The Role of Echocardiography in the Management of the Sources of Embolism

Roberta Esposito; Rosa Raia; Daniela De Palma; Ciro Santoro; Maurizio Galderisi

Disclosures

Future Cardiol. 2012;8(1):101-114. 

In This Article

Intracardiac Thrombi

Intracardiac thrombi are common findings in patients with ischemic stroke (upto 26% of patients with cerebrovascular events).[6] The echocardiographic identification of thrombi has important reflections in decision making since it represents an indication to long-term anticoagulant therapy, in order to reduce the risk of new stroke and possibly to dissolve the thrombus. Intracardiac thrombi can develop during the time course of several cardiac pathologies that favor the hematic stasis or the slackening of the blood flow (e.g., acute myocardial infarction, left ventricular [LV] aneurysms, cardiomyopathies and myocardites, valve disease and/or prosthesis, atrial fibrillation [AF]) and/or predispose to the aggregation of thrombotic material. The presence of spontaneous echo contrast, defined as 'smoke' for its echo aspect, is the most evident sign of slackened blood flow (Figure 1). Spontaneous echo contrast is considered a prethrombotic condition, associated with an increased risk for thromboembolic events.[6]

Figure 1.

Mechanisms determining the formation of left ventricular thrombi.
Left ventricular thrombi can develop due to the slackening of the blood flow which predisposes to the aggregation of blood material to the walls. It occurs in dilated cardiomyopathies or in left ventricular aneurysms after an acute myocardial infarction.

Echocardiography is the ideal tool for diagnosis and assessment of cardiac thrombi and must be utilized in all clinical conditions where the occurrence of cerebral ischemic events (transient ischemic attack, stroke) leads to the need to obtain evidence of embolic sources. A thrombus is identified as a discrete echo dense mass with well-defined margins that are distinct from the endocardium and seen throughout systole and diastole. Thrombus identification frequently requires 'off-axis' views, created 'on-line' (i.e., during the echo performance), in order to visualize peculiarities not obtainable by the standard views. The morphology and structure of thrombi have to be assessed carefully since dimensions, shape, grade of regularity and homogeneity are all characteristics defining the embolic risk and addressing the therapeutic management.

Ventricular Thrombi

Ventricular thrombi generally develop at the LV apex, with greater frequency in patients with LV aneurysms or after acute myocardial infarction (as a consequence of dyskinesia/akynesia of a given wall) (Figure 2).[7] Attention must be taken to exclude false tendons and trabeculae and to rule out artifacts, which are the most common cause of false positive results. However, TTE has a greater diagnostic accuracy (sensitivity: 90%; specificity: 85%)[8] than TEE under these circumstances (mainly because the incomplete visualization of LV apex by TEE). The accuracy of TTE is even increased by using color Doppler and/or contrast agents injected intravenously (Figure 3). Contrast agents improve delineation of the blood pool, endocardial border and thrombus allowing for more accurate detection of LV thrombus and its determinants.[9] Several echo features of LV thrombus must be evaluated including the shape (thrombus may be mural or protruding within the cavity), the motion (thrombus may be fix or present variable independent motion) and also the possible presence of adjacent LV aneurysm (i.e., a localized area of akinesia or dyskinesia that deforms LV chamber during both systole and diastole[5]). A higher risk of embolization is attributable to larger thrombus size and/or to thrombi which are mobile and protrude into the LV chamber, particularly in older patients.[10] After diagnosis, echocardiographic follow-up is needed until thrombus eradication is obtained using anticoagulants.

Figure 2.

Detection of a large thrombotic mass of left ventricular apex.
(A) Detection of a large thrombotic mass of left ventricular apex (apical 4-chamber view) in a patient with an acute inferior myocardial infarction the day before. (B) Magnified section of left ventricular apex. The relative hypogenicity reveals the recent onset of the thrombus.

Figure 3.

Apical 4-chamber view by harmonic inaging.
(A) Apical 4-chamber view by harmonic inaging in a patient with an old myocardial infarction and left ventricular dyskinetic apex. (B) The iv. injection of contrast agent allows the identification of an apical thrombus (see arrow).

