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358
D. R. Maberry and B. Fiza
and potentially aneurysm or pseudoaneurysm
formation. Myocardial dyskinesis and myocardial architectural distortion alter blood ow
through the left ventricle and lead to areas of relative blood stasis. The severity of blood stasis
increases as the left ventricle ejection fraction
decreases. Finally, acute coronary syndrome is
associated with a hypercoagulable state, specically with increased levels of von Willebrand factor, prothrombin, and brinopeptide-A that can
persist for months after the MI [3, 4]. This pathophysiology demonstrates two important phenomena about left ventricular thrombus. First,
approximately 90% of thrombi form in the rst 2
weeks after myocardial infarction [3]. Although
the risk of developing an LVT decreases with
time, one study using cardiac MRI found an additional 6% of patients with a new LV thrombus at
4months [5]. Second, myocardial dyskinesis and
decreased ejection fraction are major risk factors
for developing LV thrombus after myocardial
infarction. Interestingly, other pathologic states
with decreased ejection fraction and myocardial
dyskinesis, such as takotsubo, have an LVT incidence of only 1–2%, despite low rates of anticoagulation [6]. It is theorized that the delayed
formation of thrombi after MI and the relative
lack of thrombi in Takotsubo demonstrate the
importance of the persistent hypercoagulable
state following an acute MI [6].
[9]. The use of contrast-enhanced echocardiography improves the diagnostic yield, with a sensitivity of 61%, specicity of 99%, a PPV of 93%,
and an NPH of 91% [6]. When LV thrombus was
the specied indication and performed on very
high-risk patients (anterior MI and reduced ejection fraction), the sensitivity was 94.7% and the
specicity was 98.5% [10]. In comparison,
delayed enhancement cardiac MRI has a sensitivity of 88% and a specicity of 99% [11].
There are several well-known risk factors for
LVT that should be taken into consideration
when choosing a diagnostic modality. The primary risk factor for developing an LVT is an
acute anterior myocardial infarction. Other
important risk factors include LV ejection fraction <40%, large infarct size, severe apical dyskinesis, LV aneurysm, LV pseudoaneurysm, and
dilated cardiomyopathy [3, 11]. Of note, the risk
of LV thrombus in non-anterior MI increases as
the necrosis progresses towards the posterolateral
wall [3]. Given the limited sensitivity of echocardiography to diagnose an LV thrombus, any
patient at high risk for LVT should be referred for
a contrast-enhanced echocardiogram or a delayed
enhancement cardiac MRI [12].
Diagnosis
Denition andDierential Diagnosis
Biostatistics andRisk Factors
Multiple modalities are available for diagnosing
a left ventricular thrombus: standard echocardiography, contrast-enhanced echocardiography,
and cardiac MRI.Understanding the indications
and limitations of each of these tools is vital for
making a prompt diagnosis of LVT.A traditional
non-contrast transthoracic echocardiogram
(TTE) has a sensitivity of 24–33%, specicity of
95%, a positive predictive value (PPV) of 57%,
and a negative predictive value (NPV) of 85% for
diagnosing LVT [7, 8]. Interestingly, when evaluation for LVT is listed as the specic indication
for a TTE, the sensitivity and PPV of echocardiography increase to 60% and 75%, respectively
A left ventricular thrombus is a ventricular cavity
mass that appears adjacent to a dyskinetic segment of the myocardium with margins that are
distinct from the blood and the endocardium. To
make the diagnosis, the mass in question should
be present for the entire cardiac cycle and be visible in at least two views [10]. Finally, the thrombus should be clearly distinguishable from the
chordae tendineae, papillary muscles, and myocardial trabeculae [9]. An LVT can be further
characterized by its location, shape, mobility, and
chronicity. Most LV thrombi occur in the LV
apex, but they can occur at any location throughout the left ventricle [11, 13].
