Abstract
Echocardiography often visualizes cardiac masses which may comprise true tumors, thrombi, and vegetations. However, there are a variety of other structures that may often be misinterpreted to be significant pathology, when in fact they are not.
These include variants of normal anatomy, degenerative or acquired masses, postsurgical changes, and ultrasound artifacts. Recognition of these findings often takes experience and knowledge of common structural variants, familiarity with surgical techniques, and an understanding of the physics of ultrasound. A comprehensive review of possible findings as well as methods of confirming their nature are covered in this chapter.
Keywords
Cardiac masses, cardiac impingement, cardiac anatomic variants, degenerative cardiac changes, echocardiographic artifact, pseudotumors, pseudoneoplasms, tumor mimics
Introduction
Among cardiac masses, the three most common types are tumors, thrombi, and vegetation. However, there are a variety of other structures that can be misinterpreted as cardiac tumors. These include normal anatomic structures or variants of the heart, abnormal structures, and echo artifacts.
With the abundance of echocardiograms being performed today, it is inevitable that variants of normal structure, echo artifacts, degenerative or acquired lesions, and noncancerous masses will be detected. The sonographer and cardiologist must be able to recognize this possibility and try to distinguish between the following entities, which can be called pseudo-neoplasms. This may require additional ultrasound transducer angles and techniques, or the adjunctive use of cardiac computed tomography (CT) or magnetic resonance imaging (MRI). Potential pseudo-neoplasms and their causes are summarized in Table 39.1 . Differentiating between true masses and false pathology is obviously particularly important if one is performing echocardiography to rule out cardiac sources of embolus or flow obstruction.
| Non-Neoplastic Masses | Normal or Variant Structures | Echo Artifact | |
|---|---|---|---|
| Left atrium | Thrombus Endocardial blood cyst | Left upper pulmonary vein (LUPV) limbus (a.k.a. “Coumadin ridge”) Lipomatous hypertrophy of the interatrial septum Interatrial septal aneurysm External compression: from hernia, thoracic aorta, esophageal bezoar, scoliosis (vertebrae), pericardial thrombus (postcardiac surgery) Atrial suture anastomosis postheart transplant Inverted LA appendage (postoperative) LA appendage pectinate muscles and trabeculations | Reverberation artifact from LUPV limbus |
| Right atrium | Thrombus (deep venous or in situ) or fibrin cast (if prior indwelling catheter/wire) Vegetation (on pacemaker/AICD wires) Lipomatous hypertrophy of the interatrial septum | Eustachian valve Chiari network Crista terminalis External compression: from pectus excavatum, liver/elevated hemidiaphragm | — |
| Left ventricle | Thrombus Apical hypertrophic cardiomyopathy Hydatid cyst ( Echinococcus ) | Calcified or multilobed papillary muscles Redundant or severed mitral chordae Trabeculations | Near-field clutter |
| Right ventricle | Thromboemboli | Redundant tricuspid chordae Tricuspid papillary muscle Moderator band | |
| Valves | Lambl excrescences Caseous mitral annular calcification Vegetation Marantic endocarditis Abscess or aneurysm Blood cyst Rheumatoid nodule | Nodules of Arantius Myxomatous/degenerative changes Pannus, loose suture, bioglue or pledgets around prosthetic valves | |
| Pericardium | Pericardial or bronchogenic cyst Rheumatoid nodule Thrombus Hydatid cyst ( Echinococcus ) | Epicardial or mediastinal fat Pectus excavatum Atelectatic lung or fibrin within pleural/peritoneal spaces Vascular pseudoaneurysm |
Thrombi and vegetations are discussed fully in separate chapters ( Chapter 38 , Chapter 40 ). Thrombi should be suspected if the mass is noted in akinetic or dyskinetic areas of the ventricle, or in the left atrial appendage. Fibrin collections (which are essentially small thrombi) can also occur on pacemaker and automated internal cardiac defibrillator (AICD) wires, as well as indwelling catheter tips, and may not necessarily imply that removal is clinically necessary. Vegetations typically occur on valves that are predisposed to infection (e.g., myxomatous, bicuspid, or calcified valves) and are usually associated with some degree of regurgitation. It should be noted that chronic or old healed vegetations can remain almost indefinitely, but tend to become smaller and more echobright with time.
