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Review Article  |   August 2007
Transesophageal Echocardiography and Cardiovascular Sources of Embolism: Implications for Perioperative Management
Author Affiliations & Notes
  • Christine Ngukhoon Tan, M.B., B.S., F.R.C.A.
    *
  • Alan G. Fraser, F.R.C.P., F.E.S.C.
  • * Consultant Anesthesiologist: Department of Anaesthesia and Intensive Care Medicine, University Hospital of Wales. † Honorary Consultant in Cardiology, Wales Heart Research Institute, Cardiff University, Cardiff, United Kingdom.
Article Information
Review Article / Cardiovascular Anesthesia / Radiological and Other Imaging
Review Article   |   August 2007
Transesophageal Echocardiography and Cardiovascular Sources of Embolism: Implications for Perioperative Management
Anesthesiology 8 2007, Vol.107, 333-346. doi:10.1097/01.anes.0000270733.26234.56
Anesthesiology 8 2007, Vol.107, 333-346. doi:10.1097/01.anes.0000270733.26234.56
PATIENTS who receive anesthesia and critical care are at risk of cardioembolic stroke, which is an uncommon but highly important cause of perioperative mortality and morbidity.1,2 Embolism is associated with intracardiac lesions, cardiac anomalies, and vascular disease3 (table 1), all of which may be assessed by transesophageal echocardiography (TEE).4,5 
Table 1. Cardiovascular Sources of Embolism 
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Table 1. Cardiovascular Sources of Embolism 
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In this review, we describe how cardiovascular sources of embolism may be detected by TEE, and how TEE is important for stratifying risk and providing prognostic information to prevent, predict, or manage perioperative embolism.
Basics of TEE
Detection of Sources of Embolism
Transesophageal echocardiography is used increasingly in the perioperative period,6 and it is considered to be superior to transthoracic echocardiography for detecting cardiovascular sources of embolism.7 It has high sensitivity and specificity for defining posterior and inferior structures in the heart because of their proximity to the esophagus and stomach. High-frequency transduction (4–8 MHz) allows superior image resolution, and so TEE is better than transthoracic echocardiography at evaluating thrombi,8,9 vegetations,10 and other masses.11 There are 20 cross-sectional views for comprehensive intraoperative TEE examination, as recommended by the American Society of Echocardiography and Society of Cardiovascular Anesthesiologists.12 Of them, key TEE views for detecting cardiovascular sources of embolism can be obtained from the upper esophageal and mid-esophageal positions (fig. 1).
Fig. 1. Essential views for detection of cardiovascular sources of embolism. (  A  ) Mid-esophageal view of the left atrium (LA) and left atrial appendage (LAA) at 20°. (  B  ) Mid-esophageal view of the LA and LAA at 70°. (  C  ) Mid-esophageal view of the LA and LAA at 120°. (  D  ) Mid-esophageal four-chamber view (0°) of the foreshortened left ventricle (LV). (  E  ) Mid-esophageal two chamber view (90°) of the LV which is not foreshortened. Apex is shown. (  F  ) Mid-esophageal bicaval view (90°) showing a patent foramen ovale (PFO). (  G  ) Upper esophageal long axis view (110°) of the mid–ascending aorta (AAo) imaged through the right pulmonary artery (RPA). AA = ascending aorta; IVC = inferior vena cava; LUPV = left upper pulmonary vein; LVOT = left ventricular outflow tract; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TS = transverse sinus. (Multiplane angles may vary according to patient's anatomy.) 
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Fig. 1. Essential views for detection of cardiovascular sources of embolism. (  A  ) Mid-esophageal view of the left atrium (LA) and left atrial appendage (LAA) at 20°. (  B  ) Mid-esophageal view of the LA and LAA at 70°. (  C  ) Mid-esophageal view of the LA and LAA at 120°. (  D  ) Mid-esophageal four-chamber view (0°) of the foreshortened left ventricle (LV). (  E  ) Mid-esophageal two chamber view (90°) of the LV which is not foreshortened. Apex is shown. (  F  ) Mid-esophageal bicaval view (90°) showing a patent foramen ovale (PFO). (  G  ) Upper esophageal long axis view (110°) of the mid–ascending aorta (AAo) imaged through the right pulmonary artery (RPA). AA = ascending aorta; IVC = inferior vena cava; LUPV = left upper pulmonary vein; LVOT = left ventricular outflow tract; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TS = transverse sinus. (Multiplane angles may vary according to patient's anatomy.) 
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Limitations, Complications, and Contraindications
Masses located in the left ventricular (LV) apex, distal ascending aorta, and proximal aortic arch may be missed by TEE. Image acquisition is limited in these areas, and other imaging modalities should be considered, e.g.  , helical computed tomography and magnetic resonance imaging.13 In addition, TEE has caused complications that are primarily associated with esophageal intubation. These include trauma to the oropharynx, esophagus, and stomach resulting in odynophagia, esophageal perforation, and upper gastrointestinal bleeding.14 Therefore, the main contraindications of TEE are oropharyngeal pathology, esophageal stricture, varices, and recent upper gastrointestinal bleeding.15 
