echo workbook 123sonography

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 TeamJuly 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

Physics of Ultrasound

Ultrasound WaveNOTE:

Wave propagation through compression and decompression of tissue

NOTE: The higher the frequency the better the resolution!However you

Velocity of ultrasound is 1540 m/s in tissue and 1570 m/s in blood

However you lose penetration!

Medical Ultrasound

Frequencies between 2- 10 MHz are used!

Ultrasound waves are generated by Piezoelectric crystals

Receive signals (echoes) are used to generate images!

Safety of Ultrasound

NOTE Diagnostic ultrasound has no adverse e!ects

Diagnostic ultrasound has no adverse

Physical e!ects of Ultrasound:ects of Ultrasound:

Thermal (depends on US intensity)

Cavitations

Ultrasound Pulse

001 // Principles of Echocardiography

1

3

The higher the US frequency the higher the pulse repetition frequency

NOTE: The higher the pulse repetition frequency, the higher the frame rate and image resolution!

2D Image

2D Image

NOTE: Ultrasound is a cut plane technique. Multiple elements are used to generate a 2D image!

Types of Probes

NOTE: In echocardiography we use curvilinear probes. The advantage of such probes is their small „footprint“. Thus, it is possible image from intercostal spaces!

Image quality increases with a higher scan line density.


2

4

Image Quality

What determines overall resolution:What determines overall resolution:

Spacial resolution — lateral Contrast resolution

Spacial resolution — axial Temporal resolution

Determinants of Spacial ResolutionDeterminants of Spacial Resolution

Lateral resolution Axial resolution

Beam width/ line density Frequency

Frequency Pulse frequency

Gain

Harmonic Imaging

NOTE: Harmonic imaging uses the resonance characteristics of tissue! The send and receive frequency of the transducers di!er. Advantage: Less artefacts, better image quality

Frame Rate — InfluenceFrame Rate — Influence

The frame rate describes the number of frames / sec that are displayed . The frame rate depends on:The frame rate describes the number of frames / sec that are displayed . The frame rate depends on:

Sector width Frequency

Scan lines Depth

NOTE: High frame rates are useful in combination with the image review function! (Detection of rapid motion)

High frame rates are useful in combination with the image review function! (Detection of rapid motion)

High frame rates are useful in combination with the image review


3

5

Limitations of 2D Imaging

Attenuation Influence of tissue

Artefacts Penetration

Attenuation

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

Decrease in amplitude and intensity as the ultrasound wave travels through a medium

Absorption (proportional to frequency)

Reflection

Refraction Shadowing

Transfer of energy from the beam to the tissue

Pseudoenhancement

Enemies of Ultrasound

NOTE: Ultrasound waves can not penetrate bone and air

Bone - Absorption of US


4

6

Air - Reflection of US

NOTE: Imaging is di!cult in patient with small intercostal spaces (bone) and in patients with COPD (air)!

Artefacts

Types of Artefacts

Near field clutter Side lobe artefact

Reverberation Beam width artefacts

Acoustic shadowing Attenuation artefact

Mirror Imaging/ double images (caused by refraction)Mirror Imaging/ double images (caused by refraction)


5

7

Specific Forms

Side Lobes Reverberations

Beam Width Artefact Incorrect Gain

When do Artefacts Occur?

Good image quality (mirror artefacts)

Poor image quality

Calcification Prosthetic material

Tips to Avoid Artefacts

Know the pitfallsBeware of strong reflections

Know the anatomy Use multiple views

NOTE: Artefacts are inconsistant!!!Artefacts are inconsistant!!!


6

8

Optimizing the 2D Image (Knobology)

Important Settings

Gain Depth

Time gain compensation (TGC)

Imaging frequency

Sector width Focus

Post Processing

NOTE: Know your echo machine!Know your echo machine!

Post Processing

Grayscale Contrast

Compression Maps

NOTE: Use predefined settings for specific situations (i.e. dipatients) and for specific modalities (i.e. standard echo, contrast).

Use predefined settings for specific situations (i.e. dipatients) and for specific modalities (i.e. standard echo, contrast).

Use predefined settings for specific situations (i.e. di!cult to image patients) and for specific modalities (i.e. standard echo, contrast).

MMode

MMode

Advantage

High temporal resolution

Good for certain measurements

Allows measurement of time intervals

Timing of events


7

9

Where is it used? (see also Chapter 2)Where is it used? (see also Chapter 2)

Aorta/ left atrium (measurements, opening of 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 „flying“ W of pulmonic valve in pulm. hypertension

NOTE: MMode has lost a lot of its importance but is still valuable in specific situations!

MMode has lost a lot of its importance but is still valuable in specific MMode has lost a lot of its importance but is still valuable in specific

Other Forms of MModeOther Forms of MMode

Anatomical MMode Freedom of axis

Color Doppler MModeTiming of flow (i.e. flow propagation)

Tissue Doppler MModeMyocardial function, timing of events

Curved MModeDisplay of information (i.e. strain)

Spectral Doppler

Doppler Formula


8

10

The Doppler formula allows us to calculate velocities (i.e. blood) based on the Doppler shift between the send and receive signal!

NOTE: 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!

Doppler

PW - Doppler Low vel. (< 1,5 m/s) site specific

CW - Doppler High vel (> 1,5m/s) site unspecific

Tissue Doppler Lower velocity, higher amplitdueLower velocity, higher amplitdue

Aliasing

Depth Velocity

Width of sample volume Doppler frequency

NOTE: Aliasing will occur if the blood flow velocity exceeds the Nyquist limit. The Nyquist limit is equal to one-half of the pulse repetition frequency! Use the baseline shift to “stretch“ the Nyquist limit!

Aliasing will occur if the blood flow velocity exceeds the Nyquist limit. The Nyquist limit is equal to one-half of the pulse repetition frequency! Use the baseline shift to “stretch“ the Nyquist limit!

Aliasing will occur if the blood flow velocity exceeds the Nyquist limit. The Nyquist limit is equal to one-half of the pulse repetition frequency! Use


9

11

Tissue Doppler Imaging

Velocity Displacement

Strain Strain rate

NOTE: Tissue Doppler is also angle dependent!Tissue Doppler is also angle dependent!

Flow Dynamics

Laminar Flow Turbulent Flow

Nonturbulent motion of a fluid in which parallel layers have di!erent velocities relative to each other

Flow of a fluid in which its velocity at any point varies rapidly in an irregular manner

Max. velocity about 1.5 m/s High velocity

Vortex

NOTE: Turbulent flow is usually seen in high velocity flow (i.e. in the setting of stenosis)

A multidirectional and vortical flow with a tendency to curl or spin leads to the formation of a vortex


10

12

Bernoulli Equation

The simplified Bernoulli Equation allows an easy estimation of pressure gradients from velocities!

Where can you apply the Bernoulli equation in the heart?Where can you apply the Bernoulli equation in the heart?Where can you apply the Bernoulli equation in the heart?

Direct applications(gradients)

Indirect applications(pressure decay)

Valvular stenosis AR Quantification

Defects (i.e. VSD, Coarctation, PDA)

Diastolic function(Decceleration time)

TR signal (sPAP) dp/dt (contractility)

Prosthetic valvesMitral stenosis (PHT method)


11

13

Color Doppler

Color Encoding

Flow towards the transducer is coded in red, away from the transducer in blue!Flow towards the transducer is coded in red, away from the transducer in

NOTE: The way flow/ flow velocities are displayed is defined by the color map! Check your machine settings!

The way flow/ flow velocities are displayed is defined by the color map! Check your machine settings!

Color Doppler and Aliasing

If the Nyquist limit is reached, the color changes abruptly (red to blue, or blue to red). In the color Doppler display, you will see a mosaic pattern!

NOTE: The phenomenon of aliasing provides a good delineation of jets (i.e. PISA)


12

14

Color Doppler Frame Rate

Scan line density Emphasis (2D vs. color)

Sector width (2D) Sector width (color)

Pulse repetition frequency Depth

NOTE: Always aim for a high color Doppler frame rate!Always aim for a high color Doppler frame rate!


13

15

How to move the transducer

Displacement Rotation Angulation

NOTE: Use enough US gel! Use enough US gel!

Imaging Windows

Parasternal -2nd - 4th intercostal space left sternal boarder

Apical 4th - 5th intercostal space, lateral!

Subcostal Below xiphoid

Right parasternal2nd - 4th intercostal space

Suprasternal Jugulum sternum

NOTE: Use as many views as possible including atypical views and always image to optimize the pathology that you see or that you are looking for.

: Use as many views as possible including atypical views and always image to optimize the pathology that you see or that you are looking for.

: Use as many views as possible including atypical views and always image to optimize the pathology that you see or that you are looking for.

002 // How to Image

1

16

Image View

Apical Views

Rotate counterclockwiseRotate counterclockwiseRotate counterclockwise

4 chamber view 2 chamber view 3 chamber view

Orientation of the apical viewsOrientation of the apical views

5 chamber view5 chamber view

Coronary sinus viewCoronary sinus view

NOTE: Avoid foreshortening, place the transducer as lateral and caudal as possible

: Avoid foreshortening, place the transducer as lateral and caudal as : Avoid foreshortening, place the transducer as lateral and caudal as : Avoid foreshortening, place the transducer as lateral and caudal as

002 // How to Image

2

17

Subcostal Views

Subcostal 4 chamber viewSubcostal 4 chamber view

Vena cava inferior viewVena cava inferior view

Subcostal short axis viewSubcostal short axis view

NOTE: Perform Subcostal views in all patient Perform Subcostal views in all patient

Suprasternal View

Suprasternal viewSuprasternal view

002 // How to Image

3

18

NOTE: Suprasternal view allows you to detect, coarctation, aortic dissection and to quantify retrograde flow in the Aorta (aortic regurgitation)

Suprasternal view allows you to detect, coarctation, aortic dissection and to quantify retrograde flow in the Aorta (aortic regurgitation)

002 // How to Image

4

19

MModeMMode

MMode aorta/left atriumMMode aorta/left atrium

MMode left ventricleMMode left ventricle

Reference Values — MModeReference Values — MModeReference Values — MModeReference 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

TAPSE > 16mmMAPSE (longitudinal LV function)

> 12mm

Reference Values — Doppler Reference Values — Doppler Reference Values — Doppler Reference Values — Doppler

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

LVOT velocity (m/sec)LVOT velocity (m/sec) PW < 1,3

Pulmonic valve velocity (m/sec)Pulmonic valve velocity (m/sec) CW 0.5 - 1.0

Tricuspid valveTricuspid valve PW 0.3 - 0.7

Tricuspid regurgitation (m/sec)Tricuspid regurgitation (m/sec) CW 1,7— 2,3

E wave (m/sec)E wave (m/sec) PW < 1,3

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

Right ventricular lateral wall (cm/sec)Right ventricular lateral wall (cm/sec) TDI PW12,2 (41-60a) / 10,4 (>60a)

002 // How to Image

5

20

Color Doppler

2D before color!Look for aliasing to detect jets

Reduce PRF to detect low velocity flow

Use higher frame rates

Use multiple viewsColor as guide for CW/PW

NOTE: Don´t expect to see the full extent and size of a color Doppler jet if 2D image quality is poor

: Don´t expect to see the full extent and size of a color Doppler jet if 2D : Don´t expect to see the full extent and size of a color Doppler jet if 2D

002 // How to Image

6

21

The Left Ventricle

Quantification of LV DiameterQuantification of LV Diameter

PLAX MMODE 4 ch view

NOTE: only use MMode values if your line of interrogation is perpendicular to the LV cavity and walls

only use MMode values if your line of interrogation is perpendicular to the LV cavity and walls

only use MMode values if your line of interrogation is perpendicular

LVED Diameter — Reference Values 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

NOTE: Measure distances between the endocardial boarders, not the pericardium (lateral)

Measure distances between the endocardial boarders, not the Measure distances between the endocardial boarders, not the

LVED Diameter/BSA — Reference Values LVED Diameter/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

NOTE: Normal chamber size increases with body surface area (and body size) Normal chamber size increases with body surface area (and body size) Normal chamber size increases with body surface area (and body size)

