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27 Benign Masses, Normal Anatomic Variants, andArtifacts
347
Atrial Septal Aneurysm
Movement of the atrial septum at a distance of
1.5 cm or greater between the atria throughout
the cardiac cycle characterizes an aneurysmal
atrial septum. It is associated with a PFO and
Chiari network while also increasing the risk of
stroke [4]. Utilizing M-mode ultrasound modality through the septum at the point of maximum
motion can more precisely visualize its full displacement, augmenting measurement accuracy.
Lipomatous Hypertrophy oftheAtrial
Septum
In some individuals the interatrial septum is
thickened along the inferior and superior limbs
while sparing the fossa ovalis, giving lipomatous hypertrophy of the atrial septum its characteristic “dumbbell-like” appearance (Fig.27.4).
The maximal thickness should be greater than
1.5cm [5]. It occurs in 1–8% of individuals and
is more common in patients who are older and
obese, with a potential increased incidence in
women [1].
found in the right and left atrial appendages but
do not cross the crista terminalis into the atria
proper, which separates the pectinate muscles
of the appendages from the smooth wall of the
atria. They are distinguished from masses and
thrombi by their uniform texture and density,
along with synchronous movement with the
cardiac cycle. In contrast, a thrombus typically
exhibits asynchrony to cardiac motion and is
more common with arrhythmias and low-ow
states such as atrial brillation and heart
failure.
Left Atrium
Ligament ofMarshall
Also known as the Warfarin or Coumadin®
Ridge, this peninsula of atrial tissue separates the
left upper pulmonary vein, and left atrial appendage (Fig.27.5). Embryologically it is a remnant
of the left common cardinal vein and bers within
it can be a focus for atrial arrhythmias.
Trabeculations andPectinate Muscles
Muscular invaginations that form a web-like
appearance are termed trabeculations. In the
atria, trabeculations are referred to as pectinate
muscles. Anatomically, trabeculations are
Fig. 27.4
Transesophageal
midesophageal bicaval
view of the interatrial
septum demonstrating
lipomatous hypertrophy
of the superior limbus
(red arrow), inferior
limbus (yellow arrow),
and sparing the fossa
ovalis (green arrow). LA
left atrium, RA right
atrium, SVC superior
vena cava, IVC inferior
vena cava
Left Atrial Appendage
Like the right atrial appendage, the left atrial appendage (Fig.27.5) contains trabeculated pectinate muscles. The number and shape of its lobes vary among
individuals. It is a nidus for thrombus formation,
348
Fig. 27.5
Transesophageal
midesophageal
two-chamber view
focusing on the left
atrium, particularly the
left atrial appendage
(red star), left upper
pulmonary vein (green
star), and ligament of
Marshall (yellow arrow).
LA left atrium, LV left
ventricle, MV mitral
valve
T. Brakke and S. Brannan
with transesophageal echocardiography providing a
better evaluation of this more posterior structure than
transthoracic echocardiography. With increased use
of percutaneous left atrial appendage occlusion
devices and surgical exclusion during open heart
procedures, the left atrial appendage may appear
absent in these patients by ultrasound evaluation.
Atrial Suture Line After Cardiac Transplant
Contemporary cardiac transplant techniques normally involve anastomosing a native atrial cuff to
the donor’s left atrium, thus avoiding individually
anastomosing the pulmonary veins and the risk of
stenosis. This anastomosis is often mistaken as a
pathological structure (Fig.27.6).
Right Ventricle
Moderator Band
Also referred to as the septomarginal trabecula, the
moderator band is the most prominent muscle band
for most patients. Electrically, it contains Purkinje
bers that propagate cardiac depolarization laterally and basally to optimize ventricular output.
Structurally, it helps limit acute dilation of the right
ventricle while routing blood from the tricuspid
inow to the right ventricular outow tract.
Left Ventricle
False Tendons
Sometimes referred to as left ventricular bands,
false tendons are brous or bromuscular structures in the left ventricle akin to the right ventricle’s moderator band, though visually much less
prominent. They are associated with murmurs
and arrhythmias and may be misinterpreted as
thrombi. False tendons are more commonly single, simple, and apically located [6].