Intracardiac Lesions
Intracardiac sources of embolism include thrombi, vegetations, and tumors. They may be distinguished by their echocardiographic features and associated risk factors (table 2). The risk of embolism and examples of TEE use in these conditions are also summarized.
Table 2. Intracardiac Sources of Embolism and Their Associated Risk Factors, Echocardiographic Features, Embolic Risk, Differential Diagnosis, and Utility of TEE 
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Table 2. Intracardiac Sources of Embolism and Their Associated Risk Factors, Echocardiographic Features, Embolic Risk, Differential Diagnosis, and Utility of TEE 
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Left Atrial Thrombus
Thrombi in the left atrium (LA) appear as intracavitary masses that are usually distinct from surrounding structures. Often, they reside between the trabeculae of the left atrial appendage (LAA)16 (fig. 2), which is a multilobed end-pouch, transversed by pectinate muscles with a ridge-like appearance. (This TEE image is available on the Anesthesiology Web site at .) Sometimes, thrombi are echo-lucent and difficult to recognize. In this situation, the diagnosis may be confirmed by giving an intravenous echo-contrast agent to improve discrimination between blood and intracavitary masses.17,18 
Fig. 2. Mid-esophageal short axis view of the aortic valve (AV) and left atrium (LA) showing thrombus (  arrow  ) in the left atrial appendage. 
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Fig. 2. Mid-esophageal short axis view of the aortic valve (AV) and left atrium (LA) showing thrombus (  arrow  ) in the left atrial appendage. 
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The LAA is assessed at the mid-esophageal level. This technique involves rotation of the TEE transducer between 0° and 150° along the LAA axis, shown as dotted line along the middle of the scan views (figs. 1A–C). The sensitivity and specificity of detecting thrombi in the LA and LAA are between 81% and 98%, and between 98% and 100%, respectively.19 
The presence of thrombus in the LA is highly predictive of transient ischemic attack in patients with atrial fibrillation (AF). In a prospective study of 261 patients, the odds ratio (OR) (95% confidence interval [CI]) for transient ischemic attack in patients with LA thrombus compared with those without was 7.7 (2.1–21.6), and the annual rate of transient ischemic attack was 9.2% compared with 1.9%.20 Embolic risk would seem to correlate with mobility and shape; in a prospective study of 41 patients with LA thrombi, the incidences of embolism in patients with mobile ball-like thrombi, fixed ball thrombi, and “mountain”-type thrombi were 77, 18, and 9%, respectively.21 
Predisposing factors for LA thrombus include mitral valve pathology and abnormal LA contractile function. Structural or anatomical risk factors include an enlarged22 and bifid LAA.23 In a multicenter, observational follow-up study of 409 patients, the relative risks (95% CIs) of stroke or embolism in patients with increased length and width of LAA were 1.6 (1.05–2.5) and 2.4 (1.2–4.8), respectively.24 
Mitral Valve Disease.
Left atrial thrombus has been reported in as many as 29–33% of patients with rheumatic mitral stenosis and AF25,26 in whom it was associated with a high incidence (41%) of symptomatic arterial embolism including stroke.26 Thrombi in the LA are less common in patients with mitral regurgitation27 presumably due to attenuation of stasis by the regurgitant jet. In patients with a newly implanted mitral valve replacement, asymptomatic, early thrombosis was detected in 9.4% of 680 consecutive patients undergoing TEE.28 
Abnormal Atrial Function.
Severe dysfunction of the LA and its appendage correlates with increased risk of recurrent stroke and mortality.29 Echocardiographic features of impaired LA function include spontaneous echo contrast (SEC), reduced velocities of flow in the LAA, and atrial dysrhythmias.
  • SEC appears as smoke-like, swirling echoes resulting from the aggregation of erythrocytes and fibrinogen at low shear rates.30 It is more likely to be detected using a high-frequency ultrasonic transducer (> 5 MHz, as used in TEE) and high gain settings. The degree of SEC can be quantified using integrated backscatter, which records the acoustic intensity of the signal in decibels.31,32 SEC is relatively common (e.g.  , 17% of 290 consecutive patients undergoing TEE) and is associated with AF, mitral stenosis, and mitral prostheses.22 In patients with mitral stenosis and chronic AF, it predicts LA thrombus and embolic events (OR, 1.74 [1.23–2.48]).26 In patients with severe SEC and AF, it is associated with risk of cerebral embolism.33 