An LV thrombus can be categorized based on
the thrombus characteristics. A protruding throm-
28 Left Ventricular Thrombus Part 1
359
bus is any thrombus that projects directly into the
ventricular cavity and has multiple surfaces that
interface with the bloodstream (Fig.28.1; Video
28.1). This is contrasted with a mural thrombus,
which is at, parallel to the endocardium, and has
only one surface that contacts the bloodstream
(Fig. 28.2; Videos 28.2 and 28.3). A mobile
thrombus is any LVT that moves independently
from the myocardium. Finally, a thrombus can be
described by its chronicity. An acute thrombus
consists primarily of platelets and clotting cascade proteins. As the clot ages, broblasts create
a collagen matrix, forming a stronger, more organized clot [14]. Generally, acute LV thrombi are
irregular, protruding, highly mobile, and commonly have an echo-lucent core (Fig.28.3; Video
28.4). In contrast, chronic thrombi are less mobile
and more likely to have a mural appearance [15].
Although beyond the scope of this text, echocardiography can be used to measure the elastic
deformation of an LV thrombus as a marker for
thrombus chronicity [14].
The size, shape, and mobility of the LVT are
of diagnostic and clinical signicance. The sensitivity of echocardiography to detect an LV thrombus is variable. The likelihood of a false-negative
echocardiogram is higher for small thrombi, nonapical thrombi, and mural thrombi [9]. Clinically,
acute thrombi, large thrombi, protruding thrombi,
and highly mobile thrombi are at higher risk of
embolization [15]. Other risk factors for embolization include increasing age, a history of con-
gestive heart failure, and an adjacent
hyperdynamic myocardial segment [15].
The differential diagnosis for an LVT is broad
and includes both normal and pathologic entities.
False tendons, trabeculae, and misplaced papillary muscles are common normal variants that
can be mistaken for LVT [15]. Potentially pathologic causes of an LV mass include left ventricular broma, myxoma, papillary broelastoma,
Lamble excrescence, metastatic cancer, primary
cardiac neoplasm, and cardiac hamartoma.
Melanoma commonly metastasizes to the pericardium and myocardium. Primary cardiac
tumors are rare and are usually a primary sarcoma or lymphoma. LVT is strongly associated
with myocardial dyskinesis; if there are no adjacent areas of dyskinesis, you should seriously
consider another diagnosis [13, 15, 16].
Uncommon causes of LVT in the setting of normal LV function include eosinophilic endocarditis, antiphospholipid syndrome, protein C
deciency, myeloproliferative disorders, and cardiac trauma [15].
Echocardiography Technique
When evaluating a patient for LVT, the initial
echocardiogram examination should consist of
parasternal long, parasternal short, and apical 2,
3, and 4 chamber windows [9]. The standard apical windows may miss small LV thrombi, and
Fig. 28.1 A large,
protruding, and mobile
thrombus (red arrow) is
visualized within the left
ventricle on the
parasternal long-axis
view
360
ab
D. R. Maberry and B. Fiza
Fig. 28.2 (a) A mural thrombus is visualized in the api-
cal four-chamber view (red arrow), adherent to the left
ventricular apex and apical lateral wall. (b) A zoomed-in
Fig. 28.3 Multiple
protruding and mobile
left ventricular thrombi
are visualized in this
off-axis apical twochamber view. The
largest thrombus
demonstrates a
hypoechoic center
relative to its echogenic
margins, suggestive of
an acute thrombus
view highlights the mural thrombus and spontaneous echo
contrast (smoke) within the left ventricle
28 Left Ventricular Thrombus Part 1
361
obtaining off-axis or tangential apical views can
increase the diagnostic yield (Fig. 28.3; Video
28.4) [13]. Using probes with different frequencies, varying the gain settings, and adjusting the
depth of eld can reduce the risk of false positive
studies [5]. You can also consider measuring
Doppler ow patterns in the LV cavity, as both
apical ow stasis and apical swirling are linked to
LVT formation [15]. LV cavity Doppler ow is
also useful for differentiating between an apical
thrombus and common mimics such as a false
tendon or a myocardial trabeculae. A false tendon
is a brous band, like a chordae tendinea, that
stretches across the LV cavity but does not connect with the mitral valve. Both false tendons and
trabeculae create an echogenic line on ultrasound
that mimics the edge of an apical thrombus.
