Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5189_Библиотеки_им_академика_М_И_Перельмана.pdf
Left Atrial Thrombus
MeganH.Hicks andManenderKumarSingla
30
Etiology
Left atrial (LA) thrombus is typically the result of
blood stasis in the left atrium. The most common
site of thrombosis in the LA is the left atrial
appendage (LAA), but the formation of oating
and ball thrombus in the LA can occur [1, 2]. The
complex anatomy and histologic features of the
LAA as an embryologic remnant predispose it to
thrombogenicity, which is exacerbated in the
presence of the hypercoagulable state associated
with atrial brillation (AF) [3].
The majority of LAAs are multilobar, with
80% of patients having two or more lobes, leading to differential blood ow and predisposition
to stasis [3, 4]. There are four common morphologies that have been demonstrated to follow
genetic and regional patterns [2]. The chicken
wing is the most common shape, found in nearly
half of patients, alongside cactus, windsock, and
cauliower shapes [3, 4]. The muscle bundles
and pectinate muscles that speckle the myocardial surface also predispose the LAA to harbor
thrombus [3].
M. H. Hicks (*)
Wake Forest University School of Medicine,
Winston-Salem, NC, USA
e-mail: mhhicks@wakehealth.edu
M. K. Singla
Fortis Hospital, Ludhiana, India
Virchow described three factors responsible
for the pathogenesis of LA thrombus formation
(Virchow’s triad): (1) Wall injury via endothelial
or endocardial damage; (2) blood stasis via sluggish or turbulent ow due to atypical hemodynamics; and (3) increased coagulability [2, 5].
Collectively, this triad results in the formation of
activated platelet aggregates and leukocyte- or
brinogen-mediated erythrocyte aggregates
which present on echocardiography as spontaneous dense echocardiographic contrast (SEC) or
“smoke.” [3, 6] These aggregates can progress to
thickened, slow-moving blood called “sludge”
and eventually thrombus.
The most frequent cause of LAA thrombus
formation is AF. Nearly 15% of patients with
acute AF, dened as a duration of less than
3days, have LAA thrombi [4]. Thrombogenesis
occurs through a hyperactive clotting cascade
driven by inammation and oxidative stress [3].
Multiple cytokines and inammatory markers
known to be involved in coagulation are found to
be elevated in patients with atrial brillation,
including C-reactive protein, interleukin 6, tumor
necrosis factor-alpha, D-dimer, brinogen, prothrombin, lipoprotein a, platelet factor-4, and von
Willebrand factor [2, 3]. Thrombus can develop
even in therapeutically anticoagulated AF
patients [4, 7].
Although the mechanism of clot formation is
multifactorial, local factors such as size, morphology, and function of the LAA can play a role.
© 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_30
379
380
ab
M. H. Hicks and M. K. Singla
Increasing numbers of LAA lobes are associated
with an increased risk of LA SEC and LAA
thrombus [2, 8, 9]. As such, the non-chicken wing
shapes of LAA, especially the cauliower type,
are associated with a three-fold higher stroke risk
[2, 10, 11]. Stroke and thromboembolism risk
also correlate with an LAA volume greater than
34mL [3]. Reduced LAA blood ow velocities,
smaller LAA ostium size, a shorter distance from
ostium to the rst bend of the LAA, as well as
shorter lengths of LAA, are associated with a
greater risk of thrombus formation and thromboembolism [3].
Mitral stenosis (MS) is another important risk
factor for thrombus formation due to left atrial
stasis, portending a 17-fold increased risk in
patients with MS and AF [2, 12]. In contrast,
mitral regurgitation may be somewhat protective
due to high-velocity left atrial washing [2]. Left
ventricular dysfunction has been associated with
a decrease in LAA emptying velocity, which presumably increases stasis [3]. LAA dysfunction is
also common in dilated cardiomyopathy, even in
sinus rhythm, with LAA thrombosis noted in
many of these patients [13]. LAA dysfunction in
the absence of AF has been commonly observed
in patients with hypertrophic obstructive
cardiomyopathy.