  • The velocity of blood flow at the orifice of the LAA can be sampled using pulse-wave Doppler, with a low Nyquist limit and low wall-filter settings. Thrombogenic risk increases with decreasing LAA velocity; e.g.  , in a prospective study of 500 patients with stroke, thrombus was found in 1, 10, and 29% of patients with LAA velocities greater than 40 cm/s, 20–40 cm/s, and less than 20 cm/s, respectively.34 Above a threshold LAA velocity greater than 55 cm/s, thrombus was ruled out because this velocity has a negative predictive value of 100%.

  • AF35 and atrial flutter36 are associated with abnormal LA function, stasis, and thrombosis.37 The prevalence of intraatrial thrombus has been reported at 29–40% in patients with atrial flutter or AF compared with 3–5% in controls in sinus rhythm.36,38 Despite restoration to sinus rhythm, whether spontaneously, by electrical conversion,39 or by radiofrequency ablation,40 patients remain at risk of LA thrombosis for up to 4–6 weeks, due to transient mechanical dysfunction of the LA called atrial stunning  .41 

Utility of TEE.
Detection of LA thrombi by TEE has influenced clinical decision making. Examples include the following:
  • TEE-guided direct current cardioversion. TEE has been performed during general anesthesia before cardioversion, to exclude the presence of thrombus in the LA.42 This practice also involves routine anticoagulation because of the possibility of LA stunning, delayed thrombus formation, and thromboembolism.43 Cardioversion is contraindicated in the presence of thrombus, and a follow-up TEE can guide anticoagulation and ensure its resolution.44 

  • TEE and interventional cardiology. In patients with mitral stenosis, TEE has been used to guide percutaneous transvenous mitral commissurotomy45 and transcatheter occlusion of the LAA.46 

