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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5189_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •Resolution
- •Axial Resolution
- •Lateral Resolution
- •Elevational Resolution
- •Temporal Resolution
- •The Resolution—Penetration Interplay
- •Sound Waves
- •Ultrasound
- •Pulsed Ultrasound
- •The Range Equation
- •Ultrasound Image Formation
- •Time Gain Compensation
- •M-Mode Imaging
- •The Doppler Principle
- •Doppler Imaging
- •Continuous Wave (CW) Doppler
- •Pulsed Wave (PW) Doppler
- •Color Flow (CF) Doppler
- •Tissue Doppler Imaging (TDI)
- •Pulsed Wave TDI
- •Color TDI
- •Tissue Harmonics Imaging (THI)
- •Probe Selection
- •Curved Linear Array Transducers
- •Linear Array Transducers
- •Phased Array Transducers
- •Ultrasound Artifacts (See Chap. 3)
- •Space/Time Artifacts
- •Refraction
- •Mirror Image
- •Reverberation
- •Bayonet
- •Edge
- •Attenuation Artifacts
- •Shadowing
- •Enhancement
- •Doppler Artifacts
- •Aliasing
- •References
- •Probe Selection
- •Harmonic Imaging
- •Imaging Modes
- •Color Doppler
- •Spectral Doppler
- •Tissue Doppler
- •References
- •3: Ultrasound Artifacts
- •Reverberation Artifacts
- •Comet-Tail Artifact
- •Ring-Down Artifact
- •Mirror Image Artifacts
- •Shadowing Artifact
- •Enhancement Artifact
- •Side-Lobe Artifacts
- •Refraction Artifacts
- •References
- •References
- •Parasternal Long Axis (PLAX)
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tip
- •Parasternal Short Axis (PSAX)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Suprasternal/Supraclavicular View
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •6: Transthoracic M-Mode Echocardiography
- •Imaging Tips
- •Apical: A4C, A5C, A2C, A3C
- •Apical Four-Chamber View (A4C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Five-Chamber View (A5C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Two-Chamber View (A2C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Three-Chamber View (A3C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal: SC4, SC Long Access, IVC
- •Subcostal Four-Chamber View (SC4)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal Long Axis IVC
- •External Anatomy
- •Sonographic Anatomy
- •M-Mode Echocardiography
- •Left Ventricular (LV) Function
- •Right Ventricular (RV) Systolic Function
- •Cardiac Valves
- •Pericardial Tamponade
- •Inferior Vena Cava (IVC) Collapsibility
- •References
- •7: Transthoracic Doppler Echocardiography
- •General Approach
- •Spectral Broadening
- •Pulse Repetition Frequency
- •Pulmonary Venous Flow (Diastolic Function)
- •Hepatic Vein Flow
- •Pulse-Wave/CW Doppler (Aorta Flows)
- •References
- •8: Transesophageal Echocardiography: Insertion, Manipulation, Risks, Complications
- •Indications
- •Post Cardiac Surgery
- •Acute Cardiopulmonary Disease
- •Hypovolemia, Fluid Responsiveness
- •Endocarditis
- •Aortic Pathology
- •Insertion
- •Manipulation
- •References
- •2D Transesophageal Imaging
- •References
- •Ultrasound Assumptions
- •Reverberation Artifact
- •Side-Lobe Artifact
- •Intravascular Devices
- •3D Ultrasound
- •Stitch Artifact
- •Right Atrium: Crista Terminalis, Eustachian Valve, Chiari Network
- •Right Ventricle-Moderator Band
- •Left Ventricle: Fibroelastoma Versus Lambl’s Excrescence
- •References
- •11: LV Systolic Function
- •Structural Anatomy
- •Left Ventricular Hypertrophy
- •LV Function: Linear Measurements
- •EPSS Method
- •Caution
- •LV Function: Ejection Fraction