Variants of Normal Structure
In the right atrium (RA), remnants of normal embryonic structures (from incomplete resorption of the right sinus venosus valve) can remain and may be mistaken for pathology ( Fig. 39.1 ) . The eustachian valve is a caudal remnant that can be prominent and elongated, but will always be anchored to the RA-inferior vena cava (IVC) junction. A Chiari network is an extension of the eustachian valve, which is reported to be found in 2%–15% of normal hearts. It appears as a reticulated network of filaments with a characteristic oscillating or whiplike motion within the right atrium ( 
). This can be seen on short-axis windows of the base of the heart, right ventricle (RV) inflow views, and apical four-chamber windows; the network may be attached to one or all of: the eustachian valve, the interatrial septum, and the upper atrium. Although they are normal structures, the eustachian valve and Chiari network can become nidi for vegetations in the presence of intravenous (IV) drug use, infected lines, or pacemaker/AICD wires. They may also become associated with thrombus in rare cases. In certain invasive procedures, such as patent foramen ovale (PFO) closures or MitraClip placement, both can also interfere with the manipulation of catheters and entrap devices (see Fig. 39.1B ).
.) ( B ) Eustachian valve (yellow arrow) , seen entangled in and tethering the anterior right atrial corner (white arrow) of a Cardioseal septal occluder, which impedes it from apposing properly to the interatrial septum (IAS) in this transesophageal echocardiography (TEE) image. ( C ) Lipomatous hypertrophy of the interatrial septum, with the characteristic dumbbell shape (arrow) . ( D ) TEE view of the left atrium and left atrial appendage, illustrating the fold, or limbus (yellow arrow) between the left upper pulmonary vein (LUPV) and left atrial appendage (see also corresponding 
). Note the reverberation artifact (white arrow) below it, which mimics a thrombus floating within the appendage. AoV , Aortic valve; LA , left atrium; RV , right ventricle. In the left atrium, on both transthoracic and transesophageal echocardiography (TEE), the left upper pulmonary vein (LUPV) limbus (i.e., the fold between the LUPV and left atrial appendage), can appear prominent and has frequently been mistaken for a mass or thrombus (see Fig. 39.1D ). However, its typical position and continuity with the appendage and atrial wall should help distinguish it, along with the lack of any associated spontaneous echo contrast. Reverberation artifact from the LUPV limbus is also frequently confused with thrombus (see 
), thus giving this tissue fold the informal moniker of “the Coumadin ridge.” Lipomatous hypertrophy is a focal echogenic thickening of the epicardial fat surrounding the interatrial septum that develops frequently in elderly or obese patients, and can be exacerbated by steroid use. It is caused an expansion (hyperplasia) of normal fat cells, which are contained within the epicardial recesses between the atria. This encroaches upon (but spares) the fossa ovalis, producing a characteristic dumbbell-shaped mass on echocardiography (see Fig. 39.1C ). It is distinguished from lipoma and other neoplasms by both its characteristic location and its lack of a discrete capsule. Although lipomatous hypertrophy may become impressively large (>2 cm), no treatment is required unless there are associated atrial arrhythmias or caval obstruction.
In the left ventricle (LV), prominent or accessory papillary muscles may be mistaken for neoplasm or thrombus ( Fig. 39.2 and 
). Multiple imaging planes and sweeping the transducer to demonstrate the structure’s attachment to the LV myocardium, the relationship with mitral chordae, and the systolic contractility will help distinguish these. In some cases, IV echo contrast (to both delineate and assess for vascularization) and/or cardiac MRI may be required to definitively distinguish between these masses and malignancy or thrombus. Other LV structures such as prominent apical trabeculations or false tendons (as in Fig. 39.4A and 
) may be mistaken for thrombi. In the RV, the moderator band and tricuspid papillary muscles may mimic neoplasms.