003 // Heart Chambers and Walls

1

22

LV Diastolic Volume (4ch view) — Reference Values LV Diastolic Volume (4ch view) — Reference Values LV Diastolic Volume (4ch 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

NOTE: Volume measurements are superior to distance and area measurements

Volume measurements are superior to distance and area Volume measurements are superior to distance and area

LV Systolic Volume (4ch view) — Reference ValuesLV Systolic Volume (4ch view) — Reference ValuesLV Systolic Volume (4ch 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

NOTE: Don´t exclude the papillary muscles when tracing the LV volumes. t Their volumes should be included in the calculation

: Don´t exclude the papillary muscles when tracing the LV volumes. t Their volumes should be included in the calculation

: Don´t exclude the papillary muscles when tracing the LV volumes. t Their volumes should be included in the calculation

Pathophysiology

Principles of LV Function:

Factors influencing ejection fraction / stroke volume


2

23

NOTE: A reduction in longitudinal function is an early marker of LV dysfunction

Pathophysiology of LV failure: Cascade and Compensatory Mechanisms

NOTE: Contractility, pre- and afterload influence myocardial function. A reduction in contractility is initially compensated by an activation of the sympathetic nervous system (compensatory increase in heart rate and contractility) as well as dilatation of the LV. Stroke volume is kept adequate at rest but can not adapt to exercise (reduced functional reserve). In the endstage stroke volume is also reduced at rest (decompensation)

LV Function

Parameters of LV FunctionParameters of LV Function

Fractional shortening Cardiac output

“Eyeballing“ of LVF Cardiac Index

Ejection fraction (EF) - Simpson method

Contractility (dp/dt)

Stroke volume Tei index

TDI velocity of the myocardium

MAPSE (mitral annular plane systolic excursion)

NOTE: LVF and contractility can be reduced despite „normal“ ejection fraction. Especially in patients with small ventricles

LVF and contractility can be reduced despite „normal“ ejection fraction. Especially in patients with small ventricles

LVF and contractility can be reduced despite „normal“ ejection


3

24

Fractional Shortening — Reference ValuesFractional Shortening — Reference Values

Normal 25- 43% 27- 45%

Mild 20- 24% 22- 26%

Moderate 15- 19% 17- 21%

Severe ! 14% ! 16%

NOTE: Fractional shortening is a rough estimate of global left ventricular function. Do not use the Teichhholz formula to derive an ejection fraction from these values

Fractional shortening is a rough estimate of global left ventricular function. Do not use the Teichhholz formula to derive an ejection fraction

Fractional shortening is a rough estimate of global left ventricular function. Do not use the Teichhholz formula to derive an ejection fraction

Fractional Shortening — ContraindicationsFractional Shortening — Contraindications

LBBB / Dyssynchrony/Pacemaker

Abnormal septal motion

Regional wall motion abnormalities

Inadequate (oblique) MMode orientation

Poor image quality“Pseudo-shortening“ of the LV (very small ventricle)

NOTE: In these settings fractional shortening can either over or underestimate left ventricular function

In these settings fractional shortening can either over or underestimate left ventricular function

In these settings fractional shortening can either over or

Ejection Fraction — Simpson MethodEjection Fraction — Simpson Method

Normal > 55 %

Mild 45— 54 %

Moderate 30— 44 %

Severe < 30%

NOTE: 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.

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.

1) Ejection fractions tend to be higher in small ventricles. 2) Athletes often have ejection fractions in the low normal range. 3) Ejection fraction


4

25

Stroke Volume, Cardiac Output, Cardiac Index — Reference ValuesStroke Volume, Cardiac Output, Cardiac Index — Reference ValuesStroke 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

NOTE: The calculation of these parameters critically depend on the correct measurement of the LVOT width.

The calculation of these parameters critically depend on the correct measurement of the LVOT width.

The calculation of these parameters critically depend on the correct

dP/dt — Reference Values

Normal > 1200 mmHg/sec

Borderline 800— 1200 mmHg/sec

Reduced < 800 mmHg/sec

Severly reduced < 500 mmHg/sec

Limitations: MR signal needed, inexact, not completely load independentMR signal needed, inexact, not completely load independentMR signal needed, inexact, not completely load independent

NOTE: A rough estimate of contractility can also be obtained by eye balling the slope of the MR curve.

A rough estimate of contractility can also be obtained by eye balling A rough estimate of contractility can also be obtained by eye balling

The Right Ventricle

Characteristics

Wall thinner (<5mm) Moderator band

Trabeculations Wraped around LV


5

26

Measurement of RV (ASE Guidelines 2010)Measurement of RV (ASE Guidelines 2010)

Measurements of the Right VentricleMeasurements of the Right Ventricle

Abnormal

RV basal diameter >4.2cm

RV subcostal wall thickness

>0.5cm

RVOT PSAX distal diameter

>2.7cm

RVOT PLAX proximal diameter >3.3cm

RV systolic function

TAPSE <1.6cm

PW Peak at the annulus <10 cm/s

PW myocardial performance index

>0.4

Tissue doppler myocardial performance index

>0.55

RV diastolic function

E/A ratio <0.8 or >2.1

E/e‘ >6

Deceleration time (ms) <120ms

NOTE: The RV diameters appears larger if the transducer position is too far cranial!

The RV diameters appears larger if the transducer position is too far


6

27

Causes of RV DilatationCauses of RV Dilatation

Dil. CMP Right heart infarction

Myocarditis Pulmonary embolism

Right ventricular dysplasia

NOTE: Always search for a cause of RV dilatation! Always search for a cause of RV dilatation! Always search for a cause of RV dilatation!

Parameters of RV FunctionParameters of RV Function

Visual assessmentTDI velocity RV(normal > 1 cm/s)

TAPSE (tricuspid annular plane systolic excursion)normal > 18 mm

FAC (fractional area change)

Strain - lateral free wall

Volumetric calculations of RV ejection fraction (i.e. 3D Eco)

NOTE: Practice assessing the RV.- Do it in EVERY patientPractice assessing the RV.- Do it in EVERY patientPractice assessing the RV.- Do it in EVERY patient

FAC — Reference Values

Normal > 39 %

Mild 35—39 %

Moderate 30—35 %

Moderate- severe 25—30 %

Severe < 25 %


7

28

The Left Atrium

NOTE: LA size and volume predicts events (i.e. Afib, stroke) and is a marker of disease severity.

LA size and volume predicts events (i.e. Afib, stroke) and is a marker of LA size and volume predicts events (i.e. Afib, stroke) and is a marker of

MMode Measurements of LA — Reference ValuesMMode 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 — Reference Values

Normal (mm) " 50

Mild (mm) 51—60

Moderate (mm) 61—70

Severe (mm) > 70

LA Area — Reference Values

Normal (cm2) " 20

Mild (cm2) 20—30

Moderate (cm2) 30—40

Severe (cm2) > 40


8

29

LA Volume (Area Length Method) — Reference ValuesLA Volume (Area Length Method) — Reference Values

Normal (mL) 18- 58 22- 52

Mild (mL) 59- 68 53- 62

Moderate (mL) 69- 78 63- 72

Severe (mL) ! 79 ! 73

NOTE: LA volume measurements are superior to MMode and 2D distance measurements

LA volume measurements are superior to MMode and 2D distance LA volume measurements are superior to MMode and 2D distance

Pittfalls calculating LA volumePittfalls calculating LA volume

Inclusion of pulm. veins Tenting area of MV

Alignment / atrial foreshortening

Lateral resolution

Measuremtent not performed at end-systole

Oblique view of the LA

Parameters of LA FunctionParameters of LA Function

Doppler (MV inflow)Area changes systolic/diastolic

Pulmonary vein flow TDI / 2D Strain

NOTE: In most cases the Doppler (MV-inflow) signal is suLA function! Functional assessment of the LA is still a research application.

In most cases the Doppler (MV-inflow) signal is suLA function! Functional assessment of the LA is still a research application.

In most cases the Doppler (MV-inflow) signal is su!cient to estimate LA function! Functional assessment of the LA is still a research application.


9

30

The Right Atrium

Causes of RA DilatationCauses of RA Dilatation

Pulmonary hypertension TV- disease

RV - failure Atrial fibrillation

NOTE: The RA can be stretched in length if the LA expands The RA can be stretched in length if the LA expands The RA can be stretched in length if the LA expands

RA Length — Reference Values

Normal (mm) 29—45

Mild (mm) 46—49

Moderate (mm) 50—54

Severe (mm) ! 55

Coronary Sinus

Reference value = 4-8mm (upper limit 15m)

Causes of a dilated coronary sinus: elevated RA pressure, V. cava sin. persistens, malformation (aneurysm/diverticula)

Vena Cava Inferior

Size < 17mm, Inspiratory collapse ! 50%

NOTE: VCI size reflects fluid status, central venous pressure, tricuspid regurgitation and allows an estimation of RA pressure!


10

31

NOTE: A large vena cava inferior does not always indicate a medical condition. Some patients simply have a large vena cava inferior (even in the absence of elevated RA pressure.

Left Ventricular Hypertrophy

Forms of LVH

Relative Wall Thickness (RWT)(PWT = posterior wall thickness)(LVID = Left ventricular internal dimension)

Normal values 22— 42 %

NOTE: Most patients with hypertension have concentric LVHMost patients with hypertension have concentric LVHMost patients with hypertension have concentric LVH

Quantification of LVH — Septal Thickness SeverityQuantification of LVH — Septal Thickness Severity

Normal (mm) 6—10 6—9

Mild (mm) 11—13 10—12


11

32

Moderate (mm) 14—16 13 —15

Severe (mm) ! 17 ! 16

2D-measurements: end diastole, mid septum end diastole, mid septum

Potential problems: Measurements were not performed at enddiastole (2D)“, RV structures interfere with measurement, shape of the IVS (basal septal buldge), incorrect MMode orientation (non-perpendicular)

Measurements were not performed at enddiastole (2D)“, RV structures interfere with measurement, shape of the IVS (basal septal buldge), incorrect MMode orientation (non-perpendicular)

Measurements were not performed at enddiastole (2D)“, RV structures interfere with measurement, shape of the IVS (basal septal buldge), incorrect MMode orientation (non-perpendicular)

Sigmoidal Septum

Less than 3 cm in length Associated with HTN/

Not associated with hypertrophic CMP

Associated with LVH

NOTE: May cause obstruction and SAM (hypovolemia, hyperkinesia, catecholamines).

May cause obstruction and SAM (hypovolemia, hyperkinesia, May cause obstruction and SAM (hypovolemia, hyperkinesia,

Quantification of LV Mass (Devereux Formula)

NOTE: LV mass better reflects the extent of LVH then measurements of septal thickness. But only perform LV mass measurement in patients with good image quality!


12

33

LV Mass — Reference ValuesLV Mass — 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 PatientsAdditional Findings in Hypertensive Patients

Left atrial enlargement RV hypertrophy

Diastolic dysfunction Dilated aorta

AV sclerosis Mitral annular calcification

NOTE: If these findings are present it is likely that LVH is a consequence of hypertension

If these findings are present it is likely that LVH is a consequence of If these findings are present it is likely that LVH is a consequence of

Athletes Heart

Septum rarely > 13mm

Normal or supernormal diastolic function

Only following intensive, prolonged endurance training (> 1h/d)

RWT " 45

NOTE: Endurance training/isotonic (i.e. marathon runner) causes a more eccentric form of LVF vs. isometric exercise (weight lifting) causes a more concentric form of LVH.

Endurance training/isotonic (i.e. marathon runner) causes a more eccentric form of LVF vs. isometric exercise (weight lifting) causes a more

Endurance training/isotonic (i.e. marathon runner) causes a more eccentric form of LVF vs. isometric exercise (weight lifting) causes a more

NOTE: Deconditioning reverses LVH


13

34

Di!erential Diagnosis: Hypertension vs. Hypertrophic CMPDi!erential Diagnosis: Hypertension vs. Hypertrophic CMPDi!erential Diagnosis: Hypertension vs. Hypertrophic CMP

HTN HCMP

RR + -

Degenerative changes + -

Secondary changes + -

Young age - +

Strain

Fam. history of HCMP + +

Genetics - +


14

35

Basics of Diastolic Dysfunction

NOTE: Diastolic dysfunction is common and is associated with a worse prognosis

Causes

NOTE: Aging Dil. CMP

NOTE: Every patient with systolic

LVH Restr. CMP

with systolic dysfunction also

has diastolic dysfunction!