- •EF (Simpson’s Biplane) Method
- •Cautions
- •LV Function: Cardiac Output
- •Regional Wall Motion Abnormalities
- •Methods
- •Strain
- •Strain Methods
- •Cautions
- •References
- •Ultrasonic Enhancement Agents (UEAs)
- •M-Mode
- •Mitral Annular Plane Systolic Excursion
- •dP/dt
- •Tissue Doppler Imaging (TDI)
- •Systolic Mitral Annular Velocity (s′)
- •References
- •13: The Right Ventricle
- •The Right Ventricle
- •Right Ventricular-Focused View
- •Semi-Quantitative Right Ventricular Assessment
- •Interventricular Septum
- •Right Ventricular Dimensions
- •Right Ventricular Wall Thickness
- •Right Ventricular Area/Volume
- •Regional Systolic Functional Assessment
- •TAPSE (Tricuspid Annulus Plane Systolic Excursion)
- •Tricuspid Annular Systolic Velocity (Right Ventricular S′)
- •Global Systolic Functional Assessment
- •Right Ventricular Fractional Area Change
- •Right-Sided Hemodynamics
- •Right Ventricular-Pulmonary Artery Coupling
- •Right Ventricular Diastolic Function
- •Right Ventricular Strain
- •Conclusion
- •References
- •Left Atrium
- •Technical Considerations
- •Left Atrial Function
- •Atrial Septum
- •Right Atrium
- •References
- •15: Left Ventricular Diastolic Function
- •Introduction
- •Diastole
- •Isovolumic Relaxation
- •Early Diastolic Filling
- •Diastasis
- •Late Diastolic Filling
- •Diastolic Function Assessment
- •Normal Pattern (Grade 0)
- •LV Relaxation Abnormality Pattern (Grade 1)
- •Pseudonormalization Pattern (Grade 2)
- •Restrictive Pattern (Grade 3)
- •Mitral Annular Motion Velocity
- •Left Atrial Volume Index (LAVI)
- •Tricuspid Regurgitation (TR) Jet Peak Velocity
- •Pulmonary Vein Flow
- •ASE Recommendation 2009
- •ASE Recommendation 2016
- •References
- •16: Cardiomyopathies
- •Dilated Cardiomyopathy
- •Hypertrophic Cardiomyopathy
- •Restrictive Cardiomyopathies
- •Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D)
- •Stress-Induced Cardiomyopathy
- •Takotsubo Cardiomyopathy
- •Neurogenic Stress Cardiomyopathy
- •Cirrhotic Cardiomyopathy
- •Noncompaction Cardiomyopathy
- •Septic Cardiomyopathy
- •References
- •17: Aortic Stenosis
- •Introduction
- •Anatomic Evaluation
- •Hemodynamic Evaluation
- •References
- •Aortic Regurgitation
- •Doppler Findings
- •Vena Contracta (VC)
- •Jet Width/Area
- •Proximal Flow Convergence
- •Pressure Half-Time (PHT)
- •Pulmonary Regurgitation
- •Color Flow Doppler Findings: Jet Width, Jet Area, Jet Length, Vena Contracta
- •References
- •Mitral Stenosis
- •Etiologies
- •Planimetry
- •Continuity Equation
- •Pressure Half-Time
- •Deceleration Time
- •Mean Pressure Gradient
- •Tricuspid Stenosis
- •Etiology
- •Planimetry
- •Continuity Equation
- •Pressure Gradients
- •Pressure Half-Time
- •Consequences
- •References
- •Causes
- •Primary Causes
- •Secondary Causes
- •Jet Area
- •Vena Contracta
- •Jet Density
- •Pressure Half-Time
- •References
- •The Bernoulli Equation
- •Intracardiac Pressures
- •Left Atrial Pressure
- •Left Ventricular End-Diastolic Pressure
- •Right Ventricular Systolic Pressure
- •Case
- •References
- •22: Prosthetic Valves
- •General Imaging Principles
- •2D Imaging
- •3D Imaging
- •Doppler Evaluation
- •Case 1
- •2D Evaluation
- •Doppler Evaluation
- •Prosthetic Aortic Valve Dysfunction: Stenosis
- •Case 2
- •Prosthetic Aortic Valve Dysfunction: Regurgitation
- •Case 3
- •Case 4
- •Prosthetic Mitral Valve Dysfunction: Stenosis
- •Case 5
- •Prosthetic Mitral Valve Dysfunction: Regurgitation
- •Case 6
- •Prosthetic Valve Endocarditis
