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_3720_Библиотеки_им_академика_М_И_Перельмана
.pdf
Animal Models of Thrombosis Chapter | 6 97
https://t.me/med1917
[82] Bonnefoy A, Daenens K, Feys HB, De Vos R, Vandervoort P, Vermylen J, et al. Thrombospondin-1 controls vascular platelet recruitment and
thrombus adherence in mice by protecting (sub)endothelial VWF from cleavage by ADAMTS13. Blood 2006;107:955e64.
[83] Denis CV, Wagner DD. Insights from von Willebrand disease animal models. Cell Mol Life Sci 1999;56:977e90.
[84] Ruggeri ZM, Orje JN, Habermann R, Federici AB, Reininger AJ. Activation-independent platelet adhesion and aggregation under elevated shear
stress. Blood 2006;108:1903e10.
[85] Reininger AJ, Heijnen HF, Schumann H, Specht HM, Schramm W, Ruggeri ZM. Mechanism of platelet adhesion to von Willebrand factor and
microparticle formation under high shear stress. Blood 2006;107:3537e45.
[86] Donadelli R, Orje JN, Capoferri C, Remuzzi G, Ruggeri ZM. Size regulation of von Willebrand factor-mediated platelet thrombi by ADAMTS13 in
flowing blood. Blood 2006;107:1943e50.
[87] Johnson GS, Turrentine MA, Kraus KH. Canine von Willebrand’s disease. A heterogeneous group of bleeding disorders. Vet Clin North Am Small
Anim Pract 1988;18:195e229.
[88] Nichols TC, Bellinger DA, Reddick RL, Smith SV, Koch GG, Davis K, et al. The roles of von Willebrand factor and factor VIII in arterial
thrombosis: studies in canine von Willebrand disease and hemophilia A. Blood 1993;81:2644e51.
[89] Sweeney JD, Novak EK, Reddington M, Takeuchi KH, Swank RT. The RIIIS/J inbred mouse strain as a model for von Willebrand disease. Blood
1990;76:2258e65.
[90] Denis C, Methia N, Frenette PS, Rayburn H, Ullman-Cullere M, Hynes RO, et al. A mouse model of severe von Willebrand disease: defects in
hemostasis and thrombosis. Proc Natl Acad Sci USA 1998;95:9524e9.
[91] Benson R, Dodds W. Autosomal factor VIII deficiency in rabbits:size variations of rabbit factor VIII. Thromb Haemost 1977;38:380.
[92] French TW, Fox LE, Randolph JF, Dodds WJ. A bleeding disorder (von Willebrand’s disease) in a Himalayan cat. J Am Vet Med Assoc
1987;190:437e9.
[93] Feys HB, Roodt J, Vandeputte N, Pareyn I, Mottl H, Hou S, et al. Inhibition of von Willebrand factor-platelet glycoprotein Ib interaction prevents
and reverses symptoms of acute acquired thrombotic thrombocytopenic purpura in baboons. Blood 2012;120:3611e4.
[94] Gonzalez JV, Barboza AG, Vazquez FJ, Gandara E. Prevalence and geographical variation of prothrombin G20210A mutation in patients with
cerebral vein thrombosis: a systematic review and meta-analysis. PLoS One 2016;11:e0151607.
[95] Denorme F, De Meyer SF. The VWF-GPIb axis in ischaemic stroke: lessons from animal models. Thromb Haemost 2016;116:597e604.
[96] Sun YY, Kuan CY. A thrombotic stroke model based on transient cerebral hypoxia-ischemia. J Vis Exp 2015:e52978.
[97] Verhenne S, Denorme F, Libbrecht S, Vandenbulcke A, Pareyn I, Deckmyn H, et al. Platelet-derived VWF is not essential for normal thrombosis
and hemostasis but fosters ischemic stroke injury in mice. Blood 2015;126:1715e22.
[98] Pedder H, Vesterinen HM, Macleod MR, Wardlaw JM. Systematic review and meta-analysis of interventions tested in animal models of lacunar
stroke. Stroke 2014;45:563e70.
[99] Raymond J, Darsaut TE, Kotowski M, Makoyeva A, Gevry G, Berthelet F, et al. Thrombosis heralding aneurysmal rupture: an exploration of
potential mechanisms in a novel giant swine aneurysm model. Am J Neuroradiol 2013;34:346e53.
