
Improperly formed atrioventricu-
lar valve (shared atrioventricular
valve). Both an ASD (primum
type) and a VSD are present.
Color jet
ASD II
SECUNDUM ATRIAL SEPTAL
DEFECT – slanted apical four-
chamber view/color Doppler
Moving the transducer medially
allows more parallel alignment
to the Doppler and therefore
better visualization of the ASD jet.

190
NOTES
An ASD must be excluded
in every patient with an
enlarged RV.
The absence of a color jet
across the IAS and even a
negative contrast study do not
entirely rule out an ASD. It could
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
quantified with a balloon
during intervention. This
”stretched size” of the ASD is
relevant for device sizing.
The measurement of
LVOT/PA diameter is most
critical for shunt
calculation (measurement
errors may have grave
consequences).
When to Suspect an ASD:
• Enlarged right ventricle
• Dilated pulmonary artery
• Positive contrast study
• Abnormal septal morphology
(aneurysm, discontinuity of the
interatrial septum, etc.)
• Elevated flow in the pulmonary
artery (VTI >25 cm)
• Patient history (arrhythmias,
dyspnea, atrial fibrillation + ECG +
right ventricle enlargement)
Quantification of Atrial Septal Defects
Large > 10 mm
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.
Quantification of Shunt Flow
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
Indications for ASD closure (ESC Class I)
• Patients with significant shunts (signs
of RV volume overload) and pulmo-
nary vascular resistance < 5 Wood
units, regardless of symptoms.
• Device closure is the method of
choice for secundum ASD closure
when applicable.
ESC 2010
ASD closure must be avoided
in patients with Eisenmenger
(right-to-left shunt)
syndrome (ESC Class III).
Qp/Qs =
Flowpulm = (PA diameter/2)2 . !. VTI PA/RVOT
Flowsystem = (PA diameter/2)2 . !. VTI LVOT

191
NOTES
Intervention should be
monitored with the help
of echo (TEE, intracardiac
ultrasound).
Suitabilty for Interventional Closure
Ideal < 20 mm
Uncertain 20 – 25 mm
Too large > 25 mm
Echo Assessment following Interventional ASD Closure
• Look for a residual shunt using color
Doppler (reduce PRF) and echo
contrast
• Location and stability of the device
• Thrombus on the device
PATENT FORAMEN OVALE (PFO)
Liver
LV
RV
RA
Amplatzer
ASD OCCLUDER – subcostal
The left and the right atrial disks
of an Amplatzer occluder are
visible. The interatrial septum is
captured in between.
LA
PATENT FORAMEN OVALE –
TEE bicaval view/2D
Separation between the primum
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.
PFO
SVC
RA

192
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%.
Echo Assessment of Patent Foramen Ovale
• Frequently associated with mobile and
aneurysmatic interatrial septum
• Positive contrast study – contrast
appearance in the left atrium within 3
heart cycles after opacification of the
right atrium
• Small jet into the right atrium seen with
color Doppler (usually close to the
aortic rim)
• For color Doppler assessment, use a
subcostal view or a slanted four-cham-
ber view to improve Doppler alignment
• For contrast study use a four-chamber
view
VENTRICULAR SEPTAL DEFECTS (VSD)
Ventricular Septal Defect Types
The prevalence of VSD is
10% of all congenital
lesions of the heart in the
adult population.
Perimembranous VSD is
the most common type.
Perform a Valsalva maneuver
when looking for PFO in the
contrast study and reduce PRF
for color Doppler assessment.
A negative transthoracic
contrast study does not rule out
a patent foramen ovale. You
need a transesophageal exam.
RA
Ao
PA
Inlet or canal-type ventricular septal defect
Membranous
ventricular
septal defect
Muscular ventricular
septal defect
Subarterial or supracristal
ventricular septal defects

Perimembranous
Outlet infracristal
Outlet supracristal
Inlet
Trabecular
Perimembranous or Outlet
If you are not sure
whether a VSD is present
use the good old
stethoscope!
193
NOTES
VENTRICULAR SEPTAL DEFECTS (VSD)
Views and Locations of the Various VSD Types
RVOT RVOT
TV
TV TV
RA
RA RA
PV
PA
LV
LV
RV
LV LV
RV RV
MV
MV MV
LA
LA
LA LA
Ao
Ao
PERIMEMBRANOUS VENTRIC-
ULAR SEPTAL DEFECT – PSAX/
color Doppler
Typical jet origin and direction
of a perimembranous VSD. The
defect is located below the aortic
valve. The jet is directed more
towards right ventricular inflow.
VSD
jet
Perimembranous
VSD
LA
Ao