- •Case 7
- •Prosthetic Valve Thrombosis
- •Mechanical Valve Thrombosis
- •Case 8
- •Bioprosthetic Valve Thrombosis
- •Case 9
- •References
- •23: Infective Endocarditis
- •Introduction
- •Diagnosis
- •Echocardiographic Assessment
- •Left-Sided Endocarditis
- •Right-Sided Endocarditis
- •Prosthetic Valve Endocarditis
- •References
- •24: Cardiac Tamponade
- •Clinical Criteria
- •Cardiac Chamber Collapse
- •Inferior Vena Cava Plethora
- •Spectral Doppler Flow Variation
- •References
- •25: Ultrasound-Guided Pericardiocentesis
- •Background
- •Transthoracic Echocardiogram
- •Inferior Vena Cava Plethora
- •Right Heart Chamber Systolic/Diastolic Collapse
- •Doppler Flow Velocity Changes
- •Complications
- •References
- •Pathophysiology
- •Echocardiographic Diagnosis
- •Evolving Evidence
- •Two-Dimensional Evaluation
- •Septal Motion
- •Other 2D Findings
- •Doppler Evaluation
- •Hepatic Vein Pulse-Wave Doppler
- •References
- •Introduction
- •Normal Anatomical Variants
- •Right Atrium
- •Crista Terminalis
- •Eustachian Valve
- •Thebesian Valve
- •Chiari Network
- •Coronary Sinus
- •Persistent Left Superior Vena Cava (PLSVC)
- •Patent Foramen Ovale (PFO)
- •Atrial Septal Aneurysm
- •Left Atrium
- •Left Atrial Appendage
- •Atrial Suture Line After Cardiac Transplant
- •Right Ventricle
- •Moderator Band
- •Left Ventricle
- •False Tendons
- •Extracardiac Spaces
- •Pericardial Space
- •Sinuses
- •Exogenous Devices
- •Benign Masses
- •Myxoma
- •Fibroelastomas
- •Lambl’s Excrescences
- •Reverberations
- •Mirror Image
- •Side Lobe
- •Acoustic Shadowing
- •Conclusion
- •References
- •28: Left Ventricular Thrombus Part 1
- •Introduction
- •Etiology
- •Diagnosis
- •Echocardiography Technique
- •Contrast-Enhanced Echocardiography
- •Clinical Implications
- •References
- •29: Left Ventricular Thrombus Part 2
- •LV Thrombus Recognition: Sonographic Features
- •References
- •30: Left Atrial Thrombus
- •Etiology
- •Diagnosis
- •Clinical Implications
- •References
- •31: Right-Sided Thrombus
- •Introduction
- •Etiology
- •Diagnosis
- •Clinical Implications
- •Evolving Evidence
- •References
- •Introduction
- •Aortic Dissection
- •Abdominal Aortic Aneurysm
- •Aortic Thrombus
- •Image Acquisition
- •Pitfalls
- •References
- •33: Adult Congenital Heart Disease
- •Problems Causing Increased Pulmonary Blood Flow
- •Patent Ductus Arteriosus (PDA)
- •Atrial Septal Defect (ASD)/Patent Foramen Ovale (PFO) (Unrepaired/Repaired)
- •Problems Causing Decreased Pulmonary Blood Flow
- •Ebstein’s Malformation (Unrepaired)
- •Bicuspid Aortic Valve
- •Summary
- •References
- •Further Reading
- •Scanning Technique
- •Transudative Versus Exudative Fluid
- •Malignant Fluid
- •Empyema
- •References
- •Introduction
- •Background
- •Technique
- •Conclusion
- •References
- •36: Pulmonary Edema
- •Cardiogenic Vs. Noncardiogenic
- •Lung Zones/Locations
- •References
- •References
- •38: Diaphragm
- •Introduction
- •Measurement
- •Caveats
- •Diaphragm Thickening
- •Measurement
- •Caveats
- •Diaphragm Excursion
- •Measurement
- •Caveats
- •Measurement
- •Caveats
- •References
- •Introduction
- •Thoracentesis Technique
- •Tube Thoracostomy Technique
- •Manometry
- •Procedural Complications
- •Subpleural Mass Biopsy
- •Conclusion
- •References
- •40: Ultrasound During Intubation
- •Evidence
- •Limitations
- •References
- •41: Transcutaneous Laryngeal Ultrasonography: Vocal Fold Ultrasound
- •Introduction
- •Vocal Fold Motion Abnormalities
- •Paradoxical Vocal Cord Motion Disorder