CAD Hypertr. CMPdysfunction!

NOTE: Patients with diastolic dysfunction usually have a dilated left atrium: Patients with diastolic dysfunction usually have a dilated left atrium: Patients with diastolic dysfunction usually have a dilated left atrium: Patients with diastolic dysfunction usually have a dilated left atrium

Diastole Components

NOTE: IVRT — isovolumetric relaxation (AV closure to MV opening )

NOTE: Aortic valve

closure can be assessed with Rapid early (passive) LV filling assessed with PW Doppler in

Diastasis

PW Doppler in the LVOT (end

of signal)!Late LV filling — atrial contraction

of signal)!

Timing of Diastole

NOTE:Fusion of E and A wave can occur with tachycardia! Duration of diastasis decreases with heart rate and PQ duration!

004 // Diastolic Function

1

36

Physiology of diastolic function

NOTE: Echo assessment of diastolic function primarily reflects left atrial filling pressure!

Active Relaxation (Early diastole)Active Relaxation (Early diastole)

Internal loading conditions Contractility

Wall stress Atrial impedence

Mitral Inflow Signal

NOTE: Sample volume should be at the tip of the MV leaflets!


2

37

Mitral Inflow — Reference ValuesMitral Inflow — Reference ValuesMitral 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

NOTE: There are situations where the parameters of diastolic function are inconsistent and di

: There are situations where the parameters of diastolic function are inconsistent and di!cult to interpret.

: There are situations where the parameters of diastolic function are cult to interpret.

: There are situations where the parameters of diastolic function are : There are situations where the parameters of diastolic function are

TDI Mitral Annulus – Reference ValuesTDI Mitral Annulus – Reference ValuesTDI Mitral Annulus – Reference Values


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

Situations where TDI at the mitral annulus should not be usedSituations where TDI at the mitral annulus should not be used

Annular calcification Mitral valve prosthesis

Mitral stenosisModerate to severe mitral regurgitation


3

38

Pulmonary Venous Flow

Peak systolic PV flow vel. (S)

Peak diastolic PV flow vel. (D)

Peak reverse atrial flow vel. (AR)

AR duration (ARdur)

Signs of impaired diastolic function: decrease in systolic component, increase in peak AR, increase in AR duration

decrease in systolic component, increase

NOTE: Use right upper PV to record the PW signal! Remember to reduce PRF! Use right upper PV to record the PW signal! Remember to reduce PRF!

Pulmonic Veins – Reference ValuesPulmonic Veins – Reference ValuesPulmonic Veins – Reference Values


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

NOTE: Pulmonic vein flow, has many limitations and is rarely used in clinical practice

Pulmonic vein flow, has many limitations and is rarely used in clinical Pulmonic vein flow, has many limitations and is rarely used in clinical Pulmonic vein flow, has many limitations and is rarely used in clinical Pulmonic vein flow, has many limitations and is rarely used in clinical

Grading of Diastolic Dysfunction

NOTE: Left atrial filling pressure increases with degree of dysfunction!


4

39

A Simple Approach to Diastolic Function/Rules

Supernormal diastolic function: If echo is normal and patient is young

Normal diastolic function: If echo is normal, pat < 45a and E>A

Impaired relaxation: If A is higher than E (E/A ration is < 1), filling pressure is normal or mildly elevated

Pseudonormal diastolic function: If echo is abnormal (LVH, red LVF, etc) or pat > 65a and E is higher than A (E/A ration > 1)

DD Normal vs Pseudonormal: Check for short DT (160-200ms) , LA enlargement (34ml/m2) , E/E`(! 8-12)

Restrictive filling: If E is twice A (E/A ratio is >2), filling pressure elevated

Perform TDI: If E/E´is > 12-15 then filling pressure is elevated (PCWP > 12mmHg)

Perform Valsalva: Unloading of the atrium, LA pressure drops, unmasking of pseudonormal filling (restrictive vs. reversible restrictive)

Algorithm for estimating filling pressures in patients with normal left ventricular function (EF >55%) according to the ASE/EAE guidelines


5

40

Algorithm for estimating filling pressures in patients with reduced left ventricular function (EF <55%) according to the ASE/EAE guidelines

Specific Situations

Variations in E/A RatioVariations in E/A Ratio

Changes of LVFP with respiration?

COPD patients

High normal filling pressures (E/E`= 8 -9)High normal filling pressures (E/E`= 8 -9)

E/A FusionE/A Fusion

Tachycardia Long systole (LBBB)

Long AV delay Carotid artery maneuver

L- WaveL- WaveL- Wave

Mid-diastolic filling of the LV Elevated LVFP?

Bradycardia Short AV delays

Common in LVH Common in afib


6

41

NOTE: The presence of an L-Wave indicates elevated filling pressure!

L-Wave indicates

Atrial Fibrillation/Flutter and Heart failureAtrial Fibrillation/Flutter and Heart failure

Often associated with diastolic dysfunction

Pulm. venous flow di!cult to assess

No A wave E/E‘ increases with severity of HF

E/E‘ better than BNP and LA area

E/E‘ declines with improvement of HF

LVFP in Mitral Valve DiseaseLVFP in Mitral Valve Disease

NOTE: Diastolic

dysfunction/LV filling pressure

LA size does not necessarily reflect elevated LAFP

LA size can also be enlarged due to volume overload + afib

filling pressure should not be

assessed in the setting of MR >

grade II

E wave velocity also reflects increased stroke volume

E‘ is reduced in MS elevated in MR (stroke volume)

NOTE: Estimates filling pressure to determine the severity of disease and how the LV can cope with the problem (i.e. AS,AR; CMP)

Estimates filling pressure to determine the severity of disease and how the LV can cope with the problem (i.e. AS,AR; CMP)

Estimates filling pressure to determine the severity of disease and how the LV can cope with the problem (i.e. AS,AR; CMP)


7

42

Background

Definition NOTE: Ischemic CMP is Myocardial disease (primarily) Ischemic CMP is similar than

Impaired systolic function

similar than dilated CMP but by definition

Left ventricular dilatation

by definition NOT a form of dil. CMP!

Causes

Idiopathic (50%) NOTE: Etiology is often

Myocarditis (9%)Etiology is often not found

Ischemic heart disease (9%)

not found because biopsy is not

Peripartum CMP (7%)

is not performed!

Infiltrative disease (5%)

NOTE: Among patients with idiopathic cardiomyopathy, it is estimated that up to 50% have genetic forms

Among patients with idiopathic cardiomyopathy, it is estimated that up to 50% have genetic forms

Among patients with idiopathic cardiomyopathy, it is estimated that up

Associated ProblemsAssociated Problems

Left heart failure Atrial fibrillation

Pulmonary hypertension Mitral regurgitation

Right heart failure Tricuspid regurgitation

Dyssynchrony Thromboembolism

005 // Dilated Cardiomyopathy

1

43

Echo features

DiagnosisNOTE:

Reduced LVFNOTE:Endstage ischemic

Dilated LV (spherical)ischemic CMP and dilated CMP

Reduced -RVFdilated CMP look very similar!

Exclude other causes (CAD, valvular)similar!

How advanced is dilated CMP - Features to look forHow advanced is dilated CMP - Features to look for

Low output Reduced LVF, LVOT vel < 0.5m/sec

Atrial sizeLarge atria in more advanced forms

Mitral regurgitation Annular dilatation

Diastolic function /filling pressure

Pseudonormal / restrictive pattern

RVF, pulmonary hypertension and TR

Poor RVF, pulmonary hypertension, severe TR

Causes of Mitral regurgitation in CMPCauses of Mitral regurgitation in CMP

Dyssynchrony NOTE: MR increases

Shape changesMR increases mortality!(additional

LVF(additional volume overload of

Tenting - leaflet restrictionoverload of LV)

Annular dilatation

NOTE: Dilated CMP results in functional mitral regurgitation: Dilated CMP results in functional mitral regurgitation

NOTE: Exclude a structural form of MR. It could point to the presence of a valvular Form of CMP.

: Exclude a structural form of MR. It could point to the presence of a : Exclude a structural form of MR. It could point to the presence of a


2

44

Markers of poor prognosis

Very severe LV-dysfunction Reduced RVF

Very large LV MR

Elevated LVEFPSevere pulmonary

hypertension

Right heart failure Pleural e!usion

NOTE: RVF correlates better with prognosis than LVF (it denotes endstage heart failure)

RVF correlates better with prognosis than LVF (it denotes endstage RVF correlates better with prognosis than LVF (it denotes endstage

Specific Forms

Ischemic CMPMost common cause of heart failure, large infarcts, remodeled ventricles

Tako Tsubo CMPStress induced CMP (apical ballooning, reversible), normal coronary arteries

Peripartum CMP

Myocarditis? Risk factors: age > 30 years, multiparity pre-, eclampsia postpartum hypertension

Tachycardia mediated CMP

Atrial, ventricular tachycardiareversible

Arrhythmia mediated CMP Ectopic beats > 17.000/24h

HIV mediated CMP

Focal myocarditis, most common form of CMP in African countries (i.e. Burkina Faso)

NOTE: It is often di"cult or even impossible to distinguish dilated from ischemic cardiomyopathy from the echocardiogram

cult or even impossible to distinguish dilated from ischemic cardiomyopathy from the echocardiogram

cult or even impossible to distinguish dilated from


3

45

LV Non—Compaction

Characterized by prominent trabeculae and intertrabecular recessi

Associated with other cardiac abnormalities

Genetic disease, Risk of CMP, Family screening!

Associated with neuromuscular disorders

NOTE: There is a genetic link between non compaction and hypertrophic cardiomyopathy

There is a genetic link between non compaction and hypertrophic There is a genetic link between non compaction and hypertrophic

Chagas Disease

Trypanosoma cruzi Megaesophagus

Cardiac disease Megacolon

Most common form of CMP in Latin-AmericaMost common form of CMP in Latin-America

Right heart failure is dominant (regional + global dysfunction).Right heart failure is dominant (regional + global


4

46

Basics

Epidemiology

Prevalence: 1 in 500 NOTE: HCMP may show:

Annual Mortality:Adults 2%Childhood 4- 6%

may show:highly variable morphology, clinical presentation

Most common cause of sudden cardiac death in athletes (36%)

presentation and prognosis!

Cause

Genetic disease (sarcomere) Autosomal dominant

Syndromes (Noonan‘s, Friedreich ataxia, LEOPARD)Syndromes (Noonan‘s, Friedreich ataxia, LEOPARD)

NOTE: The onset of disease is variable: childhood, adolescence or sometimes late in life.

The onset of disease is variable: childhood, adolescence or sometimes The onset of disease is variable: childhood, adolescence or sometimes

NOTE: Perform a family screening! Perform a family screening!

Symptoms

Asymptomatic Chest pain

ECG abnormalities Syncope

Arrhythmias Sudden death

Dyspnea Palpitations

When to Consider Hypertrophic Cardiomyopathy?When to Consider Hypertrophic Cardiomyopathy?

Unexplained LVH (>15mm) LVOT/LV gradient

Non-dilated ventricleSpeckled appearance of myocardium

Asymmetric LVHTurbulent flow in the LV / LVOT

NOTE: Other cause for LVH include: hypertension, aortic stenosis, athletes heart, infiltrative heart disease.

Other cause for LVH include: hypertension, aortic stenosis, athletes heart, infiltrative heart disease.