  • TEE in cardiac surgery. Patients with LA thrombus of high embolic potential may be scheduled to undergo open cardiac surgery. TEE should be used to reconfirm its presence. For example, in a case report, complete embolization of LA thrombus to the leg of a patient was described, and TEE showed that sternotomy was no longer required.47 Conversely, TEE has been shown to refine intraoperative decision making, e.g.  , removal of thrombi and closure or amputation of the LAA.48 It is essential to verify complete surgical obliteration because residual flow within the LAA predisposes to further thromboembolism.49 

Left Ventricular Thrombus
Left ventricular thrombi may be laminar or protruding, with a smooth or irregular shape. They are usually contiguous with areas of noncontracting myocardium. Recent or actively forming thrombi may appear echo-lucent. Patients with subacute, protruding, echo-lucent, and mobile thrombi are at high risk of embolic events, compared with those who have sessile, laminated, and organized thrombi.50 
Because thrombi are often located in the LV apex, they should be suspected when an akinetic cardiac apex is thickened and rounded. A foreshortened image of the LV apex (fig. 1D) can be minimized by retroflexing the tip of the TEE probe or using other vertical scan views (fig. 1E). A deep transgastric view (0°–20°) may provide better resolution because it is within the near field of the transducer. To distinguish thrombi from artifacts, it is necessary to acquire optimal images in at least two different views, throughout the cardiac cycle. Some laminated thrombi may be difficult to visualize clearly, and endocardial border delineation may be improved by a higher transducer frequency (> 5 MHz) and contrast ventriculography.51 Harmonic power Doppler contrast has been used to detect thrombi in the apex or in a pseudoaneurysm.52 
Thrombi are more common at the apex, in aneurysms53 or pseudoaneurysms,54 or between trabeculations and in deep recesses. An aneurysm is a dilated region of infarcted LV,55 and a pseudoaneurysm is an area of contained rupture lined by pericardium.54,56 Trabeculations and deep recesses in continuity with the LV cavity are features of noncompaction, a disorder of endomyocardial embryogenesis57,58 in which intertrabecular flow can be demonstrated with color-flow Doppler and contrast-enhanced echocardiography.59,60 In isolated LV noncompaction, thromboembolic events occurred in 24% of 34 patients.61 A recent case report of an acute thromboembolic occlusion of the superior mesenteric artery has been described in association with isolated LV noncompaction.62 
Patients with poor LV function are predisposed to stasis and thrombosis. After anterior myocardial infarction with severe regional wall motion abnormalities, the overall incidence of LV thrombus was 25%.63 LV thrombus was more common in patients with larger ventricles. It occurred in 72% of 53 patients with an LV end-systolic volume index greater than 35 ml/m2compared with 33% in those with smaller ventricles.64 In severe ventricular failure, LV thrombus has been reported in patients with ventricular assist devices.65 Conversely, inferior myocardial infarction, coronary reperfusion, and preserved global LV systolic function are associated with a lower incidence of LV thrombus.63 
Echocardiographic indices that correlate with LV thrombosis include low ejection fraction, high LV wall motion score, and high E/Em ratio. An ejection fraction less than 40% was associated with earlier LV thrombus formation, in the first week after myocardial infarction.64 After acute anterior myocardial infarction, the mean (SD) wall motion score of 9.2 (2.8) in patients with LV thrombus was higher than that of 4.7 (2.1) in patients with no thrombus.63 Thrombus persisting 6 weeks after myocardial infarction was associated with apical dyskinesis.64 A high E/Em ratio (peak mitral inflow velocity [E] to peak mitral annular velocity by tissue Doppler [Em]) implies a high LV filling pressure. In 87 consecutive patients with acute myocardial infarction, the E/Em ratio (SD) was 12(5) in the group with LV thrombus compared with 7.2 (2.8) in those without thrombus. The sensitivity and specificity of E/Em greater than 9 for predicting LV thrombosis after myocardial infarction were 69% and 79%, and the positive and negative predictive values were 63% and 84%.66 
Utility of TEE.
Thrombus in the LV is associated with poor ventricular function. Patients with this condition may require coronary revascularization and insertion of a ventricular assist device:
  • During coronary revascularization, TEE should be used to check for LV thrombi particularly in ventricles that are aneurysmal.67 

  • During insertion and separation from ventricular assistance, TEE is recommended to assess ventricular function,68 in addition to examining for thrombus,65 air, valve dysfunction,69 and septal defects.68 

