Identification of Intracardiac Thrombus

Introduction

Intracardiac thrombi represent a subset of cardiac sources of embolism, are common in a variety of cardiac disease states, and account for 15%–20% of the 500,000 annual strokes in the United States. In addition, they are important sources of systemic emboli to other vascular beds. Thrombi may exist in all cardiac chambers and can either originate from an extracardiac source with migration to the heart (i.e., clot-in-transit) or arise de novo in the cardiac chambers (i.e., left atrial appendage [LAA] thrombi). In the following, we will review the appearance and differential diagnosis of thrombus and other sources of emboli and the echocardiographic methods of detecting thrombi.

Intracardiac Sources of Emboli

Similar to venous thromboembolism, arterial and intracardiac thrombi likely arise from disturbances in flow and vessel characteristics, described by Virchow triad in which there are alterations in blood flow (i.e., stasis), endothelial damage, and inherited or acquired variations in prothrombotic blood constituents. Intracardiac sources of embolism may be divided into thrombotic and nonthrombotic etiologies.

Left Ventricle

Thrombus in the left ventricle (LV) typically is as a result of myocardial infarction (MI) and subsequent local akinesis/aneurysm with stasis and exposure of prothrombotic collagen to the blood pool. As a result, thrombus almost invariably occurs in areas of hypokinesis, akinesis, or dyskinesis of the underlying LV wall segments, most commonly in the setting of an apical aneurysm. It may also occur in the setting of underlying nonischemic cardiomyopathy with reduced global ejection fraction; specific cardiomyopathies (e.g., noncompaction, Chagas, and Loeffler endocarditis) appear more predisposed to thrombus formation, presumably due to local stasis and hypercoagulability. Echocardiography is useful in detecting LV thrombi directly, as well as identifying risk factors for thrombus formation, including wall motion abnormalities and spontaneous echo contrast (SEC). There are caveats: visualization of the endocardial border and therefore clear resolution of thrombus from surrounding trabeculae may be difficult in patients with poor acoustic windows, without the use of echocardiographic contrast. Transesophageal echocardiography (TEE), despite its high resolution, may foreshorten the ventricular apex, and thus transthoracic echocardiography (TTE) is actually preferred for the identification of apical thrombi. Occasionally, even with appropriate contrast opacification, other imaging modalities such as computed tomography (CT) and cardiac magnetic resonance imaging (CMR) may be required to identify thrombus with higher fidelity.

Left Atrium

The LAA represents the most common location for atrial thrombus formation. Ninety percent of thrombi occur in the setting of atrial fibrillation of atrial flutter as a result of disorganized and ineffective contraction of the LAA causing local stasis ( Fig. 38.1 and ). When the LAA ejection velocity, measured using pulsed-wave Doppler 1 cm into the mouth of the appendage, is less than 0.4 m/s, there is an increased risk of thrombus formation ( Fig. 38.2 ). Rheumatic mitral stenosis may also contribute to left atrial (LA) enlargement, stasis, and an increased risk for LA thrombus formation and thromboembolism despite sinus rhythm. The incidence of LA thrombus with mitral stenosis in sinus rhythm is estimated to be 2.4%–13.5%, with risk factors including age greater than 44 years, LA inferosuperior dimension greater than 6.9 cm, mean mitral gradient greater than 18 mm Hg, and dense SEC. Some consider TEE warranted if any of the aforementioned risk factors are present; the absence of SEC on TEE is highly predictive of thrombus absence. In contrast to the stasis and predisposition to thrombus formation seen in mitral stenosis, significant mitral regurgitation has been associated with a lower incidence of thrombus formation and thromboembolization in individuals with rheumatic mitral valvular disease. Owing to the complex three-dimensional anatomy of the LAA with its one to four lobes, trabeculation, and interindividual variability in morphology, distinguishing thrombus from normal anatomical structures by TEE can be difficult, especially in patients with SEC ( Fig. 38.3 ).

FIG. 38.1, Transesophageal echocardiography of the left atrial appendage shows a round 2 × 1 cm structure with the echodensity and location consistent with thrombus (arrow) . Note the overlying spontaneous echo contrast. See corresponding Video 38.1 .

FIG. 38.2, Pulsed-wave Doppler at the entrance to the left atrial appendage during transesophageal echocardiography displaying (A) normal amplitude, regular contraction consistent with normal sinus rhythm, (B) variably reduced and disorganized contraction velocities in the setting of underlying atrial fibrillation, and (C) higher amplitude and more organized contraction velocities consistent with atrial flutter, compared with that of atrial fibrillation above.

FIG. 38.3, Transesophageal echocardiogram two-chamber image of the left atrial appendage, showing a multilobulated left atrial appendage with at least four lobes visualized in this particular scan plane. A small thrombus is also seen (arrow) .

Right Ventricle/Right Atrium

Although the same disease processes involved in formation of LV thrombi occur in the right ventricle (RV), the prevalence and specific predictors of RV thrombi have not been identified to date. Certain cardiomyopathies predominantly involving the RV, most notably arrhythmogenic right ventricular cardiomyopathy (ARVC), have been noted in case series to be associated with RV thrombi and may identify a group at risk of RV thrombus formation. Loeffler endocarditis (also called endomyocardial fibroelastosis) is often associated with both right and left ventricular restrictive physiology and thrombi, typically mural and involving the apices of the heart (see Chapter 24 ). In theory, one would presume that there is a higher risk for thrombus formation for mechanical prostheses in the tricuspid position due to the lower ventricular pressures in the RV versus LV, but supportive data are limited. With the increasing use of right-sided intracardiac devices such as pacemaker and defibrillator leads, whose artificial surfaces are predisposed to thrombus formation, RV thrombi are likely to be of greater importance in the future ( Fig. 38.4 and ). Venous thromboembolism that is visualized in the right atrium (RA) or RV, so called clot-in-transit, is high risk for subsequent pulmonary embolism and may appear “sausage-like” in shape on echocardiography, representing a cast of the originating lower extremity vein ( Fig. 38.5 and ; see also Fig. 35.1 and ). The RA appendage (RAA) is broad based compared with the LA and can be a source of pulmonary embolism in setting of atrial fibrillation or atrial flutter.