When color Doppler is placed over a false tendon
or trabeculae, it will show ow on both sides of
the line, conrming the presence of a false tendon
or trabeculae. An apical thrombus will not have
an internal Doppler signal [13]. Similarly, it is
important to be aware of near-eld clutter artifacts and reverberation artifacts, as both artifacts
mimic an apical thrombus but will move with
probe repositioning [13]. Finally, the diagnosis of
LVT is dependent upon clear delineation of the
LV endocardial border. If the endocardial border
cannot be clearly dened, the patient should be
considered for contrast-enhanced echocardiography or cardiac MRI [15].
Contrast-Enhanced Echocardiography
The clear delineation of the endocardial border is
a key component in diagnosing LVT and a primary limitation of the traditional non-contrast
echocardiography. The use of ultrasound contrast
to opacify the left ventricle cavity to improve
endocardial delineation signicantly increases
the sensitivity and positive predictive value of
echocardiography for diagnosing LVT.As such,
LV thrombus is listed as a primary indication for
the use of ultrasound contrast in the American
Society of Echocardiography Guidelines [17].
Ultrasound contrast is a solution of microbubbles
made up of a lipid, protein, or polymer shell lled
with a peruorocarbon or sulfur hexauoride gas.
These microbubbles undergo volumetric oscillations when they are exposed to sound waves and
reverberate at a frequency that can be detected by
vendor-specic detection modalities, allowing
for improved visualization of the endocardial
border [18].
When using ultrasound contrast agents, it is
important to make the following considerations.
First, the machine should be set to a low mechanical index, approximately 02–0.5; the exact level
will be determined by the type of contrast used.
The contrast infusion rate should be optimized so
that the LV opacication is uniform throughout.
If the contrast agent is infused too rapidly, it can
lead to signal attenuation and poor study quality.
If the contrast agent is infused too slowly, or if
the mechanical index is too high, it can lead to a
swirling artifact or a loss of apical opacication.
When used properly, contrast-enhanced echocardiography reduces the number of studies deemed
uninterpretable, increases visualization of the LV
segments, improves the ability to detect wall
motion abnormalities, and increases the detection
of LV thrombi (Figs.28.4 and 28.5) [19]. Finally,
ultrasound contrast is associated with back pain
and transient headache, but serious reactions are
rare, and it is considered safe for use in pulmonary hypertension and critically ill patients [16].
362
D. R. Maberry and B. Fiza
Fig. 28.4 Two examples of apical thrombi are demonstrated before and after ultrasound contrast enhancement.
(a) A hyperechoic region is noted near the apex (yellow
arrow); however, poor endocardial border denition limits diagnostic condence. Following contrast administration, a protruding left ventricular thrombus is clearly
delineated (yellow asterisk). (b) A large apical thrombus
is visualized both before (yellow arrow) and after (yellow
asterisk) contrast enhancement, with contrast markedly
improving thrombus visualization and endocardial border
denition.
Image adapted from Barbieri A, Mantovani F, Bursi F,
Faggiano A, Boriani G, Faggiano P. Optimal Use of
Echocardiography in Management of Thrombosis After
Anterior Myocardial Infarction. Echocardiography.