[100] Valera MC, Payrastre B, Lairez O. Nuclear imaging of thrombosis in small animal. Platelets 2016:1e6.
Chapter 7
https://t.me/med1917
Imaging Modalities for Detection and
Treatment of Cardiovascular Thrombus
Rodrigo Mendirichaga, Joel E. Fishman and Claudia A. Martinez
University of Miami Miller School of Medicine, Miami, FL, United States
INTRODUCTION
Cardiovascular thrombi are a major cause of morbidity and mortality worldwide and in the United States. Acute myocardial
infarctions (AMIs), strokes, and pulmonary emboli are examples of the devastating consequences that a thrombus can have.
Every year approximately 735,000 patients will suffer an AMI in the United States and 795,000 will experience a stroke [1].
Thrombotic disorders can be classified into those that arise predominantly due to platelet aggregates and those secondary to
fibrin deposition. Thrombi caused by platelet aggregation, typically in the arterial circulation, are called white thrombi.A
white thrombus forms when rupture of an atherosclerotic plaque exposes its necrotic core to the circulating blood, which
in turns leads to platelet aggregation and activation of the coagulation cascade. White thrombi are classically seen in
atherosclerotic lesions in the coronary circulation during an acute coronary syndrome (ACS). In contrast, clots that form in
low-pressure systems (like the venous circulation and cardiac atria) are rich in fibrin and erythrocytes. These fibrin-rich
clots are called red thrombi [2]. Red thrombi follow Virchow’s triad for thrombogenesis and can be present in pulmonary emboli and stroke from cardiac origin. Nonetheless, red thrombi can also be found in coronary arteries resulting in STsegment elevation myocardial infarction (STEMI) [3].
Imaging plays an important role in the evaluation of coronary and intracardiac thrombi. Accurate visualization of
thrombus-containing lesions (TCLs) in the coronary circulation is paramount to the selection of the appropriate therapeutic
modality to be used, particularly in the setting of complex lesions. Similarly, different imaging techniques are used to
diagnose, guide preprocedural planning, direct therapy, and provide prognostic information in patients with suspected
intracardiac thrombus. This chapter is meant to be a pictorial guidance to the different imaging modalities used to diagnose
and treat coronary and noncoronary intracardiac thrombus.
THROMBUS-CONTAINING LESION IN THE CORONARY CIRCULATION
TCLs in the coronary circulation are formed when rupture of the fibrous cap of an atherosclerotic plaque leads to exposure of
its necrotic core, which contains highly thrombogenic subendothelial tissue factor and collagen. Platelet recruitment,
adhesion, aggregation, and activation, along with activation of the coagulation cascade, result in rapid thrombus formation
[3e5].ATCLthatisrichinfibrin is often fully occlusive and results in STEMI, whereas a TCL that is rich in platelets is
often partially occlusive and results in non-ST-segment elevation ACS [3]. TCLs are more commonly found in proximal
coronary segments and bifurcating lesions and are associated with an increased risk of distal embolization, poor distal flow,
and low myocardial blush grades following percutaneous revascularization [6,7]. Large thrombus burden has been associated
with more extensive myocardial damage and major adverse events, including repeat myocardial infarction and death [8,9].
Several imaging modalities have been developed for the evalua tion of a TCL in the coronary circulation. Coronary
angiography remains the most frequently used modality for identification of thrombus. However, more sensitive modalities, including intravascular ultrasound (IVUS) and optical coherence tomography (OCT), can be used when a TCL is not
apparent angiographically, but suspicion remains high.
Cardiovascular Thrombus. https://doi.org/10.1016/B978-0-12-812615-8.00007-7
Copyright © 2018 Elsevier Inc. All rights reserved.
99
100 Cardiovascular Thrombus
https://t.me/med1917
Coronary Angiography
Coronary angiography is an invasive diagnostic procedure that allows visualization of the coronary circulation. It is the
preferred method for diagnosis of intracoronary lesions given its low risk of major complications and the possibility of
performing an intervention during the same procedure if warranted. In addition, hemodynamic data can also be obtained
during the procedure. Some of the limitations of coronary angiography include technical restrictions preventing optimal
visualization, interobserver variability, lack of visualization of the vascular wall, and inaccurate evaluation and quantification of thrombus burden [10]. TCLs are identified via coronary angiography by the presence of reduced contrast density,
staining, haziness, irregular lesion contour, filling defects, or a smooth and convex meniscus at the site of a total occlusion
[11] (Fig. 7.1).