- •References
- •Concept
- •Indications
- •Limitations
- •Views
- •The Hepatorenal Recess (Morrison’s Pouch)
- •The Splenorenal Recess
- •The Pericardial Space
- •The Pelvis
- •Pathologic Findings
- •References
- •Indications
- •Limitations
- •Bladder Ultrasound
- •Bladder Volume
- •Urinary Catheters
- •Hydronephrosis
- •Pitfalls
- •Renal Blood Flow
- •References
- •Stomach
- •Liver
- •Biliary System
- •Diagnostic Applications
- •Stomach
- •Liver
- •Biliary System
- •Paracentesis
- •Technique
- •Blakemore/Minnesota Tubes
- •Gastrostomy Tube
- •References

368
J. L. Maurer and M. E. Prekker
The published literature over several decades
highlights a number of clinical risk factors for the
diagnosis of LV thrombus: anterior AMI, large
AMI size, the magnitude of cardiac enzyme elevation, LV regional akinesis or dyskinesis including the presence of an LV aneurysm, and incident
HFrEF.According to a 2019 retrospective analysis
using two-dimensional echocardiography, the
common precipitants of LV thrombus were heart
failure (69% of cases) followed by AMI (26%)
[9]. Moreover, dilated cardiomyopathy, independent of AMI, is an established risk factor for LV
thrombus formation [10]. Thus, heart failure has
likely supplanted AMI as the most common disease associated with LV thrombosis.
3. Multiple apical views should be sought
as the LV may appear foreshortened if
the transducer is not placed at the true
apex.
4. Decreasing depth to better visualize the
apex favorably affects the pulse repetition frequency and increases the framerate of the desired image, potentially
improving image resolution [11].
5. Near-eld gain should be reduced to
mitigate near-eld artifact. This type of
artifact may mimic the appearance of an
LV thrombus and result in false positive
ndings [11].
6. Near-eld resolution of apical structures may be enhanced by using high-
LV Thrombus Recognition: Sonographic Features
frequency transducers (5–7.5MHz).
7. The presence of “spontaneous echo
contrast,” or smoke-like swirling of
The typical sonographic appearance of an LV
thrombus is an echodense mass adherent to the
endocardium with distinct margins (Figs.29.1a
and 29.2a/Videos 29.1 and 29.3) and, in some
instances, independent motion. LV thrombus formation typically occurs in regions of stagnant or
slow blood ow such as adjacent to segmental
wall motion abnormalities, LV aneurysm or pseudoaneurysm, and in the setting of diffuse LV dys-
hyperechoic speckles in the LV cavity,
is thought to represent low-velocity
blood ow and indicates greater risk of
thrombosis [12].
8. Doppler analysis of apical ow patterns
with identication of apical ow stasis
or continuous swirling of ow around
the apex may also indicate greater risk
for apical thrombosis [13].
function [11, 12]. Thus, these cardiac pathologies
often provide indirect evidence to an ultrasonographer that an LV thrombus may be present. There are three distinct morphologic features
of LV thrombus: (1) mural thrombus—thin clot
oriented parallel to the endocardium with a concave free margin and a single surface exposed to
Pro-Tips: Sonography for LV Thrombus
Detection
1. The apex is best visualized with the
patient in the left lateral decubitus position which promotes the leftward shift
of the heart from beneath the high attenuation tissue of the sternum.
2. The transducer is placed near the point
of maximal impulse (PMI) or the shortest distance between the chest wall and
the cardiac apex to maximize
resolution.