Mitral Annular Calcication
Calcication of the mitral annulus (Fig. 27.7)
creates hyperechoic foci associated with artifacts
such as acoustic shadowing or side lobe. Either
the calcication itself or the artifacts it can cause
are commonly mistaken for pathological ndings
or foreign objects. Furthermore, the artifacts can
obscure deeper structures. Because the transducer is at the apex for transthoracic imaging and
the left ventricle is in the near eld, left ventricular assessment is minimally affected by mitral
annular calcication artifacts. However, transesophageal echocardiography ultrasound beams
travel through left atrium down across the mitral
valve and nally into the left ventricle in the far
eld so artifacts created by mitral annular calci-
ab
cd
27 Benign Masses, Normal Anatomic Variants, andArtifacts
349
Fig. 27.6 The red arrows demonstrates atrial suture lines
following cardiac transplantation in (a) transthoracic apical four chamber view, (b) transthoracic parasternal long
axis view, (c) transesophageal midesophageal aortic valve
long axis view, and (d) transesophageal midesophageal
four chamber view. RA right atrium, LA left atrium, RV
right ventricle, LV left ventricle, AV aortic valve, AA
ascending aorta
ab
Fig. 27.7 Mitral annular calcication (red arrows) as shown in a transthoracic (a) apical four chamber view and (b)
parasternal long axis view
350
T. Brakke and S. Brannan
cation project into the left ventricle which can
make evaluation of systolic function and wall
motion challenging.
Extracardiac Spaces
Pericardial Space
Although the pericardial space normally contains
a very small amount of uid, it usually is not well
visualized. While most imagine uid occupying
the pericardial space, it is important to note additional materials such as calcium and adipose can
accumulate in the space, causing constrictive or
restrictive physiological effects. Commonly, peri-
cardial fat can resemble a sizable pericardial effusion. Left-sided pericardial effusions are typically
more lateral (away from the septum) and posterior
near the descending aorta (Fig.27.8a), which is
consistent with how the heart lies anatomically
within the chest. Right-sided pericardial effusions
(Fig.27.8b, c) usually occur more laterally (away
from the septum) and superiorly near the liver.
Effusions can be simple or complex, along with
localized or diffusely surrounding the heart.
Pericardial effusions are distinguished from pleural effusions on TTE parasternal views as occurring between the heart and the descending aorta
(Fig.27.8a), whereas pleural effusions are located
beyond the descending aorta.
ab
c
Fig. 27.8 Pericardial effusion (red arrows) viewed through
several transthoracic windows. (a) Parasternal long axis
view demonstrating the pericardial effusion between the
left ventricle myocardium and the descending aorta. (b)
Parasternal long axis view showing the pericardial effusion
is concentrated more along the right ventricle in this situation. (c) Subcostal view illustrating the pericardial effusion
with tamponade physiology, as the right atrium is almost
completely collapsed (green star). LA left atrium, LV left
ventricle, RV right ventricle, DA descending aorta
27 Benign Masses, Normal Anatomic Variants, andArtifacts
351
Sinuses
The transverse sinus is a reection of the pericardium located at the conuence of the posterior
aspect of the ascending aorta, anterior left atrium,
and posterior pulmonary artery. More simply, it is
a space where the great vessels leave the heart.
Meanwhile, the oblique sinus is a reection of
the pericardium located posteriorly to the entry
of the four pulmonary veins into the left atrium.
Normally, neither pericardial sinus should contain any blood or uid.
Exogenous Devices
When performing cardiac POCUS, it is imperative
to keep in mind any exogenous devices. Pacemaker
wires, pulmonary arterial catheters, central venous
catheters, mechanical support devices or cannulas,
percutaneous left atrial appendage exclusion
devices, and percutaneous atrial septal closure
devices are examples of some benign objects that
may appear in a standard cardiac ultrasound examination. Correlating expected device location to
the view and any prior radiographic studies can
help conrm the proper location or raise concern
for improper placement, which may or may not
contribute to physiological perturbations.
Benign Masses
Myxoma
Cardiac myxomas are the most common benign
cardiac tumors (27% overall) and most frequently
located in the left atrium (75% of the time) [7].
These masses are often pedunculated, attached to
an endocardial surface via a stalk, and composed
of mucopolysaccharides, giving them a friable
characteristic. The most serious consequences of
myxomas are obstructed intracardiac blood ow
and embolization of tumor materials.
Fibroelastomas
Fibroelastomas (Fig. 27.9) are small, solitary,
pedunculated, or sessile-shaped benign tumors
found on cardiac valves away from lines of closures. They are associated with thromboembolic
events, although their management from an anticoagulation and surgical removal standpoint
remains controversial.