Other cause for LVH include: hypertension, aortic stenosis, athletes

006 // Hypertrophic Cardiomyopathy

1

47

Obstructive forms Non-obstructive forms

LVOT obstruction Asymetric

Midventr. obstruction Apical

Echocardiographic Evaluation

Non obstructive CMP (Apical Type)Non obstructive CMP (Apical Type)

Asians Better prognosis

Giant negative T-waves Spades sign

NOTE:Apical hypertrophy can be diopacification

Apical hypertrophy can be di!cult to detect, use contrast for LV cavity cult to detect, use contrast for LV cavity

Views to display SAM = systolic anterior motion (of the anterior mitral valve leaflet)Views to display SAM = systolic anterior motion (of the anterior mitral valve Views to display SAM = systolic anterior motion (of the anterior mitral valve

Parasternal long axis viewParasternal short axis view at MV

Apical long axis viewMmode / Color MMode


2

48

SAM (Systolic Anterior Motion) Increases withSAM (Systolic Anterior Motion) Increases with

Hypovolemia Exercise

Medication (i.e. Nitro, diuretics)

Dobutamie

Valsalva Post-extrasystolic

NOTE: Use Valsalva or exercise to provoke a gradient during the exam. It can „unmask“ obstructive CMP

: Use Valsalva or exercise to provoke a gradient during the exam. It can „unmask“ obstructive CMP

: Use Valsalva or exercise to provoke a gradient during the exam. It can

Quantification of ObstructionQuantification of Obstruction

CW Doppler LVOT (max vel.)

Dagger shaped Doppler signal

Late or early systolic?

Provocation (valsalva, excercis, nitroglycerin)

Cave: DD AS + MR signal

NOTE: Find the site of obstruction with 2D and Color Doppler (SAM), put CW through this site, use the CW-Doppler focus.

Find the site of obstruction with 2D and Color Doppler (SAM), put CW through this site, use the CW-Doppler focus.

Mitral regurgitation in obstructive CMP

„Distortion“ of MV (SAM)

Jet directed posterior

Severity correlates with degree of obstruction

NOTE: MR can also increase with provocation and a rise in gradients MR can also increase with provocation and a rise in gradients


3

49

Other Causes of LVOT ObstructionOther Causes of LVOT Obstruction

Hypertensive CMP(sigmoidal septum)

Following operation for aortic stenosis

Post MV-repair (too long AMVL)

Hypovolemia

LVOT obstruction and AS Hypercontractile state

NOTE: The presence of SAM / obstruction does not imply that HCMP is present. IT cal also be associated with other diseases (see above)

The presence of SAM / obstruction does not imply that HCMP is present. IT cal also be associated with other diseases (see above)

The presence of SAM / obstruction does not imply that HCMP is present. IT cal also be associated with other diseases (see above)

Midventricular HCMP

Least commonCombined with LVOT obstruction

Later peak of max velocity Provocation

Gradients not high Hypercontractility

NOTE: Mid-ventricular and LVOT obstruction can be combined Mid-ventricular and LVOT obstruction can be combined Mid-ventricular and LVOT obstruction can be combined

Assessment Should Include NOTE: Septal thickness

Septal thickness! Diastolic functionSeptal thickness > 30mm = increased risk

Systolic function? Atrial size

increased risk for SCD!

NOTE: Because the LV cavity is usually small, LVF appears better than it is. In addition most patients have reduced longitudinal function, In particular in those segments which are very hypertrophied

: Because the LV cavity is usually small, LVF appears better than it is. In addition most patients have reduced longitudinal function, In particular in those segments which are very hypertrophied

: Because the LV cavity is usually small, LVF appears better than it is. In addition most patients have reduced longitudinal function, In particular in

Di!erential Diagnosis

Hypertension Amyloidosis

Aortic stenosis Sarcoid Heart disease

Athletes Fabry‘s disease

NOTE: Patient history, distribution of LVH, other echo findings and speckle tracking can be helpful to make the right diagnosis

Patient history, distribution of LVH, other echo findings and speckle tracking can be helpful to make the right diagnosis

Patient history, distribution of LVH, other echo findings and speckle


4

50

Alcohol Septal Ablation — Recommendations

Severe heart failure symptoms (NYHA classes III or IV) refractory to medications

Subaortic Doppler gradient > 50 mmHg at rest or with provocation (i.e. exercise)

Adequate coronary anatomy /Echo morphology

NOTE: Also consider surgical myectomy, especially in patients who are surgical candidates (i.e. aortic stenosis with LVOT obstruction)


5

51

Basics

Definition

Idiopathic or systemic disorder

Left and/or right ventricle

Primarily „a diastolic disease“ of the ventricles

Normal or mildly reduced systolic function

NOTE:

1) restrictive CMP is NOT the same as a restrictive filling pattern! A restrictive filling pattern can also be present in other forms of CMP

2) Subclinical systolic dysfunction (despite normal EF) is often present in the early stages of disease!

estrictive CMP is NOT the same as a restrictive filling pattern! A restrictive filling pattern can also be present in other forms of CMP

2) Subclinical systolic dysfunction (despite normal EF) is often present in the early stages of disease!

estrictive CMP is NOT the same as a restrictive filling pattern! A restrictive filling pattern can also be present in other forms of CMP

2) Subclinical systolic dysfunction (despite normal EF) is often present in the

Cause

Amyloidosis Idiopathic

Sarcoid heart disease Endomyocardial fibrosis

Radiation Chemotherapy

Carcinoid Hemochromatosis

Pathophysiology

Diastolic dysfunction Elevated filling pressure

Sti! ventricle Right heart failure

Hepatomegaly Peripheral edema

Pericardial e!usion Pleural e!usion

NOTE: Patients typically present with signs of right heart failure! Clinical and echocardiographic features can be similar to those of constrictive pericarditis!

Patients typically present with signs of right heart failure! Clinical and echocardiographic features can be similar to those of constrictive

Patients typically present with signs of right heart failure! Clinical and echocardiographic features can be similar to those of constrictive

007 // Restrictive Cardiomyopathy

1

52

Echo Features

LVH Bi-atrial enlargement

Normal LV volume Normal ventricular function

Expanded LAA Enlarged pulmonic veins

Dilated IVC Tricuspid regurgitation

NOTE: Suspect restrictive CMP in patients with normal LVF but large atria: Suspect restrictive CMP in patients with normal LVF but large atria: Suspect restrictive CMP in patients with normal LVF but large atria

How to distinguish restriction from constriction (Doppler MV Inflow and TDI MV Annulus)

Progressive decline of E‘ wave in restrictive CMP

DD: E‘ wave is preserved in constrictive pericarditis!!

Specific Forms

Amyloid Heart Disease — Echo FeaturesAmyloid Heart Disease — Echo Features

Ground glass pattern LVH

Atrial enlargement IAS thickening

Thickened valves Mild regurgitation

Diastolic dysfunction Pericardial e!usion

Pleural e!usionSystolic dysfunction (end-stage)

NOTE: The echocardiogram is often so typical that it strongly points to the diagnosis of amyloidosis

: The echocardiogram is often so typical that it strongly points to the diagnosis of amyloidosis

: The echocardiogram is often so typical that it strongly points to the


2

53

Hypereosinophilia/ Endomyocardial Fibrosis (EMF)— Echo FeaturesHypereosinophilia/ Endomyocardial Fibrosis (EMF)— Echo Features

Fibrous thickening of endocardium

Eosinophilic infiltrates left and/or right apex

Di!erent stages (necrotic/thrombotic/fibrotic)

Late stage restrictive filling pattern

NOTE: Eosiophilic thombii in EMF are present even in the absence of regional wall motion abnormalities or global LV dysfunction.

Eosiophilic thombii in EMF are present even in the absence of regional wall motion abnormalities or global LV dysfunction.

Sarcoidosis — Echo FeaturesSarcoidosis — Echo Features

Cardiac involvement = poor prognosisCardiac involvement = poor prognosis

Pericardial e!usion LV aneurysms

Wall motion abnormalities (not related to coronary perfusion territories)

Hypertrophy (segmental)

Edema Fibrosis (active?)

Endstage: Dilatation, wall thinningDilatation, wall thinning

NOTE: 20— 30 % of patients with proven sarcoidosis have cardiac involvement! MRI is more sensitive than Echo in the detection of sarcoid heart disease!

20— 30 % of patients with proven sarcoidosis have cardiac involvement! MRI is more sensitive than Echo in the detection of sarcoid

20— 30 % of patients with proven sarcoidosis have cardiac involvement! MRI is more sensitive than Echo in the detection of sarcoid

Fabry‘s Disease: ManifestationFabry‘s Disease: Manifestation

Rare multisystemic diseaseX.linked genetic disease

Alpha- Galactosidase deficiency

Renal failure

Angiokeratoma


3

54

Fabry‘s Disease: Echo featuresFabry‘s Disease: Echo featuresFabry‘s Disease: Echo features

Left ventricular hypertrophy

Right ventricular hypertrophy

Myocardial fibrosis Diastolic dysfunction


4

55

Segmental Approach

Definition of SegmentsDefinition of SegmentsDefinition of Segments

For the assessment of wall motion abnormalities, the ventricle is divided into basal, mid and distal segments.For the assessment of wall motion abnormalities, the ventricle is divided into basal, mid and distal segments.For the assessment of wall motion abnormalities, the ventricle is divided into basal, mid and distal segments.

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



Definition of the individual segments in the apical views. Note that the inferior portion of the basal septum is visible in the 4ch view.Definition of the individual segments in the apical views. Note that the inferior portion of the basal septum is visible in the 4ch view.Definition of the individual segments in the apical views. Note that the inferior portion of the basal septum is visible in the 4ch view.

008 // Coronary Artery Disease

1

56

Bulls Eye Representation

16 segment model 17 segment model (supraapical cap)

Coronary Supply

NOTE: In left dominant perfusion the posterior lateral wall and even large portions of the inferior wall are supplied by the LCx. In right dominant perfusion the RCA supplies the posterolateral wall in addition to the inferior segments.


2

57

Wall Motion Abnormalities

What Are We Looking For?What Are We Looking For?

Myocardial thickening NOTE: LV contrast

Wall motion LV contrast study improves

Hinge points endocardial boarder

Ventricular shape

boarder detection

Echogenicity

NOTE: Try your best to get the best image quality possible. This is what counts most when you are looking for regional wall motion abnormalities

: Try your best to get the best image quality possible. This is what counts most when you are looking for regional wall motion abnormalities

: Try your best to get the best image quality possible. This is what counts most when you are looking for regional wall motion abnormalities

Wall Motion Abnormalties

NOTE: If possible compare wall motion with a reference segment!

Wall Motion in Ischemic Conditions


3

58

NOTE: Ischemia, hibernation and stunning are all characterized by hypo/ akinesia AND preserved wall thickness!

Conditions of Perfusion

Stunning: reversible reduction of function of heart contraction after

reperfusion

Hibernating: Downregulation of myocardial function to match chronic

reduced blood flow

RemodelingNOTE:

Progressive LV dilation

NOTE: Predisposing factors for remodeling are

Eccentric LV hypertrophy

remodeling are large infarcts (ant. > inf.), mitral

Distortion of geometrymitral regurgitation and elevated

Hypokinesia of normally perfused segments

and elevated afterload (hypertension, AS)

More MRAS)


4

59

Aneurysm

Definition: Abnormal widening of all myocardial layers during diastole

NOTE: Elevated risk of thrombi

NOTE: There is no risk of rupture in

Increased risk of heart failureof rupture in chronic aneurysms.

Best visible in 2ch and atypical views (avoid “foreshortening“)

aneurysms.

Slow flow phenomenon within the aneurysm often present

Myocardial Tissue following Acute Coronary SyndromeMyocardial Tissue following 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


5

60

NOTE: The degree of wall motion abnormality depends of the transmurality of the infarct.