blood; (2) protruding thrombus—convex extension from the endocardium with multiple surfaces exposed to blood (Figs.29.1a-c and 29.3;
Videos 29.1 and 29.2); and (3) mobile thrombus—extension from the endocardium with independent motion of part or all of the thrombus
(Figs.29.2a-c; Videos 29.3 and 29.4). Multiple
features may co- exist in a single thrombus. In all
three thrombus morphologies, a discrete interface
between clotted and non-clotted blood is typically observed given differences in their acoustic
impedance. Thrombus chronicity also contributes
to sonographic appearance: mature thrombi may

ab
29 Left Ventricular Thrombus Part 2
c
369
Fig. 29.1 (a) Transthoracic echocardiography (TTE):
apical four chamber view depicting biventricular, apical,
protruding thrombi. (b) Contrast-enhanced TTE in the
same patient: apical four chamber view depicting biventricular, apical, protruding thrombi. Note: the left ventricular opacication (LVO) technique using an
ultrasound-enhancing agent (UEA) renders the blood in
appear hyperechoic, while immature thrombi
may be relatively hypoechoic and difcult to distinguish from blood. Larger thrombi may exhibit
heterogeneous echodensity. In many cases, the
acoustic properties of thrombus and myocardium
are similar making this diagnosis challenging; a
mural thrombus can be nearly indistinguishable
from the adjacent myocardium.
An LV thrombus must be distinguished from
the normal intraventricular anatomy such as papillary muscles, muscular trabeculae, chordal
structures, endocardium, and other
intraventricular masses. Thrombus mimics may
the left ventricular cavity hyperechoic but does not penetrate or opacify the avascular thrombi. The right ventricle
may be more difcult to see in contrast enhanced images.
(c) Non-contrast cardiac magnetic resonance (CMR)
imaging in the same patient: this horizontal long axis
(HLA) view utilizing steady-state free precession demonstrates biventricular, apical, protruding thrombi
be identied in part by, (1) an intracavitary location that would be atypical for LV thrombus (e.g.,
the base of the heart), (2) the absence of pathology associated with an LV thrombus such as segmental hypokinesis or akinesis, LV aneurysm, or
diffuse LV dysfunction, or (3) the absence of
variation in sonographic appearance of a suspicious structure over time (LV thrombi tend to
change in appearance with serial imaging).
Sonographic artifacts may also mimic an LV
thrombus. An anatomic structure exhibits an
immutable position within the LV cavity whereas
an artifact changes position or disappears with

370
ab
J. L. Maurer and M. E. Prekker
c
Fig. 29.2 (a) Transthoracic echocardiography (TTE):
apical two chamber view depicting a left ventricular
mobile thrombus adherent to the apical inferior wall. Note
the irregular endocardial border and hyperechoic structure
(thrombus). (b) Contrast-enhanced TTE: apical two
changes in orientation. Therefore, spurious structures should be interrogated with multiple
orthogonal views in order to exclude artifacts.
The use of color ow Doppler to evaluate for
ow across an area of interest may further distinguish artifacts from structures that warrant additional interrogation.
Thus, features that favor the diagnosis of LV
thrombus include apical location, adjacent position relative to hypokinetic or akinetic myocardium such as LV aneurysm, the presence of
chamber view depicting the same left ventricular mobile
thrombus located on the apical inferior wall. (c
contrast cardiac magnetic resonance (CMR) imaging of
the same patient: vertical long axis view depicting the left
ventricular, apical inferior, mobile thrombus (dark grey)
contrast,” acoustic differentiation from underlying myocardium, distinct thrombus margins,
free- motion of the intracavity thrombus margin,
static position within the LV cavity on multiple
views, and variation in appearance on serial
examinations. However, the diagnosis is not
straightforward in a substantial number of cases,
and serial echocardiography, the application of
UEAs or “echo contrast,” or CMR will be
necessary to optimize diagnostic accuracy
(Fig.29.4a-c; Videos 29.5 and 29.6).
diffuse LV dysfunction, “spontaneous echo
) Non-

29 Left Ventricular Thrombus Part 2
371
RV
a
T
LV
RV
b
RA
LV
LA
c
LV
RV
RA
LA
Fig. 29.3 There are three distinct morphologies of LV thrombi, a protruding thrombus (a), a mural thrombus (b), and
a mobile thrombus (c). Multiple morphologies may co-exist in a single thrombus
Advanced Diagnosis: Ultrasound
Enhancing Agents (UEAs)
andCardiac Magnetic Resonance
Imaging (CMR)
designed to survive transpulmonary passage and
exhibit compressibility, or the capacity to oscillate, creating a visually sharp interface between
blood and tissue. At low mechanical index (MI)
and power output, microbubbles exhibit a nonStandard two-dimensional echocardiography for
the evaluation of LV thrombus has a specicity of
96–98% and a sensitivity of 23–35%, while the
addition of UEA use has been shown to increase
sensitivity to 61–64% without compromising
specicity [6, 14, 15]. The American Society of
Echocardiography recommends that “ultrasound
enhancement should be used in patients in whom
LV thrombus cannot be ruled in or out with noncontrast echocardiography” [16].