Atrial Thrombi

Atrial thrombi involve more often the left atrium and left atrial appendage (LAA), in presence of atrial flutter and/or AF, mitral valve stenosis and mitral prosthesis. The thrombotic risk is associated with the slackening of the blood flow. In general, TTE is limited for the detection of atrial thrombi and in the majority of cases allows one only to suspect their presence. The use of color Doppler and contrast agents may be helpful,[9] but the identification of LAA thrombi remains very rare by TTE. TEE is therefore the gold standard tool (high sensitivity and specificity) since it allows a good visualization of LAA (Figure 4) and pulmonary veins, a complete exploration of atrial cavities and a comprehensive identification of even small, mural masses. TEE detection of LAA thrombi is possible since they appear as echo reflecting masses, distinct from the underlying endocardium, observed in more than one imaging plane and not related to pectinate muscles.[11] Although using TEE as the reference standard, the overall sensitivity and specificity of cardiac computed tomography for the detection of thrombi in the LAA has been found to be 96 and 100%, respectively,[12] TEE remains the preferable choice because free of radiation exposure. The thrombotic detection in the right atrium, which is very rare, must lead to suspecting the presence of venous thrombi invading the right cavity. Also in these cases TEE is the elective tool, and is able to provide evidence of extension and origin site of the mass.[13]

Figure 4.

Echocardiograms.
(A) Detection of a thrombus in the left appendage by transthocaic echocardiography (parasternal short-axis view of the great vessels).Diagnosis obtained via transthoracic echo is rare. (B) Evidence of a thrombus in left atrial appendage by transesophageal echocardiography.

Prosthetic Valve & Intracardiac Device Thrombosis

Prosthetic valves and intracardiac devices represent a major source of embolism. Prosthetic valve thrombosis is one of the most severe complications of mechanical heart valve replacement. Conditions placing the patient at greater risk of these complications include early postsurgical period, interruption of anticoagulant therapy and pregnancy. Both TTE and TEE must be performed when prosthetic or device thrombosis is suspected. However, TEE is the method of choice to diagnose the main signs, in particular for prosthetic valves: restricted leaflets or disc motion, abnormal central regurgitation, loss of physiological jets and direct visualization of thrombus or pannus formation.[5] Since the risk of embolism and complications is related to the thrombus size (thrombi >0.8 cm2 have major risk), TEE may help in the choice between surgery and thrombolytic therapy and for patients follow-up.[5] Even TEE suffers from some limitations and differential diagnosis of prosthetic valve thrombi from prosthetic endocarditis and/or from suture lines or fibrin strands may be very difficult.

Role of Echocardiography in AF

The echo assessment is crucial in this clinical setting because AF is the main determinant of LA thrombus formation (up to 15% event/year among patients with AF),[14] in relation to LA enlargement and blood flow stasis. The role of echocardiography in presence of AF is well established in guidelines[15] for several reasons: the etiological diagnosis of stroke can often be achieved by combining clinical history with echocardiography and the echo assessment allows anticoagulation therapy to commence and the potential treatment of AF with invasive therapeutic approaches; the embolic risk stratification in AF is currently based on clinical predictors (one point = history of heart failure, arterial hypertension, diabetes mellitus, age >75 years; two points = history of stroke or transient ischemic attach) according to the validated CHADS2VASC score: patients with CHADS2 ≥2 require treatment with warfarin while those with no CHADS2 risk factors can be treated with aspirin.[15] The therapeutic choice remains challenging in patients with CHADS2 = 1,[16] a subset in which echo risk factors can help to predict the thromboembolic risk ( Box 2 )[5] since they are independently associated with thromboembolism;[17] and TEE has a recognized role in guiding short-term anticoagulation for AF cardioversion. In AF lasting >48 h, besides the conventional oral anticoagulation for at least 3 weeks precardioversion, a TEE-guided approach can be used. In patients without thrombus, the cardioversion can be performed after few hours of anticoagulation (unfractioned or low-molecular-weight heparin) and soon after TEE. In patients with thrombus, lifelong oral anticoagulation and rate-control strategy shall be preferred to rhythm-control therapy, while cardioversion should be avoided because of the high thromboembolic risk.[18–20] Additional advantages of the TEE-guided approach are related to the lower incidence of hemorrhage[21,22] and a greater overall success rate in achieving sinus rhythm.[15] Moreover, a TEE-derived normal LAA function (LAA velocities ≥20 cm/s) 7 days after successful AF cardioversion identifies patients at low embolic risk, in whom the withdrawal of the anticoagulants is safe and the risk for AF recurrence low.[15] Recent application of novel TTE-derived speckle tracking echocardiography (STE) of LA function recovery after AF[23] are encouraging and could replace postcardioversion TEE in the next future.

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