Thrombus in the Right Heart
Right heart thrombi are most often caused by embolization from a peripheral venous source.70 They may become entrapped in the tricuspid valve apparatus or right ventricular (RV) trabeculations. In situ  thrombosis in the right heart is usually iatrogenic. Foreign bodies such as indwelling vascular catheters,71 pacemaker leads,72 and a prosthetic tricuspid valve73,74 are predisposing factors. Thrombi in the right heart may become infected75,76 or cause pulmonary embolism.77,78 Unlike the LV, RV dilatation and systolic dysfunction are rare causes of thrombosis, which can occur at the site of RV infarction, or within the hypokinetic aneurysmal areas of the RV free wall in arrhythmogenic RV cardiomyopathy.79,80 
Thrombi in the right atrium (RA) may be visualized in the mid-esophageal four-chamber or bicaval views between 0° and 90° on multiplane TEE. They should be distinguished from a Eustachian valve or a Chiari network, which are remnants of the right sinus venosus adjacent to the inferior vena cava (IVC). The former is commonly seen as a thin, mobile, linear structure, whereas a Chiari network is a large and fenestrated structure extending across the RA with additional attachments to its upper wall and the atrial septum.81 Unlike thrombi, these structures do not cross the tricuspid valve during diastole. In the RV, thrombus may be seen in mid-esophageal four-chamber view and in the transgastric RV inflow view between 80° and 110°.
Utility of TEE.
Pulmonary embolism may occur as a result of thrombi in the right heart.77,78 These patients may present for pulmonary embolectomy and TEE may be used to assist in their diagnosis. In a study of 46 patients having pulmonary embolectomy, TEE demonstrated RV dysfunction, tricuspid regurgitation, and leftward atrial septal bowing. However, direct visualization of the emboli was not always possible. The sensitivities for detection were 0.35, 0.26, and 0.17 in the right, main, and left pulmonary arteries, respectively. Corresponding respective specificities were 0.89, 0.95, and 1.0.82 In another study, extrapulmonary locations of thromboemboli within the right heart were detected in 26% of 50 patients who had pulmonary embolectomy. Surgical management was altered accordingly.83 
In addition, TEE would seem to be recommended when long-term central venous catheters are removed. It is thought that TEE can monitor the procedure and provide early evidence of possible thrombus migration to the pulmonary artery.84,85 
Similarly, it is likely that TEE would be useful in guiding placement of central venous catheter in the presence of right heart thrombus. Central venous catheter placement in the distribution of the IVC may be preferred in the presence of a superior vena cava thrombus. The converse would be appropriate if there were an IVC thrombus.
Vegetations
Vegetations are of low echo-reflectance compared with normal valve leaflets. They are independently mobile, lobulated structures that are most often identified downstream from the origin of a regurgitant jet. According to a meta-analysis of eight studies,10 they are detected readily by TEE, which has a sensitivity of 87–100% compared with 30–63% by transthoracic echocardiography. TEE is important for determining the Duke criteria for the clinical diagnosis of infective endocarditis,86 and a normal TEE study has high negative predictive value. The diagnosis of prosthetic valve endocarditis is more difficult because of acoustic shadowing and reverberation artifacts.9 In addition, vegetations should not be confused with other lesions, e.g.  , nonbacterial thrombotic endocarditis, valve strands, or even nodules of Arantius, which are normal anatomical features of the aortic valves.
The mobility, size, and location of vegetations are important predictors of embolism. Mobile vegetations larger than 10 mm and in the mitral position87 are associated with a high incidence of embolism.88,89 In a prospective cohort study comparing patients with vegetations larger than 10 mm to those with smaller lesions, the relative risk (95% CI) of embolization was 2.64 (0.98–7.16).90 Neurovascular embolization is associated with a high mortality.91 
Utility of TEE.
In the critical care setting, TEE is essential when the differential diagnosis in a patient with severe sepsis or multiple systemic embolism includes infective endocarditis.92 The high risk of embolism in patients with large vegetations (> 10 mm), particularly in the first 2 weeks of antibiotic therapy, may be minimized by early surgery.90 TEE should be used to plan surgery and anesthetic management.
Surgery depends on
  • The site of endocarditis

  • Multivalvular93 or prosthetic valve involvement

  • The extent of perivalvular infection, e.g.  , aneurysm, fistula, chordal rupture, leaflet perforation, and abscess formation94,95 

Patients with infective endocarditis have significant hemodynamic instability, and their anesthetic management is influenced by
  • The degree of ventricular dysfunction

  • The predominant pathophysiology of valvular dysfunction, e.g.  , regurgitation or stenosis

  • The magnitude of systemic sepsis96 

Intracardiac Tumors
Cardiac tumors may be additional sources of embolism in patients receiving anesthesia and critical care. Primary tumors are rare, with an incidence ranging from 0.001% to 0.3% in unselected patients at autopsy.11 The majority (75%), including myxoma and fibroelastoma, are benign. Malignant primary neoplasms include angiosarcoma, rhabdomyosarcoma, fibrosarcoma, leiomyosarcoma, and intracardiac lymphoma.11 Secondary neoplasms with intracardiac extension and metastasis are more common97 and can result in stroke and widespread systemic embolism. Examples include lung98,99 and renal cell carcinoma,100 which may extend into the LA via  the pulmonary veins, and into the RA via  the IVC, respectively.
Many intracardiac structures may mimic cardiac tumors. Vascularized thrombi,101 giant atrial septal aneurysms102 with thrombus,103 or coronary artery aneurysms104 could act as embolic sources. Other structures such as a prominent crista terminalis105 or lipomatous hypertrophy of the atrial septum106 are normal or incidental findings. Lipomatous hypertrophy has been reported in association with supraventricular arrhythmias107 and probable embolic phenomena, but a causal relation has not been established. Expert echocardiography is important to obviate false-positive identification and hence unnecessary surgery.108 
Cardiac Myxomas.
Cardiac myxomas account for 30–50% of primary cardiac tumors.109 They can be globular or irregular in shape (like a cluster of grapes) with a heterogeneous texture incorporating calcified, gelatinous, or cystic areas. Eighty percent of myxomas are located in the LA, where their most frequent attachment is to the fossa ovalis of the atrial septum (fig. 3; this TEE image is available on the Anesthesiology Web site at ). Other less typical attachments include the LAA and chordae of the mitral valve.110 Myxomas may be found concurrently in the LV, RV, or RA.109 Systemic embolism is thought to occur from fragmentation of tumor or dislodgement of thrombi formed on its surface.111 Highly mobile, villous tumors with friable broad bases have much higher embolic potential than the firm, well-encapsulated variety.112 Uncommonly, detachment and embolism of a whole cardiac myxoma may occur.113 
Fig. 3. Mid-esophageal bicaval view showing a left atrial myxoma (MYX) attached to the atrial septum (  arrow  ). RA = right atrium. 
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Fig. 3. Mid-esophageal bicaval view showing a left atrial myxoma (MYX) attached to the atrial septum (  arrow  ). RA = right atrium. 
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Cardiac Papillary Fibroelastomas.
Cardiac papillary fibroelastomas (or myxopapillary tumors) represent 8–10% of primary tumors of the heart. They occur most commonly on left heart valves, attached by a small pedicle to their endocardial surface, but they may occur at multiple other sites, including the papillary muscles, the LV free wall, the RV outflow tract,114 and the pulmonary valve.115 They are usually small (< 20 mm), homogeneous, round or oval-shaped masses but may also have multiple papillary fronds appearing like a sea anemone in motion. They may mimic vegetations in their independent motion, but unlike vegetations, they are often located on the ventricular side of the mitral valve or the ascending aortic side of the aortic valve.
Presenting features of fibroelastomas include systemic embolism,116 transient ischemic attack, stroke, blindness, syncope, myocardial infarction causing heart failure, and sudden death.117 Fibroelastomas may undergo fragmentation or act as a nidus for platelet and fibrin aggregation, leading to thromboembolism.118 In a summary of 725 cases reported in the literature, tumor mobility was the only independent predictor of death or nonfatal embolization.119 Thus surgical excision has been recommended if a tumor becomes mobile during follow-up by echocardiography, even when there are no symptoms.
Utility of TEE.
In the perioperative period, TEE may be used to
  • Confirm location and guide manipulation.120 Tumors may embolize, and TEE should be used to check their precise location and assist in appropriate manipulation of the heart. Tumors that embolize may cause significant hemodynamic instability requiring immediate confirmation by TEE and alteration in surgical plan.121 