Diagnosis
While cardiac computed tomography and intracardiac echocardiography have emerged as effective alternative imaging modalities, TEE remains
a mainstay of left atrial evaluation [10, 11, 14].
TEE has been reported to have a sensitivity and
specicity approaching 100% and 99%, respectively, with an estimated 86% positive predictive
value and 100% negative predictive value [3, 15].
The left atrium is visualized abutting the TEE
probe in all mid-esophageal views, with the LAA
best visualized in the mid-esophageal twochamber and aortic valve short-axis views [16]. It
is seen in the long axis abutting the Coumadin
(lateral) ridge, which separates the LAA from the
more superior and posterior left upper pulmonary
vein (Fig.30.1). Of the multiple classic morphologies of the LAA, the windsock is the easiest to
fully examine, while the fan/broccoli and C/
chicken wing morphologies present more challenges due to more extensive lobar architectures
[2, 11].
Thrombi may appear as both mobile or immobile hyperechoic tissue, usually acoustically different from the abutting endocardium [11]. To
effectively exclude thrombus, the LAA must be
examined in multiple planes. Simultaneous
orthogonal (X-plane) imaging is often useful to
Fig. 30.1 (a) Midesophageal aortic valve short axis view. (b) 3D view. LAA left atrial appendage, LUPV left upper
pulmonary vein
30 Left Atrial Thrombus
Fig. 30.2 Normal
quadriphasic LAA
velocity waveform
381
distinguish artifact or pectinate muscle from
thrombus. Both color ow Doppler and injectable ultrasound contrast with or without power
Doppler imaging may be useful adjuncts to
exclude or conrm thrombus by revealing defects
in color or contrast; this is particularly helpful
when confounding SEC is also noted [11, 17,
18].
LAA function is frequently estimated using
the LAA ow velocity, though its utility is limited in certain populations [2, 19]. Pulsed Doppler
of the LAA in normal sinus rhythm demonstrates
a quadriphasic pattern consisting of pairs of early
and late ventricular diastolic waves that represent
emptying and lling [19] (Fig.30.2). The dominant late diastolic emptying wave is usually referenced as a surrogate of LAA ejection, with the
peak velocity having been correlated with the
risk for LAA stasis and thus thrombus formation
[19]. Normal peak velocities range from 50 to
64cm/s [20]. In patients with atrial brillation,
the LAA waveform adopts a more sawtooth pattern with variable amplitude, and mean LAA
ow velocities may better represent function
[13].
SEC is common at velocities below 20cm/s
and is an independent risk factor for thrombus
regardless of anticoagulation and CHA2DS2VASc score [9, 11, 18]. Thrombus is less likely at
velocities above 40cm/s with a negative predictive value of 99–100% at LAA velocities greater
than 55cm/s [9, 21, 22]. The velocity should be
obtained at either the level of the LAA orice or
within the rst third of the visualized depth, as
velocity expectedly decreases as ow reaches the
LAA apex [13, 23].
The LAA lling velocity does decrease with
age and is highly variable in the setting of
arrhythmia [19]. Other methods of assessment of
LAA function include tissue Doppler imaging of
the LAA wall, with a velocity <10cm/s being
highly specic for SEC [19].
As catheter-based LAA occlusion has become
more frequent, 3D evaluation of the LAA has
been deployed more often. Processing of 3D data
sets allows the LAA to be aligned in three axes to
provide reliable dimensions, improved functional
assessment, and enhanced visualization and differentiation of thrombus from endocardial tissue
[11, 24] (Fig.30.3).
382
Fig. 30.3 3-D
evaluation of the LAA
orice
Clinical Implications
LAA thromboembolism is the leading cause of
morbidity and mortality in patients with atrial
brillation [2]. LA and LAA thrombi are some of
the very important causes of ischemic stroke [3].
Approximately 20% of strokes are thought to be
cardioembolic, with the majority of these in
patients with atrial brillation. The source of
75% of those is the left atrial appendage [13, 25].