The degree of wall motion abnormality depends of the transmurality

Quantification of LVF in CADQuantification of LVF in CAD

Simpson method Visual assessment

Wall motion scoring Centerline

3D methodsEndocardial contour enhancement (contrast)

NOTE: The Simpson Method DOES NOT Account for regional wall motion abnormalities in the postero-lateral and all anterior septal segments (segments seen in the apical long axis view)

: The Simpson Method DOES NOT Account for regional wall motion abnormalities in the postero-lateral and all anterior septal segments (segments seen in the apical long axis view)

: The Simpson Method DOES NOT Account for regional wall motion abnormalities in the postero-lateral and all anterior septal segments

Problem Zones (Regions DiProblem Zones (Regions Di!cult to Image)

Region Solution

Supraapical- avoid foreshortening- move transducer more lateral +image towards the apex- use 2ch view - move transducer more lateral +image towards the apex

Lateral- rotate 4ch view clockwise- move transducer more medial

Basal inferior

- passive or active motion?- hinge points?- wall thickness

Conditions which Mimic CADConditions which Mimic CAD

Dyssynchrony/ Pacemaker Left bundle branch block

Sarcoid heart disease Abnormal septal motion

Myocarditis Cardiomyopathy


6

61

Tako-Tsubo Cardiomyopathy — Stress Induced CMPTako-Tsubo Cardiomyopathy — Stress Induced CMP

Transient left ventricular apical dysfunction/ballooning

More common in: postmenopausal women

Catecholamines involved T-wave inversions

ReversibleNO coronary obstruction

NOTE: More subtle forms may also exist: More subtle forms may also exist

Patterns of Myocardial Infarction

Supraapical Infarct Distal Septum Infarct

LAD (distal, mid.,prox.), small supraapical aneurysm, low remodeling

risk

LAD (distal,mid.,prox.), low remodeling risk

NOTE: Supraapical and distal septal infarcts can also occur in proximal LAD occlusion after rapid reperfusion.

Supraapical and distal septal infarcts can also occur in proximal LAD


7

62

Proximal LAD Type AMI Small Basal inferior Infarct

LAD (before 1st septal branch, left main), always remodeling, poor

prognosis

RCA, di!cult region to interpret, low remodeling risk

Inferior Infarct Infero-Posterior Infarct

RCA, low-moderate remodeling riskRCA (dominant) or Cx (large,

prox.), moderate remodeling risk

Posterolateral Infarct Infero-Posterior-Lateral Infarct

CX, RCA, moderate remodeling riskDominant RCA, CX (large, prox.),

high remodeling risk

NOTE: Inferior/ posterior/ postero-lateral infarcts pose an elevated risk for restrictive MR!

Inferior/ posterior/ postero-lateral infarcts pose an elevated risk for


8

63

Lateral Infarct

NOTE: When assessing the patterns of myocardial infarction, always consider the possibility of multiple/sequential infarcts!

CX, LAD (diagonal branch, di!cult to interpret, low remodeling risk

NOTE: Always consider that patients can have multiple infarcts/scars in several territories

Always consider that patients can have multiple infarcts/scars in

Complications

Overview

Acute/subacute

Cardiogenic shockThrombus formation (acute)

Myocardial rupture Right ventricular infarction

Papillary muscle rupture

Ischemic VSD

Chronic

„Remodeling“ chronic heart failure

Right heart failure

Thrombus formation (late)

Mitral regurgitation

NOTE: Perform serial echo exams after infarction, it will help you to detect potential complications earlier and assess the risk for complications

: Perform serial echo exams after infarction, it will help you to detect potential complications earlier and assess the risk for complications

: Perform serial echo exams after infarction, it will help you to detect potential complications earlier and assess the risk for complications


9

64

Pseudoaneurysm

Short, narrow neck (diameter < 50% of the fundus diameter)

Outer walls formed by pericardium and mural thrombus

HematomaOften pericardial e!usion

NOTE: Risk of secondary perforation!!Risk of secondary perforation!!

Myocardial Rupture

Mortality 95% 5- 25% of deaths from MCI

Also small infarcts Tamponade

Hematopericardium Urgent surgery!!

Ischemic VSD

Incidence 0.5-1% 50% lethal

Within 4-5 daysRisk factors (hypertension,

1st MCI, AMI)

Echo Features

LV volume overload Disrupted/spliced IVS

Color doppler CW doppler

NOTE: Most common site of rupture is the distal anterior septum (ant MCI) followed by the basal inferior septum (Inf. MCI)

Most common site of rupture is the distal anterior septum (ant MCI) followed by the basal inferior septum (Inf. MCI)

Most common site of rupture is the distal anterior septum (ant MCI)

NOTE: Ischemic VSD´s are rarely a simple hole in the septum but rather the result of splicing of the IVS.

Ischemic VSD´s are rarely a simple hole in the septum but rather the result of splicing of the IVS.

Ischemic VSD´s are rarely a simple hole in the septum but rather the


10

65

Papillary Muscle RupturePapillary Muscle Rupture

Incidence 1%Posteromedial PM more common

5% of deaths from MCI Mortality 70%

Also small infarcts

Echo Features

Severe MR Flail papillary muscle

Hyperdynamic LV Low vel. MR signal

Pulmonary hypertension Dilated pulm. veins

NOTE: Often di!cult TTE assessment (tachycardia, pulmonary edema, lack of distinct MR jet due to large regurgitant orifice and low flow velocity MR) — Perform TEE!!

cult TTE assessment (tachycardia, pulmonary edema, lack of distinct MR jet due to large regurgitant orifice and low flow velocity MR) —

cult TTE assessment (tachycardia, pulmonary edema, lack of distinct MR jet due to large regurgitant orifice and low flow velocity MR) —

RV Infarction

30- 50% of inf. MCI Poorer prognosis

Posterior wall, post. septum Usually prox. RCA (Cx possible)

Echo Features

Dilated RVWall motion abnormalities

(inferior)

Reduced RVF Dilated VCI

NOTE: Look at regional and global RV function in EVERY patient with inferior MCI

: Look at regional and global RV function in EVERY patient with inferior : Look at regional and global RV function in EVERY patient with inferior

Mural Thrombus

Thrombogenicity of infarct tissue

Low flow state in infarcted area

Incidence 20% (large MCI 60%)

Usually apex (aneurysm)

Systemic embolism 2%Small thrombi di!cult to detect

Echo Evaluation

Visible in > 1 plane Mobility (risk of embolus)


11

66

Echogenicity (fresh/old) Size (treatment monitoring)

NOTE: Often di!cult to distinguish thrombi from prominent apical trabecula. Use LV contrast!!

cult to distinguish thrombi from prominent apical trabecula. cult to distinguish thrombi from prominent apical trabecula.

Mitral Regurgitation in CAD — Mechanism

Annular dilatation

Leaflet restriction

Rupture of papillary muscle (acute)

NOTE:Restriction of the posterior leaflets a frequent finding in patients with inferior infarcts (regional remodeling of the inferior wall). Restriction of both leaflets is often a consequence of global remodeling (and usually combined with annular dilatation)!

Restriction of the posterior leaflets a frequent finding in patients with inferior infarcts (regional remodeling of the inferior wall). Restriction of both leaflets is often a consequence of global remodeling (and usually combined


12

67

Basics

Natural History of Aortic Stenosis

NOTE: Prognosis of severe aortic stenosis (in general) is good until symptoms occur!!

Epidemiology NOTE: Aortic stenosis

3rd most common heart diseaseAortic stenosis shares many

Increasing prevalence with older age (2-6% in the elderly)

shares many pathological features and risk factors with

30% AV-sclerosis (precursor of AS)

factors with atherosclerosis!

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.

009 // Aortic Stenosis

1

68

Left Ventricular Failure in Aortic Stenosis

Persistent pressure overload leads to deterioration of left ventricular function and eventual heart failure.

Causes of Aortic Stenosis

Congenital abnormalities of the aortic valve are frequent causes of aortic stenosis. In some patients stenosis is present at birth in others congenital abnormal valves predispose for the development of aortic stenosis later in life.

NOTE: The cause of severe aortic stenosis in patients <50 years is almost always congenital!!

Rheumatic Aortic StenosisRheumatic Aortic Stenosis

Usually mild/moderate NOTE: The aortic valve is the

Combined with ARThe aortic valve is the second most common valve involved in

Progressive thickening and calcification

valve involved in rheumatic heart disease!


2

69

Congenital Abnormalities of AVCongenital Abnormalities of AV

NOTE: To make the diagnosis of a

Unicuspid, bicuspid, quadricuspid

diagnosis of a bicuspid valve use the short axis view and observe the opening

Syndromes (i.e. Down, Heyde)

the opening motion of the valve!

Aortic root involvement, ectasia, aneurysm

Morphology of Aortic Valve

Normal valve (tricuspid)Functional bicuspid (tricuspid with raphe) - congenital

Bicuspid - congenital Unicuspid - congenital


3

70

Echocardiographic Assessment of Aortic ValveEchocardiographic Assessment of Aortic Valve

2D

Bicuspid valve Opening, severity

Degree of calcificationLeft ventricular function (longitudinal strain)

Atrial enlargement Left ventricular hypertrophy

MMode

Eccentric AV closure „“Box“ seperation of cusps

NOTE: Coronary artery disease is frequent in calcified aortic stenosis!Coronary artery disease is frequent in calcified aortic stenosis!Coronary artery disease is frequent in calcified aortic stenosis!

Doppler Assessment of Aortic ValveDoppler Assessment of Aortic ValveDoppler Assessment of Aortic Valve

Color Doppler

Aliasing (stenotic jet)DD: sub/supra valvular stenosis;DD: sub/supra valvular stenosis;

Additional LVOT obstruction?Additional LVOT obstruction?Additional LVOT obstruction?

CW/PW Doppler

Diastolic dysfunction (filling pressure, indirect sign of severity, correlation with symptoms

Diastolic dysfunction (filling pressure, indirect sign of severity, correlation with

Elevated pulmonary pressure is indicative of beginning heart failure

NOTE: Check were aliasing (flow acceleration) occurs: at the valve (valvular AS), below the valve (subvalvular stenosis).

Check were aliasing (flow acceleration) occurs: at the valve (valvular AS), below the valve (subvalvular stenosis).

Check were aliasing (flow acceleration) occurs: at the valve (valvular AS), below the valve (subvalvular stenosis).

Check were aliasing (flow acceleration) occurs: at the valve (valvular AS),

Quantification of Aortic Stenosis

Methods

Planimetry (TEE) Pressure gradients

Aortic valve area using continuity equationAortic valve area using continuity equation

NOTE: Planimetry is often not possible because the valves in AS are too heavily calcified (di!cult tracing of aortic valve orifice

: Planimetry is often not possible because the valves in AS are too cult tracing of aortic valve orifice

: Planimetry is often not possible because the valves in AS are too cult tracing of aortic valve orifice


4

71

Evaluation of Gradients

Gradient = 4 x Vmax2 (Bernoulli equation)

Gradients are influenced by heart rate and stroke volume

Jet velocity is elevated (> 2m/s) if AVA < 2-2,5 Jet velocity is elevated (> 2m/s) if AVA < 2-2,5 cm2

NOTE: Late peak of the Doppler signal indicates severe aortic stenosis!Late peak of the Doppler signal indicates severe aortic stenosis!Late peak of the Doppler signal indicates severe aortic stenosis!

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!

Use the pencil probe!

In the setting of atrial fibrillation average the gradients of several beats and the PW-LVOT velocity

NOTE: Patients with bicuspid stenosis and patients with severe AS in general have eccentric AS jets! In these patients you will usually get the highest gradient from a right parasternal approach!

Patients with bicuspid stenosis and patients with severe AS in general have eccentric AS jets! In these patients you will usually get the highest gradient from a right parasternal approach!

Calculation of Aortic Valve Area (Continuity Equation)


5

72

The LVOT width is measured in the PLAX slightly proximal to the aortic valve, exactly where you should also place the PW Doppler sample (5 ch view)

NOTE: Measurement of the LVOT width is most critical for the calculation of the aortic valve area! Small measurement errors make large di!erences!!

Limitations of Continuity Equation)Limitations of Continuity Equation)

Measurement of LVOTGeometry of LVOT (round, oval)

PW sample volume position Flow profile LVOT

Underestimation of AVpeak vel

NOTE: To find the optimal location of the PW Doppler sample volume place it first into the AS jet and slowly move the sample volume more proximal until there is a sudden velocity drop!

To find the optimal location of the PW Doppler sample volume place it first into the AS jet and slowly move the sample volume more proximal until there is a sudden velocity drop!