For the purpose of cardiac imaging, three
UEAs are available currently: Optison, Denity
(Luminity in Europe), and Lumason (SonoVue
outside the United States). These commercially
produced, gas-lled microbubble agents are
linear oscillation pattern that generates acoustic
signals distinct from that of tissue. The backscattered acoustic signals appear as opacication
(so- called “enhancement”) on ultrasound. In the
absence of LV thrombus, UEA-facilitated left-
ventricular opacication (LVO) will demonstrate a smooth LV endocardial border, following
the ventricular contour in an uninterrupted fashion. In the presence of LV thrombus, UEAfacilitated LVO may reveal an irregular
endocardial border (Fig. 29.2b/Video 29.4).
Moreover, the use of UEAs at low MI with multipulse cancellation techniques improves visualization of the blood-endocardial boundary and
facilitates real-time visualization of wall motion

372
J. L. Maurer and M. E. Prekker
a
b
c
Fig. 29.4 (a) Transthoracic echocardiography (TTE): api-
cal two chamber view depicting prominent trabeculation
mimicking a thrombus in the setting of adjacent wall- motion
hypokinesis. (b) Contrast enhanced TTE: apical two chamber view depicting the same prominent trabeculation mim-
so that the characteristic LV thrombus milieu
may be detected [16, 17]. The utilization of UEA
LVO also mitigates apical reverberation
artifacts.
The compressibility and resonant properties of
microbubbles relative to tissue can be exploited
by different imaging techniques to enhance the
endocardial border, dene intra-cavitary structures, and evaluate for perfusion of cardiac structures. For example, the use of intermittent imaging
with destruction/reperfusion at high MI may
facilitate visualization of a perfusion defect in the
adjacent myocardium as a substrate for thrombus
formation and differentiate avascular thrombus
from vascularized cardiac tissue [16, 17].
icking a thrombus in the setting of an adjacent hypokinetic
myocardial segment. (c) Non-contrast cardiac magnetic
resonance (CMR) imaging: vertical long axis view depicting
prominent trabeculation mimicking a thrombus in the setting of an adjacent hypokinetic myocardial segment
Pro-Tips: Use of Ultrasound Enhancing
Agents (UEAs)
1. Ensure that your ultrasound equipment
is compatible with UEAs by contacting
your equipment representative.
2. You may have to adjust the power output or mechanical index within the
range of 0.2–0.5 until visualization is
most favorable.
3. Position the focus of the ultrasound
beam at the bottom of the imaging sector in order to optimize near-eld
visualization.
(continued)

ab
29 Left Ventricular Thrombus Part 2
4. There are at least three methods to deliver
UEAs: bolus with or without dilution or
infusion. UEA boluses, sometimes
diluted in saline, are satisfactory for LVO
studies. The agent must be activated and
prepared according to manufacturer recommendations and delivery method.
5. UEA bolus injection is performed
slowly in order to achieve homogenous
opacication, which facilitates clear
visualization of the endocardium and
wall thickening with minimization of
basal attenuation and apical artifact
(Fig.29.5a, b).
6. LVO may persist for several minutes.
Repeat bolus dosing may be necessary.
373
Multiple studies have demonstrated the superiority of gadolinium-enhanced CMR over transthoracic echocardiography with UEA. Thus, if
echocardiography shows a suspicious intracavitary structure, but diagnostic uncertainty remains,
then gadolinium-enhanced CMR should be considered in centers experienced with image acquisition and interpretation using this modality.
Transesophageal echocardiography (TEE) is not
recommended for the evaluation of LV thrombus.
There is an unfavorable distance between an
ultrasound probe positioned in the esophagus and
the LV apex which leads to apical foreshortening
and poor visualization at the most common locus
of LV thrombi.