Over 90% of thromboembolic strokes in nonvalvular atrial brillation are due to LAA thrombus
[3, 26]. The incidence of stroke is much higher
when atrial brillation is due to mitral stenosis
[3]. Stroke risk can be estimated using validated
scoring systems based on comorbidities like the
CHADS2 and CHA2DS2-VASc [3].
The presence of LAA thrombus on preoperative imaging prevents performing cardioversion
to restore sinus rhythm [27]. This thus perpetuates low cardiac output states through loss of the
atrial kick, which contributes up to 30% of left
ventricular lling [27, 28]. Although the mechanism is not clear, transiently worsened LAA ejection and increased SEC can occur after
spontaneous, pharmacological, or electrical cardioversion from AF or atrial utter [18].
Paradoxically depressed LAA ow velocities
have also been noted after transcatheter radiofrequency or surgical ablation [18]. This can itself
predispose to the formation of thromboembolism. This LAA stunning is known to improve
within 7–30days after cardioversion [18].
Apart from the cerebral circulation, thrombus
dislodgement from the LA can cause occlusive
M. H. Hicks and M. K. Singla
vascular symptoms in arterial branches to limbs,
the mesentery, and other distant organs.
Echocardiographic and CT imaging of the LAA
is becoming increasingly important in ruling out
thrombus prior to cardioversion or ablative procedures as well as in anatomic assessment and
procedural guidance for minimally invasive LAA
occlusion procedures.
Questions
1. Which of the following patients is LEAST
likely to be diagnosed with a left atrial
appendage thrombus?
A. 54-year-old female with atrial brillation,
1+ spontaneous echo contrast, LAA peak
velocity 40cm/s
B. 80-year-old male with ischemic cardio-
myopathy, no spontaneous echo contrast,
LAA peak velocity 28cm/s
C. 60-year-old female with restrictive dia-
stolic dysfunction, no spontaneous echo
contrast, LAA peak velocity 62cm/s
D. 74-year-old male with severe mitral steno-
sis, 2+ spontaneous echo contrast, LAA
peak velocity 18cm/s
Answer: C
Explanation: A left atrial appendage peak
emptying velocity greater than 55 cm/s is
associated with a negative predictive value of
nearly 100%, meaning that there is almost
zero chance of the patient having an LAA
thrombus. While patients with a velocity
>40cm/s are less likely to develop a thrombus, spontaneous echo contrast is an independent risk factor for developing left atrial
appendage thrombus. A velocity <40 cm/s,
30 Left Atrial Thrombus
383
particularly those less than 20cm/s suggests a
high risk for thrombus formation.
2. Which of the following letters represents the
appropriate waveform from which to measure
the left atrial appendage peak emptying
velocity?
A. A
B. B
C. C
D. D
Answer: B
Explanation: The large diastolic upstroke
above the axis indicates ow out of the left
atrial appendage toward the probe and thus
corresponds with the emptying of the
LAA.The peak velocity, measured at the apex
of this inection, will represent the LAA peak
emptying velocity.
References
1. Omoto T, Aoki A, Maruta K, Masuda T, Hirono
M. Left atrial thrombus in a patient without mitral
valve disease or atrial brillation. J Cardiol Cases.
2016;14(4):115–8.
2. Cresti A, Camara O. Left atrial thrombus—are all
atria and appendages equal? Intervent Cardiol Clin.
2022;11:121–34.
3. Kanmanthareddy A, Reddy YM, Vallakati A,
Earnest MB, Nath J, Ferrell R, Dawn B, Lakkireddy
D.Embryology and anatomy of the left atrial appendage: why does thrombus form? Interv Cardiol Clin.
2014;3(2):191–202.
4. Beigel R, Wunderlich NC, Ho SY, et al. The left
atrial appendage: anatomy, function, and noninvasive evaluation. JACC Cardiovasc Imaging.
2014;7(12):1251–65.
5. Watson T, Shantsila E, Lip GY.Mechanisms of thormbogenesis in atrial brillation: Virchow’s triad revisited. Lancet. 2009;373(9658):155–66.