Lambl’s Excrescences
A specic type of beroelastoma, Lambl’s
excrescences are smaller and thinner liform
structures usually arising from the line of valve
closure. However, they most commonly arise
from the aortic surface of the aortic valve. Like
other broelastomas, they are associated with but
not necessarily proven to cause strokes, and their
medical and surgical management is debated.
Nodule ofArantius
These nodules are located in the center of the free
edges of most aortic valve cusps, likely arising
from chronic wear and tear. They can become
calcied and appear as a mass contributing to valvular regurgitation.
Common Artifacts Appearing
asMasses
Reverberations
Recall that ultrasound transducers send out a signal
and measure the time it takes for the signal to
return. The duration between sending and receiving is converted to a distance on the display screen.
When the transducer sends out a primary ultrasound beam, it hits a reector and then travels back
to the transducer. When the beam encounters a second strong reector, the beam reects back away
from the transducer towards the initial reector and
then back to either the secondary reector again
(the cycle repeats) or back to the transducer.
Because the beam reected from a secondary
strong reector takes longer to return to the transducer than the primary beam, the machine believes
the initial target is further from the transducer than
it actually is located. Thus, the machine displays a
352
T. Brakke and S. Brannan
copy of the target deeper or more distal to the actual
a
c
Fig. 27.9 Transesophageal views of an aortic valve broelastoma (red arrows). (a) Midesophageal aortic valve
short axis view. (b) Midesophageal aortic valve long axis
view. (c) Midesophageal biplane view of the aortic valve
long axis. In this view the mass appears to originate near
the midpoint of the commissure rather than centrally
Side Lobe
b
d
along the line of closure and has a pedunculated appearance. These suggest broelastoma over a Lambl’s excrescence, the latter of which typically has a thinner and more
brinous look. (d) Three-dimentional aortic valve short
axis view with the broelastoma
target location on the screen. This copy is a reverberation artifact. Depending on the number of
cycles the beam travels between the target and the
secondary strong reector, multiple copies can
appear on the screen, with each one deeper to the
target. Examples include A-lines on lung ultrasound and mitral annular calcication on cardiac
ultrasound.
Mirror Image
These artifacts occur when an ultrasound beam
bounces once off a strong reector, back to the
target, and then to the transducer. It creates a single copy of the target twice as far as its true location from the transducer. It is essentially a “single
copy reverberation.” They can also occur in color
ow Doppler.
All artifacts occur because they violate an
assumption about ultrasound wave behavior. In
the case of side lobe artifacts, the transducer produces more than a single beam, and the extra
beams do not travel parallel to the primary beam.
The lateral edges of the transducer generate
extraneous beams that diverge and travel in a
non-parallel direction compared to the primary
beam. When these extraneous beams hit a target
and reect back to the transducer, the machine
assumes the location they arrive at on the transducer was their origination point and displays the
target correspondingly on the screen. However,
these extra beams originated elsewhere, contacted a reector in a non-parallel pathway as the
primary beam, and then traveled back to the
transducer at a non-parallel angle. Therefore, the
machine displays a copy/copies of the target at a
uniform distance from the transducer but along a
27 Benign Masses, Normal Anatomic Variants, andArtifacts
353
curvilinear line from the actual target’s location,
otherwise known as side lobe artifacts. Side lobe
artifacts appear to disrupt blood ow when
viewed in 2D or B mode, but the use of color ow
Doppler or spectral Doppler fails to demonstrate
a disruption. An example would be a calcied
aortic valve annulus appearing as a dissection
ap in the ascending aorta.
Acoustic Shadowing
Some tissues or materials have high acoustic
impedance, meaning they prevent an ultrasound
beam from traveling further. Because the beam
cannot penetrate beyond the object, it is unable to
contact distal targets and display them on the
screen. Thus, the machine displays an echolucent
“shadow” deeper/distal to the high acoustic
impedance object. For example, in midesophageal transesophageal views, a mechanical mitral
valve often casts a shadow over the left ventricular walls, making it impossible to assess for systolic function and wall motion abnormalities.
Other common causes include other types of
prosthetic valves, patches, implants, and heavily
calcied structures.
Conclusion
Point of care Cardiac ultrasound is used more
prevalently for critically ill patients in the intensive care unit setting by an increased number of
providers. Accurately distinguishing among normal anatomical variants, benign masses, and artifacts is paramount to a proper diagnosis of
physiological etiologies of hemodynamic instability and employment of subsequent treatment
modalities. This chapter has covered a number of
these commonly mistaken structures and ndings. Whenever in doubt, we recommend always
evaluating the suspected target in multiple windows, views, and modalities.