Coronary angiography can be perfor med with relatively low risk even in the most critically ill patients. Rate of
complications is less than 0.5% and mortality is less than 0.08%. Therefore, there are no true absolute contraindications.
Relative contraindications include acute gastrointestinal bleeding, severe hypokalemia, uncorrected digoxin toxicity,
anticoagulation with an international normalized ratio greater than 1.8, severe coagulopathy, previous anaphylactic
reactions to contrast media, acute stroke, acute renal failure or severe chronic kidney disease that is not dialysis dependent,
unexplained fever, untreated active infection, and severe anemia [12]. In addition, patients are also exposed to radiation,
which can become clinically significant with repeat procedures and increased exposure.
Intravascular Ultrasound
Limited evaluation, characterization, and quantification of coronary lesions with the use of coronary angiography prompted
the development of other imaging technologies allowing for better visualization of coronary lesions. IVUS allows visualization of the arterial wall by using either a single or multiple transducers at the end of a catheter that emit ultrasound
(A) (B) (C)
(D) (E) (F)
FIGURE 7.1 Still-frame images of a coronary angiography in a patient with ST-segment elevation myocardial infarction. (A) Thrombus-containing
lesion (TCL) resulting in total occlusion of the proximal right coronary artery (RCA) (asterisk). (B) Guidewire crossing (black arrow) of the TCL.
(C) Partial flow (black arrow) demonstrated distal to the obstruction following crossing of the TCL. The proximal to mid-RCA revealed a 20-mm lesion
classified as an ACCF/AHA type C lesion. (D and E) Percutaneous coronary intervention of the RCA (asterisks). (F) Postintervention angiography
demonstrating Thrombolysis in Myocardial Infarction (TIMI) 3 flow.
Imaging Modalities for Detection and Treatment of Cardiovascular Thrombus Chapter | 7 101
https://t.me/med1917
FIGURE 7.2 Still-frame images of a coronary intravascular ultrasound performed following stent deployment in a patient with ST-segment elevation
myocardial infarction. The midportion of the stent demonstrated an area of underexpansion that was present even after high-pressure balloon inflation
(white arrow). Calcium was noted in the area of underexpansion.
waves in the 10e40 MHz range. The emitted wave reflects as it encounters tissues of different densities (with different
acoustic impedance). Cross- sectional images are reconstructed via software analysis. Normal coronary artery anatomy
produces three alternating bright and dark echo layers. The first layer encountered is the intima, which produces a bright
echo signal and is the location for the formation and growth of atherosclerotic plaque. The second layer is the media, which
consists of smooth muscle cells and produces a dark zone (echo lucent) outlining the size of the vessel in a healthy
coronary artery. The third layer is formed by multiple bright echo signals from the interface between the external elastic
membrane and the adventitia [13] (Fig. 7.2).
The 2011 American College of Cardiology Foundation/American Heart Association/Society for Cardiovascular
Angiography and Interventions (ACCF/AHA/SCAI) guideline on percutaneous coronary intervention recommended IVUS
for the assessment of angiographically intermediate lesions (particularly left main coronary artery lesions), to detect
allograft vasculopathy, to evaluate mechanisms of stent restenosis or stent thrombosis, and to guide stent implantation [14].
More recently, a meta-analysis of 20 studies and 29,068 patients undergoing IVUS-guided versus angiography-guided
drug eluting stent implantation found that the use of IVUS was associated with a significant reduction in death, major
adverse cardiovascular events, and stent thrombosis. The benefit was significantly pronounced in patients with complex
lesions or ACS [15]. Current 2014 European Society of Cardiology/European Association for Cardio-Thoracic Surgery
(ESC/EACTS) guidelines on myocardial revascularizatio n recommend the use of IVUS in selected patients to optimize
stent placement (class IIa, level of evidence B), assess severi ty and optimize treatment of unprotected left main lesions
(class IIa, level of evidence B), and assess mechanisms of stent failure (class IIa, level of evidence C) [16].