  • Assist the surgeon during cannulation and cardiopulmonary bypass (CPB). Tumors that are detected in the superior vena cava or IVC may require alternative routes of cannulation.122 Complete resection of tumors may require modification of CPB to include deep hypothermic circulatory arrest.123 

  • Assess valve function. Valvular involvement and dysfunction may occur and should be assessed perioperatively, by TEE.124 

  • Assess adequacy of tumor resection. TEE is used to check for multiple tumors125 before surgery and to ensure complete resection.126 

Cardiac Anomalies
Cardiac anomalies associated with systemic embolism include patent foramen ovale (PFO), atrial septal defects, and atrial septal aneurysm.127 Anatomical variants such as Chiari remnants may also be associated with thromboembolism.128 
Patent Foramen Ovale
Patent foramen ovale is an interatrial communication with a one-way flap that allows right-to-left shunting of blood and hence thrombi. It is a remnant of the fetal circulation and occurs when the septum primum and septum secundum fail to fuse.129 At autopsy, the incidence of “probe-patent” PFO may be as high as 27–30%, but only 6% are wider than 5 mm.130 PFO is more common in patients with a mobile atrial septal flap.131 
On TEE, PFO is often visualized in the mid-esophageal four-chamber (fig. 4; this TEE image is available on the Anesthesiology Web site at ) and bicaval views (fig. 1F). The diagnosis is usually made when four or more microbubbles are seen entering the LA during the first three cardiac cycles, after opacification of the RA by agitated saline.132 Sudden release of positive airway pressure during mechanical ventilation similar to the Valsalva maneuver133 in a conscious patient may aid the right to left shunt. In addition, saline injection into the right femoral vein seems to have a higher diagnostic yield than that into the right antecubital vein.130 Sometimes, low-velocity flow across the defect in the atrial septum may be seen using color flow mapping at low Nyquist limits.134 
Fig. 4. Mid-esophageal four-chamber view of the heart showing a patent foramen ovale (PFO) and Chiari network (  long arrow  ). The velocity of blood flow across the PFO can be demonstrated by color flow Doppler (see  Anesthesiology  website). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. 
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Fig. 4. Mid-esophageal four-chamber view of the heart showing a patent foramen ovale (PFO) and Chiari network (  long arrow  ). The velocity of blood flow across the PFO can be demonstrated by color flow Doppler (see  Anesthesiology  website). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. 
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Patent foramen ovale is associated with an increased risk of paradoxical embolism and cryptogenic stroke, which are reported to be fivefold higher in patients younger than 55 yr (OR in a meta-analysis of case–control studies, 5 [3.2–7.8]).135 Cryptogenic stroke was associated with increased size and volume of a right-to-left shunt.136 In addition, paradoxical air embolism has occurred during neurosurgery when patients are in the sitting position.137 In orthopedic practice, paradoxical embolism of thrombus or fat may occur because of immobility and intramedullary reaming, respectively.138 
Utility of TEE.
In the perioperative period, TEE may be used to diagnose PFO and hence define the cause of paradoxical embolism.139 Furthermore, unexplained hypoxemia due to right-to-left shunting of blood may be explained by TEE. This situation could occur when there is an increase in pulmonary vascular resistance, e.g.  , intermittent positive-pressure ventilation, high positive end-expiratory pressure, chronic lung disease, pneumonectomy, or heart transplantation.140 
Similarly, a right-to-left shunt may occur during decompression of the left heart, e.g.  , when a left ventricular assist device is activated. TEE has been recommended to identify the presence of a PFO and to guide surgical closure before left ventricular assist device insertion.141 
Closure of PFO may also be done routinely by interventional cardiologists. This procedure is performed during general anesthesia and TEE guidance.142 TEE is used to confirm the diagnosis, guide correct positioning of the occluder device, and ensure that there is no deformation of the aortic root or obstruction of venous return to the RA.143 
Atrial Septal Aneurysm
Atrial septal aneurysm is a localized saccular deformity that bulges more than 15 mm from the plane of the atrial septum and has a width at its base greater than 10 mm.144–146 Its prevalence is usually 2–10147 but may be as high as 28% on TEE during acute changes in loading conditions at cardiac surgery.131 Atrial septal aneurysm may be visualized in the mid-esophageal four-chamber or bicaval view. Five subtypes of atrial septal aneurysm have been described.147 Atrial septal aneurysm frequently occurs with PFO,144,145 especially in its specific subtypes.131 
Atrial septal aneurysm is considered a potential source and an independent predictor of cardiogenic embolism. In a prospective multicenter study of 606 patients, the prevalence of atrial septal aneurysm was 27.7% in patients who had ischemic stroke and normal carotid arteries compared with 9.9% in the control group.144 The combination of atrial septal aneurysm with PFO was associated with an increased risk of recurrent stroke (hazard ratio, 4.17 [1.47–11.84]).148 
The pathogenesis of thromboembolic phenomena in patients with atrial septal aneurysm is unclear.149 A possible mechanism is paradoxical embolization of thrombus trapped from IVC inflow or formed within the aneurysm, through its multiple fenestrations.145 
The occurrence of atrial septal aneurysm may impair the function of ventricular assist devices. In a case report, TEE was used to show that an atrial septal aneurysm impaired blood flow into the right ventricular assist device.150 
Chiari Network
This structure is a remnant of the right sinus venosus valve that exists during fetal life. Its prevalence of 4.6% in patients undergoing TEE for unexplained arterial embolism exceeds that of 0.5% in patients evaluated for other indications.151 A Chiari network may be visualized in the RA using the mid-esophageal four-chamber (fig. 4) or bicaval view on multiplane TEE. In contrast to the nonfenestrated flap of the Eustachian valve, a Chiari network is a fenestrated, filamentous structure with a typical undulating appearance during real-time imaging that differentiates it from RA thrombus. It usually extends from the inferolateral part of the RA onto the atrial septum, near the limbus of the fossa ovalis. It should not be mistaken for a fenestrated atrial septum.152 
A Chiari network can be associated with atrial septal aneurysm and PFO, possibly because it facilitates blood flow from the IVC toward the atrial septum,153 which may allow persistence of atrial septal aneurysm and prevent spontaneous closure of PFO. Because it may preferentially direct venous thrombi from the IVC toward a PFO, paradoxical embolism is possible. In a case report of a patient undergoing percutaneous closure of an atrial septal defect, entanglement of the closure device with the Chiari network has been demonstrated by TEE perioperatively.154 
Vascular Causes of Embolism
Aortic Atheroma
Aortic atheroma is an important source of embolism and an independent risk factor for perioperative stroke.155 In a meta-analysis of six prospective follow-up studies of 1,320 patients with severe aortic arch atheroma, the odds of stroke in patients with aortic arch atheroma was almost four times greater than in controls without atheroma (OR, 3.76 [2.57–5.51]).156 In patients with embolic disease, the prevalence of atheroma in the aortic arch varies from 21% to 27%.157 Atheroembolization and, more commonly, thromboembolism seem to be the mechanisms involved.157 Aortic atheroma is common in patients older than 60 yr who require coronary revascularization; atheroma greater than 2 mm was found in 35% and mobile atheroma occurred in 3.6%.158 During cardiac surgery with CPB, the rate of stroke in patients with aortic arch atheroma is high (12%) and six times higher than the rate in controls undergoing noncardiac surgery.156 
Atherosclerotic lesions in the descending thoracic aorta may be visualized in short and long axis views; the distance of the tip of the probe from the teeth should be noted to document the level of an abnormality. At the upper esophageal level, approximately 20 cm from the incisors, the distal aortic arch may be visualized between 0° and 90° (fig. 5; this TEE image is available on the Anesthesiology Web site at ). The aortic root and proximal half of the ascending aorta can be seen in mid-esophageal or basal views between 20° and 130°, and some of the mid–ascending aorta can be imaged through the right pulmonary artery (fig. 1G). However, there are blind spots on TEE for imaging the distal ascending aorta and proximal aortic arch because of air in the bronchus between the upper esophagus and these vessels. A recent case report described the use of a saline-filled balloon cuff of an endotracheal tube (inserted only when ventilation was terminated during CPB) to improve visualization of the proximal arch.159 
Fig. 5. Upper esophageal long (  A  ) and short axis views (  B  ) of the distal aortic arch (AoA) during routine coronary revascularization surgery. Grade V, complex atheroma detected (  arrows  ). 
Image Not Available
Fig. 5. Upper esophageal long (  A  ) and short axis views (  B  ) of the distal aortic arch (AoA) during routine coronary revascularization surgery. Grade V, complex atheroma detected (  arrows  ). 
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Epiaortic echocardiography has been shown to provide additional visualization of the aorta.160,161 In a study that enrolled 100 patients for cardiac surgery, the frequency for detection of mild, distal ascending aortic atheroma during epiaortic imaging was significantly higher than during TEE or digital palpation.162 During an epiaortic scan, mapping of distribution of aortic atheroma is required. The ascending aorta may be divided into proximal, middle, and distal thirds. Each segment may have atheroma in its anterior, posterior, lateral, and medial walls.163 
The severity of atheroma may be graded according to its morphology and appearance on echocardiography.164 The modified Montgomery scale is as follows:
  • Grade I: normal