To find the optimal location of the PW Doppler sample volume place it first into the AS jet and slowly move the sample volume more proximal until

Reference Values for Aortic StenosisReference Values for Aortic Stenosis

Mild Moderate Severe

Mean gradient < 25 mmHg 25—40 mmHg> 40 mmHg (USA)> 50 mmHg (EU)

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

BITTE TABELLE MACHENValvoloarterial Impedence

Z(va) = measure of global LV loadCalculation: Zva = (SAP + MG)/SVI, where SAP is the systolic arterial pressure and MG is the mean transvalvular pressure gradient.SVI = stroke volume index.

NOTE: Valvuloarterial impedence predicts outcome < 3.5 increases risk 2.3 to 3 fold


6

73

Valvulo-arterial ImpedanceValvulo-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.

NOTE: Valvuloarterial impedence predicts outcome < 3.5 increases risk 2.3 to 3 fold!

Valvuloarterial impedence predicts outcome < 3.5 increases risk 2.3 to 3 Valvuloarterial impedence predicts outcome < 3.5 increases risk 2.3 to 3

Special Circumstances

Low Gradient Aortic StenosisLow Gradient Aortic Stenosis

Mean gradient < 30mmHg- 40mmHG

EF< 40%

AVA < 1.0 cm2

NOTE: To di!erentiate between true severe and pseudo severe AS, you should perform a dobutamine stress echo!

erentiate between true severe and pseudo severe AS, you should perform a dobutamine stress echo!

Factors in Favor of True Severe “Low Flow Low Gradient“ Aortic StenosisFactors in Favor of True Severe “Low Flow Low Gradient“ Aortic StenosisFactors in Favor of True Severe “Low Flow Low Gradient“ Aortic Stenosis

Heavily calcified valve Late peak of AS signal

LVH in absence of hypertension

Previous exams with higher gradients

NOTE: Correct classification makes a distenosis are potential candidates for valve replacement!

Correct classification makes a di!erence! Patients with true aortic stenosis are potential candidates for valve replacement!

erence! Patients with true aortic stenosis are potential candidates for valve replacement!


7

74

Dobutamine Stress Test in Low Flow Low Gradient Aortic Stenosis

“Paradoxical“ Low Flow Low Gradient Aortic Stenosis“Paradoxical“ Low Flow Low Gradient Aortic Stenosis“Paradoxical“ Low Flow Low Gradient Aortic Stenosis

Low gradients in severe AS / normal EFLow gradients in severe AS / normal EF

AVA < 1.0 cm2 EF > 50 %

Mean gradient < 40mmHg

Low stroke volume (<35ml/mLow stroke volume (<35ml/m2)

Concentric LVH � Small, restrictive LV

Calcified valve (Hypertension)

NOTE: 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

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-

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-

Aortic Stenosis and Aortic RegurgitationAortic Stenosis and Aortic Regurgitation

Often combined Bicuspid valves

AS + endocarditis Annular dilatation

AR leads to higher gradients (overestimation of AS severity)

Volume overload / LV size

NOTE: The gradients overestimate AS severity only if aortic regurgitation is moderate!

The gradients overestimate AS severity only if aortic regurgitation is The gradients overestimate AS severity only if aortic regurgitation is !


8

75

Pressure Recovery

Increase of pressure downstream from the stenosis caused by reconversion of kinetic energy to potential energy

Increase of pressure downstream from the stenosis caused by reconversion of kinetic energy to potential energy

Where is it relevant?

Small aorta < 30mm Moderate AS

High flow rate Bileaflet prosthesis

Funnular obstruction

Sub- and Supravalvular Aortic Stenosis

Subvalvular Aortic Stenosis (Membranous)Subvalvular Aortic Stenosis (Membranous) NOTE: Look at the

2nd most common LV outflow obstruction

Look at the origin of aliasing (DD: valvular/

Variable morphology

(DD: valvular/subvalvular/supravalvular

TEE study often required!

supravalvular AS)

Other Findings in Subvalvular Aortic StenosisOther Findings in Subvalvular Aortic Stenosis

Abnormal mitral valve insertion

Associated defects (50%)

PDA, VSD, bicuspid AV, pulmonic stenosis

Features of LVOT obstruction

Morphology of aortaColor flow aliasing at the site of obstruction

CW velocity despite normal AV morphologyCW velocity despite normal AV morphology

NOTE: Subvalvular obstruction leads to aortic valve destruction (jet lesion) and aortic regurgitation!

Subvalvular obstruction leads to aortic valve destruction (jet lesion) and aortic regurgitation!

Subvalvular obstruction leads to aortic valve destruction (jet lesion)


9

76

Types of Supravalvular Aortic Stenosis

NOTE: Use other imaging modalities (CT/MRI) and search for other congenital abnormalities

Indication for Aortic Stenosis Surgery/Intervention

Indications for Surgery

Symptomatic patients with severe AS (dyspnea, syncope, angina)

Symptomatic patients with reduced LV function

Asymptomatic patients with abnormal exercise test

Moderate or severe AS if other cardiac surgery is performed

NOTE: If the patient does not full-fill the criteria/indications for surgery, annual follow up should be performed. Shorter intervals are necessary if AS is severe, heavily calcified, LVF or symptoms are uncertain!

If the patient does not full-fill the criteria/indications for surgery, annual follow up should be performed. Shorter intervals are necessary if AS is severe, heavily calcified, LVF or symptoms are uncertain!

Predictors for Rapid Progression of Aortic StenosisPredictors for Rapid Progression of Aortic StenosisPredictors for Rapid Progression of Aortic Stenosis

Non-linear and variableValve morphology (bicuspid)

Severity of AS Degree of calcification

Subclinical myocardial dysfunctionSubclinical myocardial dysfunction


10

77

NOTE: The indication for aortic valve surgery must be individualized. Consider: age, co-morbidities, risk of myocardial fibrosis in LVH, longitudinal dysfunction, degree of calcification, patient preference and expectations, rate of progression etc.

The indication for aortic valve surgery must be individualized. Consider: age, co-morbidities, risk of myocardial fibrosis in LVH, longitudinal dysfunction, degree of calcification, patient preference and expectations, rate

The indication for aortic valve surgery must be individualized. Consider: age, co-morbidities, risk of myocardial fibrosis in LVH, longitudinal dysfunction, degree of calcification, patient preference and expectations, rate

TAVI (Transcatheter Aortic Valve Implantation)

Consider interventional valve replacement in:

Symptomatic/severe aortic stenosis

High risk patients

Suitable anatomy (AV annulus diameter)

Eligible anatomic access for transapical or transfemoral valve implantation

NOTE: Indications for TAVI may change with improvements of the methodology!

Indications for TAVI may change with improvements of the


11

78

Basics

Cause of Chronic Aortic RegurgitationCause of Chronic Aortic Regurgitation

Degenerativ Aortic dilatation

Congenital Postendocarditis

Rheumatic Aortic valve prolaps

NOTE: Mild aortic regurgitation is a common finding and not a „disease“. It can be caused by degenerative disease, aging and aortic valve sclerosis.

Mild aortic regurgitation is a common finding and not a „disease“. It can be caused by degenerative disease, aging and aortic valve sclerosis.

Mild aortic regurgitation is a common finding and not a „disease“. It can be caused by degenerative disease, aging and aortic valve sclerosis.

Hemodynamics in AR

Volume overload NOTE: An elevation of

Dilated LV

An elevation of LVFP (diastolic dysfunction)

Hyperdynamic

dysfunction) usually denotes LV deterioration

Filling pressure �/�

LV deterioration (and symptoms!)

Afterload �

Indirect findings in AR

Dilated LV Hyperdynamic function

Eccentric LV hypertrophy Mildly enlarged LA

MR (annular dilatation) Diastolic dysfunction

NOTE: Dont expect very severe dilatation of the LV in combined AR and AS.Dont expect very severe dilatation of the LV in combined AR and AS.Dont expect very severe dilatation of the LV in combined AR and AS.

010 // Aortic Regurgitation

1

79

Imaging and Quantification of AR JetImaging and Quantification of AR Jet

PLAX NOTE: Look at vena contracta PSAX (visualize origin of jet) Look at vena contracta and PISA! Use

4 ch view/ 3 ch view

and PISA! Use integrative approach to quantification.

Suprasternal (to determine retrograde flow)

to quantification.

NOTE: 1) AR may be di!2) Retrograde flow is very important 3) use both color Doppler and PW Doppler to study retrograde flow.

: 1) AR may be di!cult 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.

cult to quantify in tachycardia and higher heart rates.2) Retrograde flow is very important 3) use both color Doppler and PW

Aortic Regurgitation — Reference Values


Vena contracta < 3mm 3-6mm > 6mm

Jet width (% of LVOT) < 25 25—65 > 65

Flow convergence (PISA)

not visible small large

PHT AR (msec) > 500—600 200—500 < 200

NOTE: Holodiastolic retrograde flow in the aorta = severe AR: Holodiastolic retrograde flow in the aorta = severe AR: Holodiastolic retrograde flow in the aorta = severe AR: Holodiastolic retrograde flow in the aorta = severe AR

PitfallsNOTE:

Complex, eccentric, or multiple jets.

Poor alignment of CW with AR jet

NOTE: AR signal should

have a vel. above 4,5 m/sec! Otherwise signal quality is

Calcified valves (di!cult to see proximal flow convergence zone)

Machine settings (PRF)

signal quality is inadequate to look

at deceleration time


2

80

Hemodynamic calculation of regurgitant volume and fraction

SVMV = CSAMV x VTIMV = D2 x 0.785

SVLVOT = CSALVOT x VTILVOT = D2 x 0.785

NOTE: Hemodynamic calculations of AR are rarely used. Main limitation is the inaccuracy of calculating the MV cross sectional area.

: Hemodynamic calculations of AR are rarely used. Main limitation is the inaccuracy of calculating the MV cross sectional area.

Reference Values Mild Moderate Severe

Regurgitant volume (ml/beat) < 30 30—59 ! 60

Regurgitant fraction (%) < 30 30—49 ! 50

PISA Method

ARflow = 2� x r2 x Vr

r = radius of flow convergence,

Vr = corresponding aliasing velocity,

Rvel = max. Vel of AR jet,

ERO = e"ective regurgitant orifice


3

81

Reference Values Mild Moderate Severe

ERO (cm2)< 0,1 0,1—0,29 ! 0,3

Acute Aortic Regurgitation

Causes

EndocarditisNOTE:

Cusp ruptureNOTE:

LV Size = normal or mildly dilated

Aortic dissectionor mildly dilated

and hyperdynamic

Iatrogenic (trauma)

Echofeatures of acute AREchofeatures of acute AR

Small/mildly dilated LV Tachycardia

“Initially“ hyperdynamic LV

Holodiastolic retrograde flow (Ao. desc.)

Short deceleration AR Premature MV-closure

Indications for surgery

Indication in symptomatic patients with severe AR

Reduced LVF (LVEF < 50%)

Dilated LV (LVEDD > 70mm LVES > 50mm (25mm/m2))

If EF is too poor (< 30— 35%) � Heart transplantation

NOTE: Consider AV surgery even in moderate AR if cardiac surgery for other causes (i.e. CABG, or MV replacement) is indicated

: Consider AV surgery even in moderate AR if cardiac surgery for other


4

82

Introduction

MS facts

Diagnosis of MS is made by 2D echo (doming of AMVL)

MMode not used anymore to diagnose or quantify MS

Color Doppler is indicative of MS (Candle flame appearance)

CW Doppler is used to quantify MS

Causes

Rheumatic (85,4%) NOTE: Prevalence Rheumatic fever (75% valvular

involvement)

Prevalence depends on socioeconomic

Stenotic annular calcification (12,5%)

socioeconomic status of the country

Congenital (0,6%)

NOTE: Rheumatic heart disease is very common in developing countries.: Rheumatic heart disease is very common in developing countries.: Rheumatic heart disease is very common in developing countries.