Fig. 29.5 (a) Contrast enhanced transthoracic echocar-
diography using proper UEA technique: apical two chamber view. Note the homogenous LV opacication and
focus positioned at the bottom of the imaging sector with
optimal visualization of a papillary muscle. (b) Contrast
enhanced transthoracic echocardiography using poor
UEA technique: apical two chamber view. Suboptimal
visualization of an LV structure is the result of positioning
the focus at the top, rather than at the bottom, of the imaging sector. Contrast swirling is observed

374
Clinical Implications andTreatment
ofLV Thrombus
The natural history of an LV thrombus is
unpredictable and may entail regression with
or without therapy, partial regression, change
in morphology, or calcication. The most
feared complication of LV thrombus is embolization. In the absence of therapeutic anticoagulation, the risk of LV thrombus embolization
has historically ranged from 13% to 22% [2,
18]. Embolization risk is greater among pro-
truding and mobile thrombi. After 3months,
the risk of systemic embolization may be lower
as the thrombus matures and incorporates into
LV wall segments. A 2020 observational study
evaluating the prognosis of patients treated
with anticoagulation for a conrmed LV thrombus identied an overall incidence of major
adverse cardiac events of 37% [18]. Over a
median follow-up period of 632 days in this
study, mortality was 19%, stroke was diagnosed in 13%, and major bleeding occurred in
13% [18].
Systemic anticoagulation reduces the risk
of LV thrombus embolization. Professional
society guidelines for the management of
STEMI complicated by LV thrombus, including the American College of Cardiology/
American Heart Association (ACC/AHA) and
the European Society of Cardiology (ESC),
recommend anticoagulation therapy for at
least 3–6 months duration [19, 20]. The
American Heart Association/American Stroke
Association (AHA/ASA) guidelines for the
secondary prevention of ischemic stroke recommend anticoagulation therapy for at least
3months duration for patients with LV thrombus who are diagnosed with stroke or transient ischemic attack [21]. Professional
societies unanimously agree that screening
for an LV thrombus should be pursued in the
setting of frequently coexistent pathology.
However, the optimal timing for screening,
imaging frequency, and duration of follow-up
imaging in the setting of an identified LV
thrombus all remain controversial.
J. L. Maurer and M. E. Prekker
Evolving Evidence: The Choice of
Anticoagulant to Treat LV Thrombus
Historically, guidelines have recommended
vitamin K antagonists (VKAs) for the treatment or prevention of LV thrombus [19,
21]. Heparins are often used until the target
INR is achieved. The efcacy of direct oral
anticoagulants (DOACs) in LV thrombus
treatment could perhaps be extrapolated
from experience treating atrial brillation
(AF) and venous thromboembolism (VTE).
Accordingly, the use of DOACs to treat LV
thrombi has increased, and the literature
now contains reports of thrombus regression with apixaban, rivaroxaban, and dabigatran. However, in a 2020 retrospective
cohort study, DOAC treatment was associated with a higher risk of systemic embolization in patients with an LV thrombus
compared with warfarin use [22]. We recommend that the risks and benets of
DOAC use in patients with LV thrombus be
weighed on a case-by-case basis.
The combination of anticoagulation
therapy and dual antiplatelet therapy
(DAPT), so-called “triple therapy,”
increases the risk of bleeding two- to threefold compared to anticoagulation therapy
alone. There are no randomized clinical trials comparing “double therapy” (oral
anticoagulation plus a single antiplatelet
agent) with “triple therapy” in acute coronary syndrome (ACS) patients with LV
thrombus. However, data gleaned from
studies comparing double versus triple
therapy for patients with ACS and other
conditions suggest that double therapy is
associated with reduced bleeding risk and
potentially similar efcacy compared with
triple therapy [23, 24]. Future clinical
research should clarify the role of DOAC
therapy for patients with LV thrombus as
well as compare the benets and harms of
double vs triple therapy for ACS patients
with LV thrombus who require platelet
inhibition after PCI.

29 Left Ventricular Thrombus Part 2
375
Summary Points
• The typical sonographic appearance of an LV
thrombus is an echodense mass adherent to
the endocardium with distinct margins and, in
some instances, a motion that is independent
• The majority of LV thrombi form in the LV
apex, often in conjunction with an LV apical
aneurysm.
• Careful echocardiographic evaluation with
multiple apical views should be performed if
the diagnosis of an LV thrombus is suspected.
• There are three common morphologic variants
of LV thrombus (mural, protruding, and
mobile), but a single thrombus may exhibit
more than one of these features.