2020;37(8):1287–1295
Permission Granted from John Wiley and Sons and
Copyright Clearance Center
ab
cd
28 Left Ventricular Thrombus Part 1
363
Fig. 28.5 Visualization of Apical Thrombi Before and
After Ultrasound Contrast Enhancement. Panels (a) and
(c) show an apical two-chamber view acquired before and
after contrast administration, respectively. In panel (a),
the endocardial border at the apex is poorly dened, limiting diagnostic clarity. Contrast enhancement in panel (c)
reveals a well-delineated apical thrombus. Panels (b) and
(d) depict an apical three-chamber view before and after
contrast. While no thrombus is identied in panel (b) due
to suboptimal visualization, panel (d) demonstrates
improved endocardial border denition and conrms the
presence of an apical thrombus following contrast
administration
Image adapted from: Srichai MB, Junor C, Rodriguez LL,
Stillman AE, Grimm RA, Lieber ML, etal. Imaging and
pathological characteristics of left ventricular thrombus: a
comparison of contrast-enhanced magnetic resonance
imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. American Heart Journal. 2006;152(1):75–84
Permission Granted from Elsevier Publishing
364
D. R. Maberry and B. Fiza
Clinical Implications
Patients with an LV thrombus are at increased risk
of cardioembolic events and require anticoagulation and repeat imaging to evaluate for thrombus
resolution [8]. When the diagnosis of LVT is
made, the patient should be started on anticoagulation with warfarin and a heparin bridge. Directacting oral anticoagulants (DOACs) can be used,
but a recent retrospective study found that patients
treated with DOACs had a higher incidence of
stroke after 1year [20]. The rate of LVT-related
cardioembolic events is approximately 5.5% and
can be as low as 3% in patients who are therapeutic on warfarin more than 50% of the time [20]. It
is important to recognize that the risk of a cardioembolic event is highest during the rst 2 weeks
after thrombus formation and then gradually
decreases over the next 3months [20].
Delayed enhancement Cardiac MRI is considered the diagnostic standard, but it has limited
availability, limited ability to perform serial
exams, increased cost, and may not be tolerated
by the patient. The diagnosis of LV thrombus can
be made on point-of-care (POC) ultrasound if a
ventricular cavity mass with distinct margins is
seen adjacent to a dyskinetic segment of the myocardium. It is important to understand the limitations of point-of-care ultrasound in making this
diagnosis. It is crucial that high-risk patients with
a negative POC ultrasound are referred for additional testing with contrast-enhanced echocardiography or a cardiac MRI.It is also reasonable
to consider repeat contrast-enhanced echocardiography in 2 weeks for high-risk patients with a
negative initial scan [20].In patients with an LVT
on their initial study, a repeat echocardiogram
may be performed in 2–4weeks to assess for resolution of the thrombus, as 62.3% of patients may
have total resolution of the thrombus with a
median time to resolution of 103days [21]. This
has important therapeutic implications, as patients
with thrombus resolution can discontinue their
anticoagulation while patients with persistent
LVT remain at a higher risk of complications [20].
Summary Points
• Left ventricular thrombus (LVT) affects 5.4%
of all MIs and 7–15% of anterior MIs [3].
• LV thrombus should also be considered in
patients with severe apical dyskinesis, LV
aneurysm, LV pseudoaneurysm, and dilated
cardiomyopathy [3, 11].
• Patients with LVT are at increased risk of cardioembolic events and require anticoagulation
and further imaging to monitor for thrombus
resolution [21].
• Traditional transthoracic echocardiograms
have a sensitivity of 24–33% and specicity of
95% [7, 8].
• Specifying LVT as the indication for the study
increases the sensitivity [9].
• Contrast-enhanced echocardiography
improves delineation of the endocardial border and increases the sensitivity to 61% and
specicity of 99% [6].
• The likelihood of a false-negative echocardiogram is higher for small thrombi, non-apical
thrombi, and mural thrombi [9].
• Obtaining off-axis or tangential apical views,
using probes with different frequencies, varying the gain settings, and adjusting the depth
of eld can reduce the risk of false positive
studies [5, 13].
• LV cavity Doppler ow is useful for differentiating between an apical thrombus and common mimics such as a false tendon or a
myocardial trabecula [13].
• Contrast-enhanced echocardiography should
be considered in all high-risk patients and in
any study where the endocardial border is not
clearly dened [17].
Questions
1. Which of the following ultrasound modalities
can be used to differentiate between a left
ventricular thrombus and similarly appearing
non-pathologic conditions such as a false ten-
don or a trabecula?