Limitations on the use of IVUS include presence of distortion artifacts, which severe ly limit the ability to assess true
arterial characteristics; presence of halo or near-field artifacts, which may limit the ability to evaluate intimal pathology;
and inability to access vessels under 1.5 mm in size, as the device cannot be safely positioned because of the risk of total
occlusion [13].
Optical Coherence Tomography
Coronary OCT is a high-resolution imaging modality analogous to IVUS that uses light instead of sound for the generation
of images. OCT uses a light source with a wavelength ranging from 1280 to 1350 nm to reproduce cross-sectional images
of coronary arteries by measuring the echo time delay and the intensity of light that is reflected (backscattered) from
internal structures in tissue [10]. OCT offers a significantly improved resolution compared with IVUS, given that localization of the returned signal origin is improved due to the much shorter wavelength of light compared with sound [17].
Time domain OCT characteristics compared with IVUS are shown in Table 7.1.
Light penetrates blood poorly because of the presence of red blood cells and the different refractive indices of plasma
and red blood cells. Therefore, a blood-free environment needs to be created for optimal visualization during OCT. This is
most commonly achieved with the use of a proximal occlusion balloon and infusion of a transparent medium flush to allow
102 Cardiovascular Thrombus
https://t.me/med1917
TABLE 7.1 Tissue Domain Characteristics of Optical Coherence Tomography and Intravascular Ultrasound
a
OCT
Energy source Near-infrared light Ultrasound (20e45 MHz)
Wavelength (mm) 1.3 35e80
Resolution (mm) 15e20 (axial); 20e40 (lateral) 100e200 (axial); 200e300 (lateral)
Frame rate (frames/s) 15e20 30
Pullback rate (mm/s) 1e3 0.5e1
Maximum scan diameter (mm) 7 15
Tissue penetration (mm) 1e2.5 10
IVUS, intravascular ultrasound; OCT, optical coherence tomography.
a
Based on LightLab M2/M3 time domain OCT imaging system.
b
Based on Volcano, Bos ton Scientific, and Terumo IVUS systems.
IVUS
b
(A) (B) (C) (D)
FIGURE 7.3 Still-frame images of a coronary artery as seen by optical coherence tomography. These images demonstrate a stent deployed in a patient
with non-ST-segment elevation myocardial infarction. A thrombus (asterisk) is noted in the right coronary artery (A and B) just prior to and (C and D)
encroaching into the stented segment. The metallic strut produces a characteristic shadow that can be seen in (C) and (D) (white arrows).
for proper visualization (occlusive technique) [18]. However, a nonocclusive technique has also been described and is
favored by some operators [17]. Experience with both the occlusive and the nonocclusive techniques of OCT has
demonstrated the procedure to be safe [17,19,20]. OCT has proven to be feasible, have a high procedural success rate, be
able to navigate through tight lesions that an IVUS catheter is unable to cross, provide superior visualization and differentiation of the lumen and arterial wall interface, and detect subtle abnormalities following stent implantation compared
with IVUS [16,17,19]. Coronary OCT is the only technique capable of providing acute measurements of fibrous cap
thickness, detecting minor cap disruptions, and differentiating red and white thrombi with great accuracy [16]. OCT
analysis defines red thrombus as a high-backscattering lesion with signal-free shadowing protrusion, whereas white
thrombus is depicted as a low-backscattering mass, which is rich in signal and projects into the lumen [10] (Fig. 7.3).
OCT provides excellent image resolution, which allows for detailed assessment of the coronary arteries, a TCL, and
previously implanted stents. The 2014 ESC/EACTS guideline on myocardial revascularization recommends the use of OCT
to assess mechanisms of stent failure (class IIa, level of evidence C) and to optimize stent implantation in selected patients
(class IIb, level of evidence C). Further studies are required to fully define the clinical scope of coronary OCT [16,21].
Some of the limitations of OCT include limited availability, restricted depth penetration, difficult visualization of largediameter vessels at proximal target sites (particularly ostial lesions in the left main and right coronary arteries), and limited
visualization through blood fields [17].