6. Pathan F, Hecht H, Narula J, Marwick TH.Roles of
transesophageal echocardiography and cardiac computed tomography for evaluation of left atrial thrombus
and associated pathology: a review and critical analysis. JACC Cardiovasc Imaging. 2018;11(4):616–27.
7. Erickson M, Yadav H, Sneij E, Austin J, Manyam
H. Incidence of left atrial appendage thrombus
despite 3 weeks of anticoagulation and the need for
precardioversion echocardiography. Ann Noninvasive
Electrocardiol. 2022;27(5):e12989.
8. Wang F, Zhu M, Wang X, etal. Predictive value of
left atrial appendage lobes on left atrial thrombus
or spontaneous echo contrast in patients with nonvalvular atrial brillation. BMC Cardiovasc Disord.
2018;18:153.
384
M. H. Hicks and M. K. Singla
9. Fatkin D, Kelly RP, Feneley MP.Relations between
left atrial appendage blood ow velocity, spontaneous
echocardiographic contrast and thromboembolic risk
invivo. JACC. 1994;23(4):961–9.
10. Smiseth OA, Baron T, Marino PN, Marwick TH,
Flachskampf FA.Imaging of the left atrium: pathophysiology insights and clinical utility. Eur Heart J.
2022;23:2–13.
11. Abdelmoneim SS, Mulvagh SL. Techniques to
improve left atrial appendage imaging. J Atr
Fibrillation. 2014;7(1):85–94.
12. Al-Saady NM, Obel OA, Camm AJ. Left atrial
appendage: structure, function, and role in thromboembolism. Heart. 1999;82(5):547–54.
13. Agmon Y, Khandheria BK, Gentile F, Seward
JB. Echocardiographic assessment of the left atrial
appendage. JACC. 1999;34(7):1867–77.
14. Ge J, Chen T, Chuanzhen M, Maduray K, Zhong
J. Can intracardiac echocardiography completely
replace transesophageal echocardiography to guide
left atrial appendate closure? The comparisons of
intracardiac echocardiography with transesophageal
echocardiography. J Card Surg. 2022;37:2766–75.
15. Manning WJ, Silverman DI, Gordon SP, et al.
Cardioversion from atrial brillation without prolonged anticoagulation with use of transesophageal
echocardiography to exclude the presence of atrial
thrombi. N Engl J Med. 1993;328:750–5.
16. Shanewise JS, Cheung AT, Aronson S, etal. ASE/SCA
guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the Society
of Echocardiography Council for Intraoperative
Echocardiography and the Society of Cardiovascular
Anesthesiologists Task Force for Certication in
Perioperative Transesophageal Echocardiography. J
Am Soc Echocardiogr. 1999;12:884–900.
17. Hamper UM, DeJong MR, Caskey CI, Sleth S.Power
Doppler imaging: clinical experience and correlation
with color Doppler US and other imaging modailities.
Radiographics. 1997;17(2):499–513.
18. Bansal M, Kasliwal RR. Echocardiography for left
atrial appendage structure and function. Indian Heart
J. 2012;64(5):469–75.
19. Ito T, Suwa M. Assessment of left atrial appendage function by echocardiography. Heart Fail Rev.
2023;28(5):1177–87.
20. Donal E, Yanada H, Leclercq C, Herpin D.The left
atrial appendage, a small, blind-ended structure.
Chest. 2005;128(3):1853–62.
21. Herring N, Page SP, Ahmed M, etal. The prevalence
of low left atrial appendage emptying velocity and
thrombus in patients undergoing catheter ablation
for atrial brillation on uninterrupted peri-procedural
warfarin therapy. J Atr Fibrillation. 2013;5(6):761.
22. Handke M, Harloff A, Hetzel A, et al. Left atrial
appendage ow velocity as a quantitative surrogate
parameter for thromboembolic risk: determinants and
relationship to spontaneous echocontrast and thrombus formation—a transesophageal echocardiographic
study in 500 patients with cerebral ischemia. J Am
Soc Echocardiogr. 2005;18(12):1366–72.