A. Pulse wave Doppler.
B. Continuous wave Doppler.
28 Left Ventricular Thrombus Part 1
365
C. Color Doppler.
D. M-mode.
Explanation: LV cavity Doppler ow is
useful for differentiating between an apical
thrombus and common mimics such as a false
tendon or a myocardial trabecula. A false tendon is a brous band, like a chordae tendinea,
that stretches across the LV cavity. Both false
tendons and trabeculae create an echogenic line
on ultrasound that mimics the edge of a ventricular thrombus. When color Doppler is
placed over a false tendon or trabeculae, it will
show ow on both sides of the line, conrming
the presence of a false tendon or trabeculae. An
apical thrombus will not have an internal
Doppler signal [13]. Pulse wave Doppler allows
you to measure low velocities in a small, gated
area. Continuous wave Doppler can measure
both the direction and the velocity of ow along
a given path but cannot determine the exact
location [22]. M-mode allows you to visualize
motion and timing in a selected region [23].
2. You are caring for a 55-year-old man with
acute heart failure after an anterior myocardial infarction. He is now 7 days out from PCI
and has been progressing as expected. You are
completing your morning exam when you
notice that his right leg is cold and no longer
has a palpable dorsalis pedis pulse. You perform a bedside echocardiogram and notice a
moderately reduced ejection fraction with
anterior wall dyskinesis but do not visualize
an LV thrombus. Which of the following scenarios is most likely to result in a falsenegative echocardiogram for LV thrombus?
A. A left ventricle apex thrombus of any size.
B. A large mural thrombus.
C. A small apical thrombus.
D. A small, non-apical, mural thrombus.
E. A small, non-apical, protruding
thrombus.
Explanation: In a study by Weinsaft etal.
(2011) comparing echocardiography and
delayed enhancement cardiac MRI in 243
patients, they found that small thrombi and
mural thrombi were the most likely to be
missed on transthoracic echocardiography.
In this study, the positive predictive value
was also related to the image quality of the
echocardiogram [9]. A second study by
Weinsaft etal. published in 2009 found that
non-apical thrombi were less likely to be
detected [7].
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Left Ventricular Thrombus Part 2
JohnL.Maurer andMatthewE.Prekker
29
Learning Objectives
1. Identify risk factors for LV thrombus
formation.
2. Recognize the sonographic features of an LV
thrombus.
3. Know the utility of ultrasound-enhancing
agents and the limits of imaging modalities
for the diagnosis of LV thrombus.
4. Understand the clinical implications and treatment of an LV thrombus.
In: “Echocardiography and Ultrasonography in the ICU:
A Comprehensive Text” Eds. Michael Lanspa, MD, MS,
and Andrew Levinson, MD, MPH
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_29.
J. L. Maurer
Department of Critical Care, University of Minnesota
Physicians, Minneapolis, MN, USA
e-mail: Jmaurer10@umphysicians.umn.edu
M. E. Prekker (*)
Department of Medicine, Division of Pulmonary,
Allergy, and Critical Care Medicine, Hennepin
County Medical Center, Minneapolis, MN, USA
e-mail: Matthew.prekker@hcmed.org
LV Thrombus Formation:
Pathophysiology andClinical
Context
LV thrombosis most commonly occurs within the
LV apex (Figures/Videos 29.1, 29.2, 29.3 and 29.4)
where there is blood stasis in the setting of acute
myocardial infarction (AMI) or heart failure with
reduced ejection fraction (HFrEF). In the case of
AMI, most LV thrombi are diagnosed within
2weeks of the inciting event and commonly within
the rst 72h [1]. In the era of percutaneous coronary intervention (PCI), the reported incidence of
LV thrombus-complicating AMI has declined to
1.6–4% [2–4]. However, incidence estimates are
inuenced by diagnostic modality and screening
intervals. For example, studies utilizing gadolinium-enhanced cardiac magnetic resonance imaging (CMR) have reported an LV thrombus incidence
of 8–15% following AMI [5, 6].
The pathophysiology of LV thrombosis is
driven by Virchows triad (circulatory stasis,
endothelial injury, and hypercoagulability). In
the setting of AMI, regional LV akinesia or dyskinesia may lead to blood stasis [7]. Transmural
or endocardial injury contributes to LV thrombus
formation by exposing blood to a damaged endothelial surface. Patients with acute coronary syndrome (ACS) may exhibit an increased basal
level activation of the coagulation system
following clinical ACS resolution which may
predispose to late thrombosis [8].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_29
367