Cardiac/Coronary Computed Tomography Angiography and Cardiac Magnetic Resonance
Imaging
Noninvasive anatomic evaluation of the coronary circulation can be obtained with the use of cardiac/coronary computed
tomography angiography (CCTA) or cardiac magnetic resonance imaging (CMRI). While providing a purely anatomical
Imaging Modalities for Detection and Treatment of Cardiovascular Thrombus Chapter | 7 103
https://t.me/med1917
evaluation of the coronaries, CCTA and CMRI have the advantage of avoiding the small risk of serious complications
associated with the invasive nature of coronary angiography. CCTA has become a primary noninvasive test for coronary
artery evaluation and has been validated in large multicenter studies. Acute coronary lesions typically present with
enlargement of the vessel diameter and ring-like enhancement, depicting thrombus with surrounding contrast agent.
However, not all TCLs have this appearance [22]. Advantages of CCTA include a short scanning time, low technical
burden, and high negative predictive value, adding value in low- to intermediate-risk patients [23e25] . The 2012
ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline on the diagnosis and management of patients with stable ischemic
heart disease considered CCTA a reasonable option for symptomatic patients with an intermediate pretest probability of
coronary artery disease after initial risk stratification [26].
Given that the diagnostic accuracy of CCTA is closely related to the quality of the images obtained, multidetector row
scanners with at least 64 rows and prefer ably more are preferred to increase anatomic coverage and reduce the total scan
time. Patient-related factors that can interfere with the diagnostic quality of CCTA include (1) inability to sustain a breath
hold for at least 5 s, (2) heart rate greater than 70 beats per minute (target heart rate is typically achieved with the use of
beta blockers), (3) presence of an irregular heart rhythm, (4) presence of coronary calcification or stents, and (5) segments
with diameter <1.5 mm [27e29]. In addition, CCTA is contraindicated in patients with severe allergy to iodinated contrast
and is relatively contraindicated in patients at high risk of contrast-induced nephropathy. The total amount of contrast used
during CCTA is typically <120 mL. CCTA also exposes the patient to ionizing radiation, although with current prospectively triggered CCTA scan method’s radiation exposure can be limited to 3 mSv or less. The Society of Cardiovascular Computed Tomography presented a guideline for the performance and acquisition of coronary computed
tomographic angiography in 2016 [30].
CMRI has also undergone significant resear ch for its ability to evaluate the coronary circulation. CMRI is an attractive
modality because it offers the potential of assessing the coronary artery anatomy, cardiac function, inflammation, and stress
perfusionefibrosis in the same study [31]. Some advantages over CCTA include the absence of radiation and iodinated
contrast exposure; however, CMRI has been generally superseded by CCTA for evaluation of coronary stenosis and
thrombosis. This is largely due to the better spatial resolution of CCTA and the lesser degree of scanner and operator
dependence compared with CMRI. Settings in which CMRI is a viable imaging option include patients in whom radiation
exposure is of high concern (e.g., pediatric patients), patients with renal failure given that no contrast administration is
required, and possibly patients with heavily calcified coronary artery segments [32]. In this situation, however, most
practices will use conventional coronary angiography. Challenges to CMRI include (1) inability to follow breathing
instructions, (2) irregular heart rhythms, and (3) presence of metallic foreign bodies or medical devices, which may cause
artifacts. CMRI requires longer scanning times than CCTA. Current clinical indications for coronary assessment via CMRI
are limited to the detection of abnormal origin of coronary arteries, coronary ectasia, or coronary aneurysms (class I) and
coronary artery bypass evalua tion (class II) [31,33].
NONCORONARY THROMBUS
Left-Atrial Thrombus
Risk factors for the development of left-atrial (LA) throm bi include mitral valve pathology or prosthesis, decreased leftventricular function, and abnormal LA contraction in the setting of atrial arrhythmias. Thrombus formation in the left
atrium with the subsequent risk of arterial embolization is a well-known complication of atrial arrhythmias, particularly
atrial fibrillation (AF). The risk of stroke is increased by four- to five-fold across all age groups in the presence of AF and
up to 17-fold when associated with mitral stenosis [34,35]. LA thrombus formation in AF follows Virchow’s triad for
thrombogenesis, with abnormal blood flow within the left atrium as the primary abnormality leading to thrombosis. Blood
flow is particularly stagnant in the left atrial appendage (LAA). The LAA is a tubular, hooked, and trabecular blind-ending
structure in a narrow junction with the venous component of the left atrium [35]. The LAA orifice or “os” is typically
located superiorly and laterally. The normal diameter of the os ranges from 10 to 24 mm [36]. The LAA is the most
common location for LA thrombus formation. Imaging of the left atrium and LAA has gained significant interest in part
because of procedural advances targeting LAA percutaneous closure for stroke prophylaxis in pati ents with AF.