194
NOTES VENTRICULAR SEPTAL DEFECTS (VSD)
VSD Quantification
• Use atypical views to visualize the
myocardial discontinuation
• Color Doppler detection of flow
across the interventricular septum
• Restrictive VSD has a high velocity
(> 4.5 m/sec) and occurs in small or
medium-sized defects
• Non-restrictive VSDs have a low
velocity (< 4.5 m/sec), indicating
a large defect
Aneurysmal Transformation in VSD
• Partly or completely sealed VSD by
fibrous tissue proliferation of the septal
leaflet of the tricuspid valve
• Best visualized on a five-chamber view
• No risk of rupture
Associated Lesions
Membranous VSD Supracristal VSD Inlet VSD
Septal aneurysms Aortic valve prolapse ASD I
Subaortic stenosis Cleft mitral valve
Double chambered RV
PATENT DUCTUS ARTERIOSUS (PDA)
Hemodynamics of PDA – Different Presentations
• Variable, depending on size
• Left-to-right shunt
• Elevation of pulmonary artery pressure
• Eisenmenger reaction
• Hemodynamically insignificant (small)
PDA is present in 2% of the adult
population and is often
associated with coarctation and
VSD. Always suspect a PDA in
the setting of a dilated
hyperdynamic left ventricle in
the absence of other forms of LV
volume overload.
Interventional VSD
closure is only possible in
muscular VSD with a
distance > 3mm from the
aortic valve.
Contrast is not helpful in
ventricular septal defects.

Patients with high-
velocity PDA jets are
candidates for closure
(exception: small
asymptomatic PDA).
195
NOTES
Coronary fistulas are
found in 0.2% of coronary
angiograms.
PATENT DUCTUS ARTERIOSUS (PDA)
Visualization of the Patent Ductus Arteriosus
• Parasternal short axis (pulmonary artery
bifurcation)
• Suprasternal view
• Systolic + diastolic flow in spectral and
color Doppler
• Dilatation of the pulmonary artery is
common
• 2D (suprasternal view) often allows
measurement of PDA size
CORONARY FISTULAS
Coronary Fistulas
• Abnormal communication between
coronary artery and heart chamber
• 90% into right ventricle
• RV volume overload
• Coronary steal
Echo Features of Coronary Fistulas
• Dilated coronary artery (> 0.6 cm)
• Enlargement of heart chambers
• Turbulant flow
• Continous flow (shunt) to right heart
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 pulmonary
hypertension and
eventually shunt reversal
(right to left) and the
Eisenmenger reaction.
PDA jet
PATENT DUCTUS ARTERIOSUS –
PSAX/Color Doppler
Shunt (color jet) between the
aorta and the pulmonary artery at
its bifurcation. The jet is present
during systole as well as diastole.
Ao
Ao
r-PA

196
NOTES TETRALOGY OF FALLOT
• Stenosis of the pulmonary artery (right
ventricular outflow obstruction)
• Ventricular septal defect
• Deviation of the origin of the aorta to
the right (overriding aorta)
• Concentric right ventricular
hypertrophy
Echocardiographic Assessment in Fallot
Ventricular septal defect and overriding aorta
• Assess the characteristic and large VSD
on multiple views and define the
location and number of VSDs
• The degree of aortic override is best
assessed on parasternal long-axis and
apical views.
• The extension of the defect from the
membranous septum is best seen in
the parasternal short axis
• Assess the relationship between the
defect and the tricuspid and aortic
valve.
Right ventricular outflow tract obstruction
• Use parasternal short-axis views.
• Assess the infundibulum and pulmo-
nary vale.
• Infundibular muscle bundles often
contribute to the RVOT obstruction
• The pulmonary valve annulus is often
hypoplastic (important information in
regard of a transannular patch).
• The pulmonary valve tends to look
thickened and may be dome-shaped.
Hemodynamic assessment
• A large and generally unrestricted
defect permits equalization of right and
left ventricular pressures.
• The direction and degree of shunting
strongly depend on the severity of right
ventricular outflow tract obstruction.
Aortic arch and coronary arteries
• Use suprasternal views to investigate
the aortic arch and exclude the
presence of aortopulmonary colla-
terals and the presence of a patent
ductus arteriosus.
• The anatomy of the proximal coronary
arteries should be assessed using
parasternal short-axis views
• Exclude a right aortic arch (present in
25%)
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
pulmonary hypertension and
eventually shunt reversal
(right to left) and the Eisen-
menger reaction.
In patients with a more severe
RVOT obstruction, PW and col-
or Doppler will demonstrate a
significant right-to-left shunt at
the VSD. In patients with a large
left-to-right shunt, left atrial
and left ventricular dilatation
will be present.
Right ventricular outflow
obstruction tends to occur at
multiple levels - infundibular,
RVOT, often hypoplastic annu-
lus valve abnormalities
(bicuspid valve).
When assessing patients after
Fallot repair, look for residual
pulmonary regurgitation.
RVOT obstruction
Right ventricular
hypertrophy
Overriding aorta
Large ventricular
septal defect