Rheumatic fever

Group A streptococcal (GAS) tonsillopharyngitis - Antibody cross reactivity

Arthritis joints

Chorea minor Subcutaneous nodules

PancarditisUsually a!ects childern at age 6-15

Congenital Mitral StenosisCongenital Mitral Stenosis

Rare (0,6% of CHD)

Combined with other cong. defects

Forms: Annulus hypoplasia, parachute, double orifice

011 // Mitral Stenosis

1

83

NOTE: Shone complex is an association of congenital mitral stenosis and other left-sided in— and outflow obstructions (coarctation, valvular/subvalvular aortic stenosis)

Shone complex is an association of congenital mitral stenosis and other left-sided in— and outflow obstructions (coarctation, valvular/subvalvular aortic stenosis)

Hemodynamics of MS

LA-LV gradient Elevated pressure in LA

Elevated pressure pulm. capillaries

Pulm. cong. / edema

PHT / reactive PHT Tricuspid regurgitation

Right heart failure Atrial fibrillation

NOTE: In mitral stenosis there is no „burdon“ on the left ventricle (no pressure or volume over load.

In mitral stenosis there is no „burdon“ on the left ventricle (no pressure In mitral stenosis there is no „burdon“ on the left ventricle (no pressure

Echocharacteristics of MSEchocharacteristics of MS

Doming (diastolic bulging of the AMVL)

Reduced valve opening

Commissural fusion Leaflet tip thickening

Secondary calcificationSubvalvular involvement (thickened and fused tendinae)

NOTE: Older patients with MS are have more calcified valvesOlder patients with MS are have more calcified valvesOlder patients with MS are have more calcified valves

Associated problems

Thickened aortic valveReduced LVF (rheumatic myocarditis)

Enlarged LA Pulmonary hypertension

Other valve involvement Aortic regurgitation

Tricuspid stenosis Thrombus

NOTE: Many of these findings develop and progress over time. Also consider these in your management strategy

: Many of these findings develop and progress over time. Also consider these in your management strategy

: Many of these findings develop and progress over time. Also consider


2

84

Risk of Thrombus NOTE:

Systemic embolism in 20% of all MS patients

NOTE: Most thrombi are seen in the left atrial appendage.

80% of patients are in Afibatrial appendage. Thus you will miss them with

45% have spontaneous left atrial contrast

them with transthoracic Echo!!

Quantification

MV Area — Reference Values

Normal (cm!) 4— 6 cm!

Mild (cm!) > 1,5 cm!

Moderate (cm!) 1— 1,5 cm!

Severe (cm!) < 1 cm!

Problems with MV Planimetry (PSAX)Problems with MV Planimetry (PSAX)

Image quality Alignment

Timing Calcification

Atrial fibrillation Incompl. comm. fusion

Operator experience

NOTE: Planimetry is the most direct way to quantify MS. It does not rely on hemodynamic assumption. It is also technically the most challenging method

: Planimetry is the most direct way to quantify MS. It does not rely on hemodynamic assumption. It is also technically the most challenging method


3

85

Forms of Mitral Stenosis

Classic form Funnular form

NOTE: The funnular form is usually seen it there is strong involvement of the subvalvular apparatus

: The funnular form is usually seen it there is strong involvement of the

MS Gradients — Reference ValuesMS Gradients — Reference Values

Mild (mmHg) < 5 < 8

Moderate (mmHg) 5— 10 8— 15

Severe (mmHg) > 10 > 15

NOTE: Gradients are higher in the setting of additional MR!Gradients are higher in the setting of additional MR!Gradients are higher in the setting of additional MR!

PHT — Pitfalls

Diastolic dysfunction Aortic regurgitation

Following valvuloplastyConcave shape of tracing

Degenerative calcified MSAdditional AR where the AR signal interferes with MV inflow signal


4

86

Color Doppler , PISA and Continuity EquationColor Doppler , PISA and Continuity Equation

Candle flame

PISA for quantification

MVA = Mitral volume flow/ Peak velocity of diastolic mitral flow

Continuity Equation ( does not work if AR and MR are both present)

Quantification of Mitral Stenosis in Atrial FibrillationQuantification of Mitral Stenosis in Atrial Fibrillation

Planimetry Several di!erent measurements

Mean gradientsAverage 5 cycles with small variation of R-R intervals close to normal HR

PHTAvoid mitral flow from short diastoles/ average di!erent cardiac cycles

Valvuloplasty

Indication and Results

Indication

Clinically significant MS (valve area < 1,5 cm" or < 1,8 cm" in unusually large patients)

Results

Good immediate results (valve area > 1,5 cm" with no regurgitation) can be obtained in over 80%

NOTE: PHT method is not reliable immediately after valvuloplasty!PHT method is not reliable immediately after valvuloplasty!


5

87

Prevalvuloplastic Echo-evaluationPrevalvuloplastic Echo-evaluation

Mobility Subvalvular thickening

Valve thickening Calcification

Calcification of commissures

Thrombus

Mitral regurgitation Tricuspid regurgitation

NOTE: Complications of MV valvuloplasty are 1) acute MR, 2) iatrogenic ASD, 3) embolism, 4) tamponade (perforation) 5) local complications/bleeding

Complications of MV valvuloplasty are 1) acute MR, 2) iatrogenic ASD, 3) embolism, 4) tamponade (perforation) 5) local complications/bleeding

Complications of MV valvuloplasty are 1) acute MR, 2) iatrogenic ASD, 3) embolism, 4) tamponade (perforation) 5) local complications/bleeding


6

88

Basics

Natural History of Severe MRNatural History of Severe MR

10 year survival of 57% NOTE: Severe MR is not

5 year all cause mortality in asymptomatic MR patients is 22%

Severe MR is not a benign condition!

5 year risk for cardiac events in asymptomatic MR patients is 33%

Hemodynamics of MR

In acute MR ejection fraction is high and the size of the left ventricle is normal or only mildly enlarged (unadapted). In chronic MR ejection fraction is „supranormal“ and the left ventricle is dilated (adapted). In decompensated MR the left ventricle is significantly enlarged and ejection fraction begins to drop.

NOTE: In a setting of significant MR an ejection fraction of 55% to 60% (which is otherwise considered normal) already denotes left ventricular failure.

012 // Mitral Regurgitation

1

89

Consequence of Mitral RegurgitationConsequence of Mitral Regurgitation

Volume overload Elevated filling pressure

Pulmonary hypertension Tricuspid regurgitation

Reduced systolic wall stress Unloaded left ventricle

NOTE: Patients with even severe MR can stay asymptomatic for long periods Patients with even severe MR can stay asymptomatic for long periods Patients with even severe MR can stay asymptomatic for long periods

Causes

Primary (structural) causesPrimary (structural) causes

Mitral valve prolaps Degenerative disease

Rheumatic HD Endocarditis

Drugs Congenital

Mitral annular calcification

Systemic diseases

Secondary (functional) causesSecondary (functional) causes

Annular dilatation Restrictive leaflets

SAM Atrial enlargement

NOTE: Echocardiography provides important clues as to the cause of MR! Combinations of several etiologies is not uncommon (i.e. annular dilatation and restrictive leaflets).

Echocardiography provides important clues as to the cause of MR! Combinations of several etiologies is not uncommon (i.e. annular dilatation

Echocardiography provides important clues as to the cause of MR! Combinations of several etiologies is not uncommon (i.e. annular dilatation

Quantification of Mitral Regurgitation

Integrative ApproachIntegrative Approach

Color DopplerJet (flow convergence, vena contracta)

2D- Imaging Indirect signs

NOTE: Your ability to image jets is often more important than quantitative parameters! Use multiple views!!

Your ability to image jets is often more important than quantitative parameters! Use multiple views!!

Your ability to image jets is often more important than quantitative


2

90

Quantification Based on Color DopplerQuantification Based on Color Doppler


Vena contracta (mm)

< 3 3—6,9 ! 7

Jet area (%)

Small, central jet (<20% of LA area)

VariableLarge, central jet (>

40% of LA area)

NOTE: The proximal portions of the jet (vena contracta and flow convergence zone are more important for the quantification of MR opposed to the jet area, length or width

The proximal portions of the jet (vena contracta and flow convergence zone are more important for the quantification of MR opposed to the jet area,



Color Doppler Confounders

Geometry of regurgitant orifice Multiple jets

Coanda e"ect („wall hugging“ jets)

Driving force (systolic pressure)

LA compliance

NOTE: The PRF setting greatly influences the size of the jet! Always use the same PRF otherwise a comparison is nor possible

The PRF setting greatly influences the size of the jet! Always use the same PRF otherwise a comparison is nor possible

The PRF setting greatly influences the size of the jet! Always use the

Indirect Signs

NOTE:Dilated LV

NOTE:The size of the left atrium does not Hyperdynamic LVF atrium does not allow quantification

LA enlargement

allow quantification of mitral regurgitation.

IAS bulging (towards RA)regurgitation.


3

91

Retrograde Flow in Pulm. VeinsRetrograde Flow in Pulm. Veins

Normal flow Blunted flow Systolic flow reversal

NOTE: In most instances you will not need pulmonic. vein Doppler to quantify MR. In addition a good signal can only be obtained in 50-75 % of patients. Di!cult interpretation in Afib.

: In most instances you will not need pulmonic. vein Doppler to quantify MR. In addition a good signal can only be obtained in 50-75 % of patients.

cult interpretation in Afib.

: In most instances you will not need pulmonic. vein Doppler to quantify MR. In addition a good signal can only be obtained in 50-75 % of patients.

PISA Method

Flow through hemispheric surface = flow through orifice!

NOTE:Shift aliasing limit to lower velocity 20- 40cm/s (larger hemisphere)

NOTE:PISA is also a city in Italy....

EROA = [(2r2 x Vpisa)/ Vmr]

Italy....

Regurgitant flow = Q = 2 x r2 x � x Nyquist vel.

NOTE: Use magnifications (Zoom/RES) to increase your measurement accuracy

: Use magnifications (Zoom/RES) to increase your measurement : Use magnifications (Zoom/RES) to increase your measurement

Limitations of PISA

Geometry of orifice Multiple Jets

Deliniation of PISA Excentric origin of Jets

Dynamic MR Motion of the annular plane


4

92

NOTE: There is much controversy as to wether PISA should be used. Most likely new 3D echo techniques will make PISA more reliable. (better approximation of PISA geometry).

There is much controversy as to wether PISA should be used. Most likely new 3D echo techniques will make PISA more reliable. (better approximation of PISA geometry).

There is much controversy as to wether PISA should be used. Most likely new 3D echo techniques will make PISA more reliable. (better

Reference Values for Parameters of MRReference Values for Parameters of MRReference Values for Parameters of MR


Regurgitant Volume (ml/beat)

< 30 30—44, 45—59 ! 60

RegurgitantFraction (%)

< 30 30—39, 40—49 ! 50

EROA (cm2) < 0,2 0,2—0,29, 0,3—0,39 ! 0,4

Volumetric methods

MR volume = MR inflow — aortic outflow (NO AR!!)MR volume = MR inflow — aortic outflow (NO AR!!)MR volume = MR inflow — aortic outflow (NO AR!!)

Signs of Acute MR

Hyperdynamic LV normal size Tachycardia

2D morphology Low velocity (shock)

Triangular shaped MR - spectrum

Elevated MV- inflow velocity

NOTE: The diagnosis of acute MR can be divelocity MR jets (shock), tachycardia and tachypnea.

The diagnosis of acute MR can be di"cult, because patients have low velocity MR jets (shock), tachycardia and tachypnea.

cult, because patients have low

Mechanisms of Mitral Regurgitation

Why is the Mechanism Important?Why is the Mechanism Important?NOTE:

EtiologyNOTE:Usually transthoracic echo

Prognosis (reversible)transthoracic echo is su"cient to determine the

Managementdetermine the mechanism. If not: use TEE!

Repair?If not: use TEE!


5

93

What should be examined?

Valve morphology (thickened, myxomatous)

Extent of involvement

Origin of regurgitant defect

Why is the valve incompetent (mechanism)

NOTE: The extent of morphologic abnormalities of the mitral valve does not necessarily correlate with the severity of mitral regurgitation!!