Despite offering lower sensitivity than transesophageal echocardiography (TEE) for the identification of LA thrombus,
transthoracic echocardiography (TTE) is sometimes used as the initial test in the evaluation of the left atrium [37]. TTE
offers limited sensitivity for the evaluation of LA thrombus, largely due to the posterior location of the left atrium and poor
visualization of the LAA. Some of its advantages include its noninvasive nature, widespread availability, and low cost.
Nevertheless, large LA/LAA thrombi can occasionally be identified with the use of TTE, circumventing the need for
104 Cardiovascular Thrombus
https://t.me/med1917
FIGURE 7.4 (A) Transesophageal echocardiogram performed in a patient planned to undergo electrical cardioversion revealing a large left atrial
appendage (LAA) thrombus measuring approximately 1.3 2.7 cm (asterisk). (B) Three-dimensional transesophageal echocardiography reconstruction
demonstrating the large LAA apical thrombus and a second small thrombus at the os of the LAA (arrows).
further invasive testing. In addition, the use of intravenous contrast and measurements of LAA wall velocities by tissue
Doppler have been proposed to increase its sensitivity [38].
TEE has proven to be more sensitive in identifying LA thrombus than TTE. As such, TEE has become the imaging
modality of choice for diagno sis of an LA/LAA thrombus and is performed in the evaluation of a cardiac source of
embolism and before planned cardioversion or ablation to restore sinus rhythm in patients with AF. The posterior location
of the left atrium allows for excellent visualization with TEE. LA thrombi present as intraluminal masses of variable
morphology with a lower echogenicity than the surrounding LA walls, although an organized thrombus can appear more
echogenic and may calcify (Fig. 7.4). The sensitivity and specificity of TEE for identifying a thrombus in the LAA are
100% and 99%, respectively [36]. Nevertheless, the LAA is a complex structure with variable morphology and multiple
lobes, and small thrombi (<2 mm) can still be missed [39]. To fully define the LAA, experts recommend gradually
changing the scanning plane angle from 0 to 150 degrees, allowing for the visualization of the LAA in its widest
dimension. If a LA thrombus is identified via TEE, its embol ic potential should be analyzed. This includes mobility,
morphology, size, and connection to the LA wall [40]. Limitations of TEE for the evaluation of a suspected LA thrombus
include (1) incorrect diagnosis of prominent pectinate muscles or artifact as thrombi, (2) possibility of overlooking the
presence of a thrombus in a multilobed LAA, and (3) limited-quality near-field image of the LA body adjacent to the TEE
probe [40]. Table 7.2 lists absolute and relative contraindications to TEE [36,41]. The 201 6 ESC/EACTS guid eline f or th e
management of AF recommends TEE to exclude cardiac thrombus as an alternative to preprocedural anticoagulation
when early cardioversion is planned (class I, level of evidence B) and to ensure thrombus resolution in patients in whom
a cardiac thrombus was identified during a previous TEE prior to proceeding with cardioversion (class IIa, level of
evidence C) [42]. Meanwhile, the 2016 American Society of Echocardiography guideline for the use of echocardiography in the evaluation of cardiac sources of embolism recommends TEE as the initial or supplemental test for evaluation
for cardiovascular source of embolus with no identified noncardiac source [43].
Intracardiac echocardiography (ICE) is an invasive, catheter-based, imaging modality that allows visualization of
cardiac structures and blood flow with the use of Doppler imaging. ICE has been increasingly utilized since the late 1990s
to guide noncoronary interventions, including radio-frequency catheter ablation in patients with AF [44]. ICE can provide
adequate imaging of the LAA from close anatomic structures like the right-ventricular outflow tract or pulmonary artery
[45]. It has therefore been studied as a complement to TEE to detect LA/LAA thrombi in patients with AF undergoing
radio-frequency catheter ablation [46,47]. Some authors have suggested that ICE can replace the need for TEE in some
cases [48,49].