23. Goldberg TH, Gordon SC, Spevack DM, Gordon
GM. Disparities in emptying velocity within
the left atrial appendage. Eur J Echocardiogr.
2010;11(3):290–5.
24. Nucifora G, Faletra F, Regoli F, etal. Evaluation of
the left atrial appendage with real-time 3-dimensional
transesophageal echocardiography. Circ Cardiovasc
Imaging. 2011;4:514–23.
25. Dudzińska-Szczerba K, Kulakowski P, Michalowska
I, Baran J.Association between left atrial appendage
morphology and function and the risk of ischaemic
stroke in patients with atrial brillation. Arrhythm
Electrophysiol Rev. 2022 Apr;11:e09.
26. Wang D, Forbes TJ, Lee JC, Eng
MH.Echocardiographic imaging for left atrial appendage occlusion. Intervent Cardiol Clin. 2018;7:219–28.
27. Hautmann M, Zacher M, Fuchs S, et al. Left atrial
appendage thrombus formation, potential of resolution and association with prognosis in a large realworld cohort. Sci Rep. 2023;13:889.
28. Namana V, Gupta SS, Sabharwal N, Hollander
G. Clinical signicance of atrial kick. QJM.
2018;111(8):569–70.
Right-Sided Thrombus
KarimEl-Kersh andBilalAtharJalil
31
Learning Objectives
1. Identify the causes of right-sided thrombi
(RST).
2. Know the different echocardiographic patterns of RST.
3. Understand different treatments for RST.
Introduction
Intra-cardiac thrombi include both left- and rightsided thrombi (RST). While left-sided thrombi,
such as those in the left atrial appendage and the
left ventricle, are not uncommon, RSTs are
exceedingly rare yet carry a high mortality [1].
The broad categories of RST include true thrombi
and tumor thrombi. This chapter discusses the
etiology, diagnosis, echocardiographic appear-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_31.
K. El-Kersh
Division of Pulmonary, Critical Care, and Sleep
Medicine, Department of Medicine, University of
Arizona College of Medicine, Phoenix, AZ, USA
e-mail: Karimelkersh@arizona.edu
B. A. Jalil (*)
Divisions of Cardiovascular Critical Care and
Advanced Heart Failure, Heart and Vascular Institute,
West Virginia University, Morgantown, WV, USA
e-mail: bilal.jalil@wvumedicine.org
ance, and clinical implications of right-sided
thrombi. Pulmonary embolism and right-heart
dysfunction are discussed in a separate chapter.
Etiology
There are two broad categories of RST: true
thrombi and tumor thrombi. True thrombi can be
further subdivided into thrombi-in-transit, which
represent embolized thrombi from peripheral
veins that get trapped en route within the right
heart, and those associated with devices such as
central venous catheters and implantable cardiovascular leads.
Mobile RSTs are diagnosed in about 4%–18%
of patients with acute pulmonary embolism (PE),
with the higher incidence being reported in critically ill patients [2, 3]. The increased utilization
of echocardiography in the risk stratication of
PE patients has led to an increased detection of
RST; however, the true incidence remains
unknown. Mobile RST typically represents
embolized thrombi from a more peripheral vein
that temporarily lodges in the right atrium or
right ventricle and is considered life-threatening
[4]. Several predisposing factors are implicated
in the temporary entrapment of mobile thrombi
in the right heart. These may include the presence
of a prominent Eustachian valve, a low cardiac
output state, tricuspid regurgitation, and pulmonary hypertension [5].