  • Grade II: mild intimal thickening greater than 2 mm

  • Grade III: moderate, atheromatous plaque less than 4 mm

  • Grade IV: severe, protruding atheromas 4 mm or greater

  • Grade V: complex, ulcerated, and mobile atheroma of any size

It has high sensitivity and specificity and excellent reproducibility.165 Evaluation of the thickness of atherosclerotic plaques in the aorta compares well with magnetic resonance imaging.166 
The risk of stroke correlates with the size and complexity of atheroma:
Plaque Thickness.
Increasing plaque thickness is associated with higher risk of stroke. Compared with controls without atheroma, the OR (95% CI) of stroke was 4.4 (2.8–6.8) in patients with plaques between 1 and 3.9 mm, and 13.8 (5.2–36.1) for plaques 4 mm or greater.167 Similarly, Cohen et al.  168 reported an OR (95% CI) of 12.6 (7.7–17.6) for stroke in patients with plaques 4 mm or greater in the aortic arch. From analysis of receiver operator characteristics, plaque thickness greater than 3.5 mm was reported as the best predictor of cardiovascular events.169 
Complex Plaque.
Protruding plaques with ulceration, superimposed mobile thrombi, or noncalcified (fat-laden) areas confer additional independent risks for stroke and peripheral embolism. Compared with controls, the OR (95% CI) of embolism in patients with complex plaques was 17.1 (5.1–57.3).170 
SEC in the Aorta.
The presence of SEC in the thoracic aorta was associated with recent stroke in a prospective study of 224 patients and 85 controls undergoing TEE.171 Compared with controls without aortic SEC, the OR (95% CI) of stroke in patients with SEC in the aorta was 2.8 (1.65–4.46; P  < 0.001).
Surgical Manipulations of the Proximal Aorta.
Aortic clamping172 or cannulation173 and aortic arch endarterectomy are associated with a threefold increase in perioperative stroke.174 
Utility of Echocardiography.
Detection of ascending aortic atheroma has been shown to influence clinical decision making during cardiac surgery.175–177 Examples include modifications in
  • Aortic cannulation

  • Aortic cross clamping

  • Proximal aortic vein anastomosis

  • Cannulation for cardioplegia

  • Deep hypothermic circulatory arrest for partial or complete ascending aortic replacement178 