More recently, CCTA and CMRI have emerged as noninvasive modalities for the assessment of the left atrium and
LAA. Patients with AF referred for catheter ablation typically undergo CCTA for three-dimensional assessment of the
Imaging Modalities for Detection and Treatment of Cardiovascular Thrombus Chapter | 7 105
https://t.me/med1917
TABLE 7.2 Relative and Absolute Contraindicat ions to Transesophageal Echocardiography
Relative Absolute
Restriction of neck mobility (i.e., atlantoaxial joint
disease, severe cervical arthritis)
Coagulopathy or thrombocytopenia Esophageal pathology (i.e., laceration, tumor,
Recent upper gastrointestinal bleed Active upper gastrointestinal bleed
Esophageal varices Recent upper gastrointestinal surgery
Barret’s esophagus Esophagectomy
Active peptic ulcer disease or esophagitis
Symptomatic hiatal hernia
History of dysphagia
Prior gastrointestinal surgery
Prior radiation to neck and mediastinum
Perforated viscus
stricture, diverticulum, scleroderma)
(A) (B)
FIGURE 7.5 Cardiac computed tomography angiography demonstrating a dilated left atrium and a thrombus at the apex of the left atrial appendage
(arrow) measuring 1.4 cm in the maximal dimension. The thrombus is seen in both (A) the early and (B) the delayed sequence.
atrial and pulmonary vein anatomy. Given its high spatial resolution CCTA is well suited to define the LAA anatomy and
could spare the need for an invasive test like TEE in the evaluation of patients undergoing catheter ablation [50] (Fig. 7.5).
As such, the interest in CCTA for the identification of LA/LAA thrombus has increased significantly. In a meta-analysis of
19 studies and 2955 patients with AF referred for electrical cardioversion or pulmonary vein isolation, or who had a
cardioembolic stroke, CCTA had a sensitivity of 96% and specificity of 92% for the identification of LA/LAA thrombus in
patients compared with TEE. Most importantly, the negative predictive value for thrombus was 99%. Because LAA filling
by iodinated contrast does not reliably occur until approximately 70 s after injection, typical immediate imaging may
demonstrate an artifactual hypodensity in the LAA, termed “pseudothrombus.” Consequently, early imaging for pulmonary
vein anatomy is typically immediately followed by a delayed scan for the LAA. A subanalysis including only studies that
employed delayed imaging demonstrated a sensitivity and specificity of 100% and 99%, respectively, whereas negative
predictive value reached 100% [51]. Routine use of delaye d imaging results in a significant reduction of false-positive tests
and increases clinical ef ficiency [52] (Fig. 7.6). CCTA may ultimately eliminate the need for TEE in up to 80% of patients
with AF referred for ablation [53].
106 Cardiovascular Thrombus
https://t.me/med1917
(A) (B)
FIGURE 7.6 Cardiac computed tomography angiography revealing a dilated left atrium. (A) Early phase demonstrates a left atrial appendage (LAA)
hypodensity suggestive of a thrombus (arrow). (B) Delayed sequence demonstrates complete opacification of the LAA, confirming the diagnosis of a
pseudothrombus.
CMRI has also been used effectively in this setting. In contrast to CCTA, CMRI avoids the need for radiation or
iodinated contrast exposure. With the use of delayed enhancement, some studies of CMRI have demonstrated a sensitivity
of 100%, specificity of 99%, and diagnostic accuracy of 99% [54]. However, results have been varied, and some studies
have shown TEE to remain superior to CMRI for identification of LAA thrombus [55]. CCTA has an advantage over
CMRI in identifying calcification.
Left-Ventricular Thrombus
Left-ventricular thrombus (LVT) is classically seen within 24 h (and up to 2 weeks) of an AMI, particularly a STEMI
involving the left anterior descending artery and resulting in severe left ventricular (LV) dysfunction. Risk factors for the
development of an LVT include infarct size and location, impairment of global or regional LV function, multivessel
coronary artery disease, elevated cardiac biomarkers, and a decreased mitral E-wave deceleration time [56e58]. Other
predisposing conditions include LV apical aneurysms, dilated cardiomyopathy, and LV apical ballooning syndrome. LVT
is rarely seen when LV function is preserved [59].