© 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_31
385
386
K. El-Kersh and B. A. Jalil
The other group of true thrombi are those
associated with the presence of indwelling central venous catheters or cardiovascular device
leads. The presence of a foreign body can be an
inciting factor for thrombi formation, which is
usually seen in the right atrium. Right atrial
thrombi (RAT) have been documented in endstage renal disease patients with indwelling
hemodialysis catheters with an incidence of 5.4%
[6]. They have also been reported in patients with
central venous catheters and pulmonary artery
catheters in autopsy studies with an incidence
between 29–33% [7]. Mobile thrombi on implantable cardiovascular device leads have been documented as high as 30% [8]. These catheter- and
device-related thrombi are harder to recognize
using transthoracic echocardiography (TTE), and
since patients with RAT are asymptomatic, the
incidence of RAT is likely underestimated [9].
“Tumor thrombi” is a misnomer, as these are
not true thrombi but rather represent venous
extension of tumors from the inferior vena cava
to the right atrium. These can be seen in advancedstage hepatocellular and renal cell carcinomas
and are often considered poor prognostic indicators [10, 11].
Diagnosis
RSTs are usually diagnosed by TTE initially, and
they can be occasionally noted in contrast to
chest computed tomography (CT) studies aimed
to assess for an acute PE.Thrombi are seen as
hyperechoic densities within the right atrium,
right ventricle, or the right ventricular outow
tract. Their appearance is characterized by their
shape (serpiginous or globular) and motion
(mobile or immobile), and they are usually classied into three types based on their echocardiographic appearance. Type A thrombi are usually
seen in patients with acute PE and deep vein
thrombosis and are highly mobile and serpiginous in morphology. Type B thrombi are nonmobile and may arise from an in-situ thrombosis
related to cardiac structural abnormalities or the
presence of foreign bodies. Type C thrombi are
highly mobile and appear globular and multilobular, similar in appearance to right atrial myxomas [12]. The types of thrombi are depicted in
Fig.31.1a–c and Videos 31.1, 31.2, and 31.3.
The best views to evaluate for RST are those
that best delineate the right atrium, the right ventricle, and the right ventricular outow tract. The
apical 4-chamber view (Fig.31.2 and Video 31.4)
and the subcostal 4-chamber views (Fig.31.1c
and Video 31.3) visualize the right-heart chambers well. Additionally, the subcostal view of the
inferior vena cava can identify tumor thrombi traversing through the inferior vena cava into the
right atrium (Fig. 31.3 and Video 31.5). Rightventricular inow views may be used to better
visualize the right heart chambers and to help differentiate a freely mobile thrombus from vegetation attached to tricuspid valve leaets (Fig.31.4
and Video 31.6). The parasternal short- and longaxis views can be used to identify RST and to
assess the right ventricular outow tract
(Fig.31.5a, b and Videos 31.7 and 31.8).
With the increasing use of TTE in PE risk
stratication, the detection of RST is expected to
increase. The sensitivity of TTE could be reduced
due to poor acoustic windows, normal anatomic
variants such as the presence of a prominent
Eustachian valve, Chiari network, crista terminalis, false chordae tendineae, and the presence of
congenital heart disease [13]. Contrast echocardiography may be of additional value in delineating the presence of thrombi that are not well
visualized on non-contrast-enhanced images and
may help to differentiate thrombi from tumors
(Fig. 31.6a, b and Videos 31.9 and 31.10).
31 Right-Sided Thrombus
387
a
c
b
Fig. 31.1 A depiction of the types of thrombi. (a) A trun-
cated apical 4-chamber view focusing on the right ventricle showing a type A mobile thrombus in the right atrium
with a serpiginous appearance. (b) Apical 4 chamber view
showing a type B non-mobile thrombus in the right ventricle adherent to the interatrial septum. (c) Subcostal
view showing a type C multilobulated thrombus in the
right atrium
Fig. 31.2 Apical 4
chamber view showing a
mobile thrombus in the
right ventricle
388
Fig. 31.3 A subcostal
view of the inferior vena
cava showing tumor
thrombus within the
hepatic vein and
extending into the
inferior vena cava and
the right atrium
K. El-Kersh and B. A. Jalil
Fig. 31.4 A rightventricular inow view
showing a mobile
globular appearing
thrombus in the right
atrium with to-and-fro
motion traversing the
tricuspid valve