Furthermore, off-pump coronary artery bypass grafting179 with minimal aortic manipulation172 may be performed. Stroke rate was reduced from 2.2% in patients with severe atheroma and partial aortic cross clamp to 0.2% using the “no-touch” technique.180 It is envisaged that these alterations may minimize the risk of atherothromboembolism and hence the occurrence of perioperative stroke. Off-pump coronary artery bypass grafting in high-risk patients with atheromatous aorta has been associated with lower risk of stroke and death.181 
Other Sources of Embolism
Less common sources of embolism or features that have been associated with embolism and that may be detected by TEE include air embolism, mitral annular calcification, and valve strands.
Intracardiac Air Embolism
Air or microbubbles may be seen readily within the cardiac chambers during intraoperative TEE. They may occur during neurosurgical procedures performed with the patient in a sitting position,182 or during surgery involving any sites above the level of the heart. The incidence of venous air embolism during neurosurgical procedures has been reported to be high at 43%,183 and venous air embolism with paradoxical air embolism has also been documented.182 
After open heart surgery, clusters of air or numerous microbubbles are invariably seen within the cardiac chambers. Despite careful standard mechanical deairing, delayed release of air trapped in the pulmonary vessels is common. Numerous highly echo-reflective particles can be seen entering the LA from the pulmonary veins, in the mid-esophageal four-chamber view.184 These echo-reflections by bubbles are relatively large and sparsely distributed, unlike the pattern seen with SEC. Bright, echogenic structures within the wall of myocardium often indicate intracoronary air embolism (fig. 6; this TEE image is available on the Anesthesiology Web site at ). This complication has been implicated in cardiac events after CPB.185 Myocardial injury with transient ST elevation on electrocardiogram, conduction disturbances, and regional wall motion abnormalities, are more frequent in patients with intracavitary pooled air than in those with minimal appearance of microbubbles.186 
Fig. 6. Mid-esophageal long axis view of the left ventricle (LV) after aortic valve replacement (AVR) showing intracoronary air embolism. Note the presence of bright echogenic microbubbles (air) within the LV anteroseptal wall. LA = left atrium. 
Image Not Available
Fig. 6. Mid-esophageal long axis view of the left ventricle (LV) after aortic valve replacement (AVR) showing intracoronary air embolism. Note the presence of bright echogenic microbubbles (air) within the LV anteroseptal wall. LA = left atrium. 
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During coronary revascularization with cardiopulmonary bypass, cerebral microembolization during the administration of drugs or blood187 may be detected by transcranial Doppler ultrasound. The number of perfusion interventions and hence episodes of microembolization may contribute toward long-term cognitive dysfunction, e.g.  , reduction in learning, memory, attention, and concentration.188 
Mitral Annular Calcification
Mitral annular calcification (MAC) is a chronic, noninflammatory, degenerative process typically affecting the posterior annulus and appearing as an echo-dense, semilunar mass. It may extend to involve the intervalvular fibrosa, mitral leaflets, aortic annulus, and papillary muscle.189 MAC occurs in 10% of patients older than 50 yr.190 It is associated with aortic sclerosis and aortic annular calcification,191 coronary artery disease,192 atherosclerosis,193 and end-stage renal disease.194 
Mitral annular calcification seems to be an independent risk factor for cardiovascular disease and embolic stroke even in patients without AF, congestive heart failure, or coronary artery disease. The relative risk (95% CI) of stroke in individuals with MAC was 3.12 (1.77–5.25).195 In the Framingham Heart Study, MAC was independently associated with an increased risk of stroke, with a hazard ratio (95% CI) of 1.5 (1.1–2.0) and a 10% increase in cardiovascular morbidity and mortality for each 1-mm increase in MAC.196 Mobile elements associated with MAC that have been demonstrated in patients with end-stage renal disease197 include thrombi,198 vegetations,199 and caseous abscess.200 Therefore, emboli may be thrombotic or calcific.
Valve Strands
Valve strands are thin (< 1 mm), long (< 10 mm) filiform projections from heart valves that have undulating independent motion. Typically, they are observed near the closure line of the mitral valve. It was first suggested that they might be composed of fibrin, but morphologic analysis of strands recovered from native and prosthetic valves has revealed collagen.201 
Valve strands were reported in 39% of elderly patients who had TEE for suspected cardioembolic stroke, giving an OR (95% CI) of ischemic stroke in patients with mitral valve strands of 2.2 (1.4–3.6; P  < 0.005).202 In other studies, however, no relation with brain infarction or clinical embolic events was demonstrated.203 
Conclusion
We have shown that TEE is invaluable in patients who are at risk of cardioembolic events. It enables risk stratification, influences medical therapy, and refines clinical decision making in patients with thrombus, vegetations, tumor, aortic atheroma, and other sources of embolism.204 It is envisaged that its routine use may improve patient outcome in the perioperative period.
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Fig. 1. Essential views for detection of cardiovascular sources of embolism. (  A  ) Mid-esophageal view of the left atrium (LA) and left atrial appendage (LAA) at 20°. (  B  ) Mid-esophageal view of the LA and LAA at 70°. (  C  ) Mid-esophageal view of the LA and LAA at 120°. (  D  ) Mid-esophageal four-chamber view (0°) of the foreshortened left ventricle (LV). (  E  ) Mid-esophageal two chamber view (90°) of the LV which is not foreshortened. Apex is shown. (  F  ) Mid-esophageal bicaval view (90°) showing a patent foramen ovale (PFO). (  G  ) Upper esophageal long axis view (110°) of the mid–ascending aorta (AAo) imaged through the right pulmonary artery (RPA). AA = ascending aorta; IVC = inferior vena cava; LUPV = left upper pulmonary vein; LVOT = left ventricular outflow tract; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TS = transverse sinus. (Multiplane angles may vary according to patient's anatomy.) 
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Fig. 1. Essential views for detection of cardiovascular sources of embolism. (  A  ) Mid-esophageal view of the left atrium (LA) and left atrial appendage (LAA) at 20°. (  B  ) Mid-esophageal view of the LA and LAA at 70°. (  C  ) Mid-esophageal view of the LA and LAA at 120°. (  D  ) Mid-esophageal four-chamber view (0°) of the foreshortened left ventricle (LV). (  E  ) Mid-esophageal two chamber view (90°) of the LV which is not foreshortened. Apex is shown. (  F  ) Mid-esophageal bicaval view (90°) showing a patent foramen ovale (PFO). (  G  ) Upper esophageal long axis view (110°) of the mid–ascending aorta (AAo) imaged through the right pulmonary artery (RPA). AA = ascending aorta; IVC = inferior vena cava; LUPV = left upper pulmonary vein; LVOT = left ventricular outflow tract; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TS = transverse sinus. (Multiplane angles may vary according to patient's anatomy.) 
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Fig. 2. Mid-esophageal short axis view of the aortic valve (AV) and left atrium (LA) showing thrombus (  arrow  ) in the left atrial appendage. 
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Fig. 2. Mid-esophageal short axis view of the aortic valve (AV) and left atrium (LA) showing thrombus (  arrow  ) in the left atrial appendage. 
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Fig. 3. Mid-esophageal bicaval view showing a left atrial myxoma (MYX) attached to the atrial septum (  arrow  ). RA = right atrium. 
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Fig. 3. Mid-esophageal bicaval view showing a left atrial myxoma (MYX) attached to the atrial septum (  arrow  ). RA = right atrium. 
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Fig. 4. Mid-esophageal four-chamber view of the heart showing a patent foramen ovale (PFO) and Chiari network (  long arrow  ). The velocity of blood flow across the PFO can be demonstrated by color flow Doppler (see  Anesthesiology  website). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. 
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Fig. 4. Mid-esophageal four-chamber view of the heart showing a patent foramen ovale (PFO) and Chiari network (  long arrow  ). The velocity of blood flow across the PFO can be demonstrated by color flow Doppler (see  Anesthesiology  website). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. 
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Fig. 5. Upper esophageal long (  A  ) and short axis views (  B  ) of the distal aortic arch (AoA) during routine coronary revascularization surgery. Grade V, complex atheroma detected (  arrows  ). 
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Fig. 5. Upper esophageal long (  A  ) and short axis views (  B  ) of the distal aortic arch (AoA) during routine coronary revascularization surgery. Grade V, complex atheroma detected (  arrows  ). 
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Fig. 6. Mid-esophageal long axis view of the left ventricle (LV) after aortic valve replacement (AVR) showing intracoronary air embolism. Note the presence of bright echogenic microbubbles (air) within the LV anteroseptal wall. LA = left atrium. 
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Fig. 6. Mid-esophageal long axis view of the left ventricle (LV) after aortic valve replacement (AVR) showing intracoronary air embolism. Note the presence of bright echogenic microbubbles (air) within the LV anteroseptal wall. LA = left atrium. 
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Table 1. Cardiovascular Sources of Embolism 
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Table 1. Cardiovascular Sources of Embolism 
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Table 2. Intracardiac Sources of Embolism and Their Associated Risk Factors, Echocardiographic Features, Embolic Risk, Differential Diagnosis, and Utility of TEE 
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Table 2. Intracardiac Sources of Embolism and Their Associated Risk Factors, Echocardiographic Features, Embolic Risk, Differential Diagnosis, and Utility of TEE 
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