TTE remains the initial modality of choice for the evaluation of a suspected LVT. On TTE, LVT appears as a mural or
pedunculated echodensity with acoustic properties similar to those of normal myocardium. The accuracy of TTE is
dependent on the clear delineation of endocardial borders. As such, a contrast agent should be used to increase sensitivity
and specificity [60,61]. This may be particularly important for obese patients or those with chronic obstructive lung
disease, in which the image quality may be unsatisfactory. With contrast injection, LVT appears as a filling defect
separated from the myocardium. Nevertheless, interobserver variability remains an important concern. In addition, false
tendons, trabeculations, and papillary muscles can be mistaken for a thrombus, whereas small clots and mural clots may be
overlooked [59] (Fig. 7.7).
Given the limitations of TTE for the identification of LVT, the use of more sensitive imaging modalities, including
CMRI, have been explored, particularly in patients with ischemic heart disease. CMRI with delayed enhancement is the
modality of choice for documentation of myocardial necrosis and fibrosis in the setting of myocardial infarction. In
addition, CMRI has demonstrated greater sensitivity and specificity for LVT detection compared with TTE [62e64]. This
is partly due to delayed enhancement used for detection of myocardial fibrosis, which can also be used with long inversion
recovery times for differentiation of enhancing cardiac masses from nonenhancing “bland” thrombus [65]. CMRI thus
identifies both the infarct extent and its sequela of thrombus and is now considered the “gold standard” for the identification of LVT (Fig. 7.7) [33].
Imaging Modalities for Detection and Treatment of Cardiovascular Thrombus Chapter | 7 107
https://t.me/med1917
(A) (B) (C)
FIGURE 7.7 Still-frame images of a transthoracic echocardiogram in the (A) parasternal short-axis and (B) apical two-chamber view performed in a
patient presenting with an anterior ST-segment elevation myocardial infarction demonstrating severely reduced left-ventricular systolic function, wall
motion abnormalities, and a large apical thrombus (white arrow). (C and D) Cardiac magnetic resonance imaging revealed extensive myocardial infarction
in the anteroseptal distribution extending circumferentially around the apex of the left ventricle, as documented by transmural delayed enhancement and
thinning of the myocardium (black arrows). Severe left-ventricular dysfunction was again noted, with an estimated left-ventricular ejection fraction of
16% and an end-diastolic volume of 254 mL. A large apical thrombus with a maximal thickness of 2 cm is again demonstrated (asterisks). The thrombus
extends to the anteroseptal wall in the middle and apical thirds of the left ventricle.
(D)
CCTA h as also been explored as an alternative for the evaluation of LVT. The main advantages of CCTA include its
short scanning times and widespread availability [66]. LVT appears as a filling defect immediately adjacent to the
myocardial wall, commonly in an area of previous AMI. CCTA relia bly identifies areas of wall thinning related to
myocardial infarction; nevertheless it is less specific than CMRI for identifying infarct extent and fibrosis. One application
for which CCTA may be suitable, whereas CMRI is not, is the evaluation of pump thrombosis in patients with end-stage
heart failure managed with a ventricular assist device (VAD) [67] (Fig. 7.8). Pump thrombosis is increasingly recognized
as one of the most important complications affecting patients following VAD placement. Pump thrombus can develop
within the left ventricle, inflow cannula, motor, outflow graft, or aortic root [68]. The diagnosis is suggested by changes in
pump performance and the development of hemolysis. TTE performed at incremental VAD speeds is recommended as part
of the evaluation of suspected pump thrombosis, but is not always diagnostic [69,70]. CCTA offers the advantage of
providing full visualization of the inflow cannula, ou tflow cannula, and anastomotic sites, with the limitation of providing
inadequate imaging of the metallic components of the VAD secondary to streak artifact [68]. Bey ond individual cases,
more rigorous studies evaluating the use of CCTA to confirm suspected pump thrombosis have yielded conflicting results
[68,70,71].
(A)
FIGURE 7.8 Still-frame images of a cardiac computed tomography angiography demonstrating an aortic root thrombus (asterisks) in a patient with a
left-ventricular assist device. (A) Axial and (B) reconstructed coronal views. The thrombus measures 2.6 3.2 2.8 cm and extends from the aortic
annulus to the left coronary sinus, causing occlusion of the proximal left coronary artery. The figure is blurred due to streak artifact arising from the
metallic components of the VAD.
(B)
Соседние файлы в папке Библиотека им академика М.И. Перельмана