Summary Points
• Every physician performing echocardio-
graphic assessment of the heart needs to dis-
tinguish between normal anatomical variants
and pathological ndings by becoming familiar with common variants that cause confusion
and reconrming suspicions with multiple
views and modalities.
• Benign cardiac masses such as myxomas and
broelastomas are found incidentally on cardiac ultrasounds and may or may not require
medical or surgical attention.
• Several ultrasound artifacts like reverberation,
side lobe, and acoustic shadowing can hamper
the full evaluation of the heart in a particular
view and falsely create abnormal appearing
structures.
Questions
1. A 72-year-old male with a past medical his-
tory of diabetes mellitus type 2, hypertension,
hyperlipidemia, and chronic obstructive pulmonary disease presents to the emergency
room after experiencing new-onset left facial
droop and slurred speech thirty minutes prior
to arrival at the hospital. Which of the following normal anatomic variants is this patient
most likely to show on echocardiographic
imaging:
A. Patent foramen ovale.
B. Chiari network.
C. Left atrial appendage.
D. Atrial septal aneurysm.
E. Crista terminalis.
F. A, B, and C.
G. A, B, and D.
H. A and B.
Answer 1:
G— A patent foramen ovale, Chiari network, and atrial septal aneurysm are all associated with an increased risk of stroke, which is
the clinical diagnosis for this patient. The crista
terminalis (E) separates the pectinate muscles
of the right atrial appendage from the smooth
wall of the right atrium and is most commonly
visualized at the junction of the superior vena
cava and right atrium on transesophageal echocardiography in the midesophageal bicaval
view. The left atrial appendage (C) is a normal
structure that should be found in every patient,
except for those who have undergone surgical
354
T. Brakke and S. Brannan
or percutaneous left atrial appendage exclusion. It is a nidus for thrombus in low-ow
states, such as atrial arrhythmias like atrial
brillation and heart failure. This patient did
not endorse any history of dysrhythmias, palpitations, heart failure, or other risk factors for
having a thrombus in the left atrial appendage.
Therefore, a patent foramen ovale, Chiari network, and atrial septal aneurysm are more
likely in this patient.
2. A 64-year-old female with normal heart function, coronary artery disease, and severe aortic valve insufciency is admitted on
veno-arterial extracorporeal membrane oxygenation support to the cardiovascular intensive care unit following combined coronary
artery bypass grafting and aortic valve
replacement for failure to separate from cardiopulmonary bypass due to cardiogenic
shock. Which of the following could have prevented this from occurring?
A. Perform a 3D assessment of the aortic
valve.
B. Insert a pulmonary arterial catheter for
added monitoring under TEE guidance.
C. Perform a bubble study through a left
upper extremity peripheral IV.
D. Conrm the arterial cannula placement on
TEE.
Answer 2:
C—While undergoing a combined on- pump
coronary artery bypass grafting and aortic
valve replacement surgery, the heart is arrested
by administering cardioplegia either antegrade
(into the aortic root so that it goes down the
coronary arteries) or retrograde (through a cannula placed into the coronary sinus). Antegrade
ow down the coronary arteries is dependent
upon sufcient pressurization of the root
between the aortic cross- clamp and a competent aortic valve. In this case, the patient has
severe aortic valve insufciency, which results
in antegrade cardioplegia leaking into the left
ventricle rather than going down the coronary
arteries. Therefore, the surgeon placed a retrograde cardioplegia line in the coronary sinus to
frequently dose the cardioplegia.
In patients with a persistent left superior
vena cava (PLSVC), primarily left upper
extremity venous blood drains into the coronary sinus directly and eventually into the
right atrium. This results in the coronary sinus
usually being dilated greater than 1 cm and
should clue echocardiographers into its possible existence. Conversely, when administering retrograde cardioplegia through a coronary
sinus catheter, the retrograde cardioplegia
travels backward into the systemic circulation
rather than to the myocardium for myocardial
protection. Therefore, this patient had a
PLSVC with frequent administration of retrograde cardioplegia resulting in no cardioprotection. Diagnosing PLSVC involves
conducting a bubble study through a left upper
extremity PIV and observing opacication of
the coronary sinus rather than the right-sided
superior vena cava. Had this been done before
the institution of cardiopulmonary bypass, a
different myocardial protection plan could
have preserved this patient’s heart function on
pump.