• Utilization of an ultrasound enhancing agent
(UEA), with appropriate mechanical index or
power output adjustments, improves the sensitivity of transthoracic echocardiography for
the diagnosis of LV thrombus.
• Left-ventricular opacication (LVO) using
UEAs improves visualization of the bloodendocardial boundary and facilitates: (1) LV
thrombus diagnosis and (2) evaluation of
abnormalities in wall motion.
• Systemic anticoagulation reduces the risk of
LV thrombus embolization and treatment is
generally prescribed for at least 3–6months.
Questions
1. A 40-year-old woman presents 2weeks after
childbirth for progressive dyspnea, peripheral
edema, and new onset right-sided weakness.
She is admitted to the intensive care unit for
acute hypoxemic respiratory failure requiring
mechanical ventilation. Head imaging demonstrated an acute ischemic stroke. While performing bedside echocardiography you
estimate an ejection fraction of <30% and are
concerned that an LV thrombus may be present. Which of the following maneuvers would
be may assist in the diagnosis of an LV
thrombus?
A. Place the patient in the left lateral decubi-
tus position and the transducer at the point
of.
B. maximal impulse.
C. Avoid foreshortening of the left ventricu-
lar apex and obtain multiple orthogonal
views.
D. Slowly administer an IV bolus of ultra-
sound contrast while pursuing left ventricular apical views.
E. All of the above.
Answer D
Peripartum cardiomyopathy (PPCM) is a
well-established risk factor for LV thrombus,
especially in the setting of an ejection fraction of <35%. In the setting of concurrent
heart failure and stroke symptoms, evaluation for an LV thrombus is critical. Standard
two- dimensional echocardiography for the
evaluation of LV thrombus has a specicity
of 96–98% and a sensitivity of 23–35%,
while the addition of UEA use has been
shown to increase sensitivity to 61–64%
without compromising specicity [6, 14,
15]. The American Society of
Echocardiography recommends that “ultrasound enhancement should be used in
patients in whom LV thrombus cannot be
ruled in or out with noncontrast echocardiography” [16]. Time-gain compensation
(TGC) should be adjusted such that neareld gain is reduced in order to mitigate
near-eld artifacts and false positive evaluation. Decreasing depth to better visualize the
apex favorably affects the pulse repetition
frequency (PRF) and increases the frame rate
of the desired image. Depth of eld settings
of 7–9cm may be most favorable.
2. A 55-year-old man with a history of ischemic
heart disease is admitted from a clinic for further evaluation of fatigue, cough, dyspnea,
and severe peripheral eosinophilia. After
admission, he exhibits a complete heart block
with a ventricular escape rhythm prompting
transfer to the intensive care unit. Bedside
echocardiography with the use of an
ultrasound- enhancing agent demonstrates
reduced LV function and a mobile echodense
mass adherent to the apical endocardium.
Which of the following statements is false?

376
J. L. Maurer and M. E. Prekker
A. Embolization risk is greater among pro-
truding thrombi and especially mobile
thrombi.
B. A true intra-cavitary structure should
exhibit an immutable position within the
LV cavity whereas an artifact will change
position or disappear with changes in
orientation.
C. In patients with heart disease, the admin-
istration of UEAs may be poorly tolerated
evidenced by studies that have demonstrated a greater risk of adverse events
with the application of perutren compared with placebo.
D. In the absence of absolute contraindica-
tions, anticoagulation therapy should be
instituted for a minimum of 3 months
duration and guided by follow-up
imaging.
Answer C
This patient most likely has
Hypereosinophilic syndrome (HES) complicated by cardiac disease. Hypereosinophilic
myocarditis is associated with heterogeneous
mechanisms. A large body of published clinical
data, evaluating the application of UEAs under
conditions of stress and coronary artery disease,
has established the safety of UEAs. Accordingly,
the FDA has approved three agents for cardiac
indications after extensive safety evaluations,
including direct comparisons with placebo, that
showed no signicant difference in total or specic adverse events [16, 25].
Acknowledgments Special thank you to the following
for their generous contributions to this chapter: Dr.
Michelle Carlson, MD, FACC; Melissa Madsen, cardiac
sonographer; and Dr. Laura Hubbard, PharmD.
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