TETRALOGY OF FALLOT
TRANSPOSITION OF THE GREAT ARTERIES
• Lesion in which the aorta arises from
the right ventricle and the pulmonary
artery from the left ventricle.
• Its prevalence is 4.7 per
10,000 live births.
• It is not associated with any
common gene abnormality.
• The most common form is the dextro
type (D-TGA), in which the aorta arises
from the right ventricle and the
pulmonary artery from the left ventricle
(ventriculoarterial discordance).
• Levo- or L-looped transposition of the
great arteries (L-TGA) is very rare and is
commonly referred to as congenitally
corrected TGA. Venous blood returns
from the correctly located right atrium
to the discordant left ventricle via the
mitral valve and into the lung via the
pulmonary artery. Oxygenated blood
flows through the pulmonary veins to
the left atrium into the discordant right
ventricle, and via the tricuspid valve into
the systemic circulation through the
aorta (atrioventricular and ventriculoar-
terial discordance).
• The D-TGA leads to cyanotic heart
disease while L-TGA usually does not
present with cyanosis (unless the
patient has associated cardiac defects).
197
NOTES
In D-TGA a shunt on the
atrial/ventricular/great
vessels (PDA) is required to
live, either present at birth or
artificially created (e.g.
Rashkind’s procedure)
Patients with L-TGA are at
risk for (systemic) heart
failure because the morpho-
logical right ventricle (which
was not formed to sustain a
high pressure system)
supplies the systemic
circulation.
D-TGA L-TGA
AO
Ao
Mitral valve
Tricuspid
valve
LV
RV
LA
PA PA
RA
RA
RV
LV
LA
TETRALOGY OF FALLOT –
PLAX/2D
A patient with a tetralogy
of Fallot, a large VSD and an
overriding aorta.
VSD
Overriding aorta

198
NOTES TRANSPOSITION OF THE GREAT ARTERIE
Cardiac Lesions Associated With D-TGA
• A ventricular septal defect in any
region of the ventricular septum
(50% of patients).
• Left ventricular outflow tract
obstruction (25%)
• Abnormalities of the mitral and
tricuspid valve, e.g. straddling tricuspid
valve (septal chordal attachment of the
tricuspid valve extending into the left
ventricle), overriding valves.
• Coronary abnormalities
Echocardiographic Assessment in D-TGA
• Subcostal views show the pulmonary
artery arising from the posterior left
ventricle.
• Parasternal short-axis views show the
aorta rising anteriorly from the right
ventricle.
• Look for associated cardiac lesions.
Cardiac Lesions Associated With L-TGA
• Ventricular septal defect (70-80% of
patients), most commonly perimem-
branous VSD.
• Pulmonary outflow (i.e. left ventricular)
tract obstruction (30- 60% of patients).
The obstruction is commonly subval-
vular due to an aneurysm of the
interventricular septum fibrous tissue
tags or a discrete ring of subvalvular
tissue.
• Tricuspid valve abnormalities (90% of
patients) e.g. tricuspid valve regurgitati-
on, Ebstein-like malformation of the
tricuspid valve accompanied by right
ventricular dysfunction and failure
(20- 50% of patients).
• Mitral valve abnormalities (50% of
patients) e.g. abnormal number of
cusps, straddling chordal attachments
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 are in opposite posi-
tions, the valve on the left side of
the screen is more apical (lower
in the screen) than the valve on
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.
It can be identified because it is
heavily trabeculated.
RV
RA
LV
Tricuspid valve
Mitral valve
LA

199
NOTES
TRANSPOSITION OF THE GREAT ARTERIE
Echocardiographic Assessment in L-TGA
• Systemic location of the tricuspid valve
and morphologic right ventricle. It is
best seen on an apical four-chamber
view or parasternal short-axis views.
• Subcostal imaging usually provides the
clearest view of the pulmonary artery
arising from the morphologic left
ventricle.
• Look for associated cardiac lesions.
The diagnosis of L-TGA is
often missed at adult cardiac
echo laboratories!
L-TGA – Atypical long-axis view,
subpulmonic ventricle/2D
The subpulmonic ventricle, which
is anatomically the left ventricle,
ensures pulmonary circulation.
Pulmonic valve
Mitral valve
LV
PA
RA

200
NOTES

Echo_Factsheets_-_Companion_Syllabus_to_the_Masterclass_Lectures_2Nd_Edition.pdf

More Related Content

Similar to Echo_Factsheets_-_Companion_Syllabus_to_the_Masterclass_Lectures_2Nd_Edition.pdf (20)

More from SpandanaRallapalli (20)

Recently uploaded (20)

Echo_Factsheets_-_Companion_Syllabus_to_the_Masterclass_Lectures_2Nd_Edition.pdf