Performing a 3D assessment of the aortic
valve (A) can further evaluate the patient’s
aortic insufciency and would prompt the use
of retrograde cardioplegia. It would still
require evaluation for a PLSVC. Placing a
pulmonary arterial catheter under TEE guidance (B) can be a useful monitor in some situations, but for this patient, it would not have
improved myocardial protection. Conrming
arterial cannula placement (D) would not have
improved this patient’s myocardial
protection.
3. What is the most common location to nd a
myxoma?
A. Left atrium.
B. Right atrium.
C. Left ventricle.
D. Right ventricle.
Answer 3:
The most common location for a cardiac
myxoma, which is the most common benign
cardiac tumor, is the left atrium (A) in approximately 75% of patients. The other locations
27 Benign Masses, Normal Anatomic Variants, andArtifacts
355
can be home to myxomas but are less frequent
than the left atrium.
References
1. Sidebotham D, Merry A, Legget M, Wright
G. Practical perioperative transoesophageal echocardiography. 3rd ed. New York City, NY: Oxford
University Press; 2018.
2. Pejković B, Krajnc I, Anderhuber F, Kosutić
D. Anatomical variations of the coronary sinus
ostium area of the human heart. J Int Med Res.
2008;36(2):314–21.
3. Otto C.Textbook of clinical echocardiography. 6th ed.
Philadelphia, PA: Elsevier; 2018.
4. Mas JL, Arquizan C, Lamy C, Zuber M, Cabanes L,
Derumeaux G, etal. Recurrent cerebrovascular events
associated with patent foramen ovale, atrial septal
aneurysm, or both. N Engl J Med. 2002;3(11):93.
5. Mattioli AV, Aquilina M, Oldani A, Longhini C,
Mattioli G.Atrial septal aneurysm as a cardioembolic
source in adult patients with stroke and normal
carotid arteries. A multicentre study. Eur Heart J.
2001;22(3):261–8.
6. Ahmad ZS, Koshy C, Koshy GA.Echocardiographic
study of left ventricular false tendons. J Indian Acad
Echocardiogr Cardiovasc Imaging. 2019;3(3):150–5.
7. Swaminathan M, Mathew J, Nicoara A, Ayoub
C. Clinical manual and review of transesophageal echocardiography. 3rd ed. New York City, NY:
McGraw Hill; 2019.
Left Ventricular Thrombus Part 1
DonaldR.Maberry andBabarFiza
28
Learning Objectives
1. Discuss the pathophysiology of LV
thrombus.
2. Examine the utility of using contrast enhancement to improve the echocardiographic diagnosis of LV thrombus.
3. Review echocardiographic techniques for
reducing erroneous ndings of LV thrombus.
Introduction
Left ventricular thrombus (LVT) is a potentially
fatal complication of anterior myocardial infarction and dilated cardiomyopathies. Prompt and
accurate diagnosis of LVT is crucial as the presence of LVT can signicantly impact both acute
and long-term management strategies. The diagnosis of LVT can be challenging to establish with
point-of-care ultrasound but can be achieved with
meticulous imaging techniques and a thorough
understanding of the echocardiographic charac-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_28.
D. R. Maberry · B. Fiza (*)
Division of Critical Care Medicine, Department of
Anesthesiology, Emory School of Medicine,
Atlanta, GA, USA
e-mail: donald.reed.maberry@emory.edu;
babar.za@emory.edu
teristics of LVT.This chapter details the epidemiology, pathophysiology, and role of point-of-care
echocardiography in diagnosing
LVT.Additionally, we discuss the diagnostic limitations of ultrasonography and the role of
contrast- enhanced echocardiography in the LVT
diagnostic algorithms.
Etiology
Epidemiology andPathophysiology
Left ventricular thrombus was a common complication of myocardial infarction before the widespread use of PCI treatments [1]. Early studies
using 2D echocardiography alone to diagnose
LVT reported an incidence of 4–17% in all cases
of myocardial infarction and 10–34% for anterior
myocardial infarctions [1, 2]. In contrast, contemporary studies using cardiac magnetic resonance (CMR) report an overall incidence of LVT
of 5.4% and 7–15% of anterior MIs [3].
The formation of left ventricular thrombi
occurs because of Virchow’s triad, which consists
of three factors: hypercoagulability, stasis, and
endothelial injury [3]. During a myocardial
infarction, subendothelial ischemia leads to tissue damage and localized inammatory changes
that activate platelets and the coagulation cascade. Simultaneously, the decrease in cardiac
blood ow leads to areas of myocardial dyskinesis
© 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_28
357