The extent of morphologic abnormalities of the mitral valve does not necessarily correlate with the severity of mitral regurgitation!!

How to Visualize MV Segments

NOTE: Don‘t forget to image the commissural regions!


6

94

Mitral Valve Prolaps

Anterior leaflet (posterior + lateral jet) Posterior leaflet (anterior + medial jet)

Both leaflets (central Jet)Commissural (jet at commissure origin)

Mitral Flail Leaflet

Anterior leaflet (posterior + lateral jet) Posterior leaflet (anterior + medial jet)

Mitral Valve Leaflet Restriction

Both leaflets (central jet) Posterior leaflet (lateral, posterior jet)


7

95

Other Causes

Annular dilatation (central jet) MR in HCMP (posterior jet direction

Valve perforation (jet through leaflet)Valve perforation (jet through leaflet)

NOTE: Other mechanisms for MR include: Annular calcification, leaflet retraction, and leaflet shrinkage.

: Other mechanisms for MR include: Annular calcification, leaflet

Unfavorable Factors for RepairUnfavorable Factors for Repair

Extensive involvement (more than two segments) NOTE:

Anterior vs. posterior leaflet

NOTE:

Know your surgeon!

Commissural defectssurgeon!

Calcification

NOTE: Repair techniques include: quadrangular resection with sliding plasty, chordal transfer and use of artificial chords. Mitral valve repair always includes implantation of an annuloplasty ring

: Repair techniques include: quadrangular resection with sliding plasty, chordal transfer and use of artificial chords. Mitral valve repair always includes implantation of an annuloplasty ring

: Repair techniques include: quadrangular resection with sliding plasty, chordal transfer and use of artificial chords. Mitral valve repair always includes


8

96

Mitral Valve Prolaps

Forms of Mitral Valve Prolaps

M. Barlow (classic MVP, myxomtous)

Fibroelastic deficiency

Pseudoprolaps (small ventricles, RV enlargement)

Secondary causes

NOTE: The normal mitral valve plane has the shape of a saddle, don‘t base the diagnosis solely on a 4-chamber view

The normal mitral valve plane has the shape of a saddle, don‘t base the diagnosis solely on a 4-chamber view

The normal mitral valve plane has the shape of a saddle, don‘t base the

Myxomatous Mitral Valve (Floppy valve, M. Barlow)Myxomatous Mitral Valve (Floppy valve, M. Barlow)Myxomatous Mitral Valve (Floppy valve, M. Barlow)

Prevalence = 2-3 % Rapid multiplication of cells

Rocking motion of annulus

Involvement of entire subvalvular apparatus

Billowing Excessive tissue

Segmental involvement

NOTE: M. Barlow is a structural disease of the mitral valve. Don‘t base your diagnosis only on the presence of a prolapse!

M. Barlow is a structural disease of the mitral valve. Don‘t base your diagnosis only on the presence of a prolapse!

M. Barlow is a structural disease of the mitral valve. Don‘t base your

Flail Leaflet

Etiology of Flail Leaflet

NOTE: Mitral valve prolaps

NOTE: Ruptured chordae can be

Endocarditischordae can be found in over 50% of

Degenerative50% of myxomatous valves!

Rheumaticvalves!


9

97

Echo Criteria — Flail LeafletEcho Criteria — Flail LeafletNOTE:

Chordal structures in the LANOTE: Flail leaflet can be very subtle,

Concave (LA) position of leaflet

be very subtle, especially if secondary chords are

Double contour

chords are involved!

NOTE: The degree of MR depends on the location and type of chord that is ruptured. Flail leaflet does not always imply severe MR

: The degree of MR depends on the location and type of chord that is ruptured. Flail leaflet does not always imply severe MR

: The degree of MR depends on the location and type of chord that is

Other Causes of Mitral Regurgitation

Degenerative MR Rheumatic MR Endocarditis

Common Doming of AMVL Valve destruction

Thickened MVOther rheumatic features

Perforation

Annular calcification

Combined MS + MR

Leaflet rupture

NOTE: The etiology and mechanism of MR are often closely related!The etiology and mechanism of MR are often closely related!The etiology and mechanism of MR are often closely related!The etiology and mechanism of MR are often closely related!

Congenital Abnormalities of MVCongenital Abnormalities of MV

NOTE: Chordal abnormalities

NOTE: Cleft MV is often combined with

Papillary muscle abnormalitiescombined with

ASD I Cleft MV


10

98

Indication for Surgery

Indication NOTE: Repair is better

LVEF < 60 %Repair is better than replacement.

ESD > 45mmreplacement. Chordal

New Afib preservation should be

sPAP >50mmHg

should be performed whenever

or if patients is symptomaticwhenever possible.

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

Mitral Clip ProcedureMitral Clip Procedure

NOTE: MitraClip procedure is an interventional therapy where a clip is placed attaching the anterior to the posterior leaflet. Similar to the surgical procedure know as the „Alfieri“ stitch.Studies have shown that this technique can reduce mitral regurgitation and improve symptoms

Other Factors to ConsiderOther Factors to Consider

Type of valve Age of patient

Contraindication to warfarine

Co-morbidities

Additional indication for heart surgery (CABG, other valve, aneurysm)

Alternative new approaches (i.e.: mitral clip)


11

99

Echocardiographic Approach in Asymptomatic PatientsEchocardiographic Approach in Asymptomatic Patients

Monitor LVF and size

NOTE: Prognosis

Check for pulmonary hypertensionPrognosis

depends on preoperative

Atrial size/risk for Afibpreoperative

LVF! Other tests!

Earlier surgery if repair is likely!


12

100

Basics

Morphology

3 leaflets NOTE: The posterior

Larger than MV (3.2-6.4 cm2) The posterior

leaflet is usually very small!

More apical and thinner leaflets than MV

very small!

NOTE: The location and size of the papillary muscles is highly variableThe location and size of the papillary muscles is highly variableThe location and size of the papillary muscles is highly variable

How to Image the Tricuspid ValveHow to Image the Tricuspid Valve

RV PLAX ant. + post. leaflet

RV inflow-outflow viewant./sept. +post leaflet

RV optimized 4 ch view sept. + ant. leaflet

RV inflow: E/A wave lower than MV inflow, velocity varies with respirationE/A wave lower than MV inflow, velocity varies with respirationE/A wave lower than MV inflow, velocity varies with respiration

NOTE: The TV is more di!cranial 4 chamber view ( 1 IC space higher.

The TV is more di!cult to image than the mitral valve, use a more cranial 4 chamber view ( 1 IC space higher.

cult to image than the mitral valve, use a more

Causes of Tricuspid Regurgitation

Prognosis of TR

Survival poor if TR severe NOTE: Trivial (physiologic) TR + PHT (physiologic) TR is common!

+ reduced LVF

is common! (70% of adults)

+ reduced RVF

NOTE: TR severity is a good marker of disease progression in many conditinos (CMP, valvular heart disease, pulmonary hypertension etc.)

TR severity is a good marker of disease progression in many conditinos (CMP, valvular heart disease, pulmonary hypertension etc.)

TR severity is a good marker of disease progression in many conditinos (CMP, valvular heart disease, pulmonary hypertension etc.)

013 // Tricuspid Valve Disease

1

101

Causes of Functional Tricuspid RegurgitationCauses of Functional Tricuspid Regurgitation

Left heart disease Mitral valve disease

Pulmonary hypertension RV dilation (ASD/left right shunt)

NOTE: Functional (secondary) TR is much more common than structural (primary) TR!

Functional (secondary) TR is much more common than structural Functional (secondary) TR is much more common than structural

Causes of Primary TRNOTE:

Rheumatic (TR comb. with TS)NOTE: If the plane of the tricuspid valve is

Trauma (blunt trauma, flail/rupture)

tricuspid valve is displaced towards the apex consider

Pacemaker lead associated

the apex consider rudimentary form of M. Ebstein or

Endocarditis

of M. Ebstein or Tricuspid valve dysplasia!

Congenital (i.e. M. Ebstein)dysplasia!

NOTE: Tricuspid Dysplasia is common in dogs (i.e. Labrador Retrievers)

Tricuspid Dysplasia is common in dogs (i.e.

Carcinoid Tricuspid RegurgitationCarcinoid Tricuspid Regurgitation

Release of vasoactive substances (i.e. serotonin) leads to:Release of vasoactive substances (i.e. serotonin) leads to:

Endocardial fibrosis (TV, PV, RV endocardium, LV (PFO)

TV leaflet restriction

Wide coaptation defectcan be associated with pulmonic stenosis

NOTE: Left valve involvement can be found in the presence of ASD or PFO!Left valve involvement can be found in the presence of ASD or PFO!Left valve involvement can be found in the presence of ASD or PFO!

Morbus Ebstein

Variable morphology Large anterior leaflet

Leaflet tetheringApical displacement (atrialized RV)

Associated with: ASD, VSD, PDA, CoA, RVOT obstructionASD, VSD, PDA, CoA, RVOT obstruction

NOTE: The origin of the TR jet is far in the right ventricle caused by apical displacement of the tricuspid valve!

The origin of the TR jet is far in the right ventricle caused by apical displacement of the tricuspid valve!

The origin of the TR jet is far in the right ventricle caused by apical


2

102

Quantification of Tricuspid Regurgitation

Quantification

Flow convergence Vena contracta

Jet area Jet length

Eye-balling

NOTE: The degree of tricuspid regurgitation can vary to some extent with respiration! Observe several beats with Echo!!

The degree of tricuspid regurgitation can vary to some extent with respiration! Observe several beats with Echo!!

The degree of tricuspid regurgitation can vary to some extent with

Tricuspid Regurgitation — Reference ValuesTricuspid Regurgitation — Reference ValuesTricuspid Regurgitation — Reference Values


PISA Nyquist limit 28 cm/s

< 0.5 cm 0.6 - 0.9 cm > 0.9 cm

Vena contractaNyquist limit 50-60 cm/s

>0.7 cm

Signs of Severe TR

Dilated RV Dilated RA

Dilated VCISystolic flow reversal (hepatic veins)

Flattened IVS (diastole) Visible coaptation defect

TV Surgery — Rules

Surgery before RV failure

Surgery if TR ! moderate in heart surgery

No surgery if RVF is severely reduced

Repair is better than replacement

NOTE: If patients with severe TR develop signs of right heart failure (pleural e!usion, peripheral edema ascites) then it is often to late for surgery (irreversible RV dysfunction)

If patients with severe TR develop signs of right heart failure (pleural usion, peripheral edema ascites) then it is often to late for surgery

(irreversible RV dysfunction)


3

103

Tricuspid Stenosis

OverviewNOTE:

In 9 % of rheumatic heart diseaseNOTE: Look for doming of

Congenital TS (very rare)doming of TV in 2D and

Functional TS due to masses (very rare)and turbulent flow in the

Endocarditis ( very rare)flow in the color doppler!

Following repair/replacement!doppler!

NOTE: TS can also occur following TV repair (undersizing of TV annuloplasty wing)

TS can also occur following TV repair (undersizing of TV annuloplasty TS can also occur following TV repair (undersizing of TV annuloplasty

Hemodynamics

RA-RV gradient (increase with inspiration)

Elevated pressure in RA

Dilated RA Dilated VCI

NOTE: Symptoms of TS can mimic those of right heart failureSymptoms of TS can mimic those of right heart failureSymptoms of TS can mimic those of right heart failure

Quantification of Tricuspid StenosisQuantification of Tricuspid Stenosis

PHT: TVA = 190/PHT (is not validated)

Mean gradient: Significant TS if > 5mmHg

Severe TS: TVA < 1.0 cm2

NOTE: Look for turbulent flow in the color doppler across the TV in all patients with mitral stenosis!! Doming of the tricuspid valve is often dito visualize! Thereby you won‘t miss associated TS!

Look for turbulent flow in the color doppler across the TV in all patients with mitral stenosis!! Doming of the tricuspid valve is often di!cult to visualize! Thereby you won‘t miss associated TS!


4

104

VIDEO LECTURES

PATIENT DEMOS

BLOG

INSTRUCTIONAL GAME

FACT-SHEET

echo workbook 123sonography

Documents