Chapter 3. Anatomic Variants and Ultrasound Artifacts

Anatomic variants are variations in normal anatomy that can be misinterpreted as pathological conditions. Many anatomic variants are remnant structures from embryological development and fetal circulation, particularly in the atria. Anatomic variants are seen in multiple image planes and persist despite changes in transducer frequency, gain, compression, and depth. Ultrasound artifacts are errors in imaging most commonly due to a violation of the assumptions that are inherent in any ultrasound system. All imaging systems assume that sound travels in a straight line, travels directly back from a reflector, and travels at exactly 1540 m/s through soft tissue. Additionally, it is assumed that the ultrasound beam is very thin, reflections are entirely from structures within the main axis of the beam, and the intensity of reflections is related only to the tissue characteristics of the reflector.1 Artifacts cross known anatomic planes and boundaries and typically disappear with alternate imaging planes and when remedial actions are taken. It is vital to be familiar with the common anatomic variations and ultrasound imaging artifacts to ensure accurate echocardiographic interpretation and to avoid unnecessary interventions.2

The atria and the sinus venosus evolve in the 4th week of embryonic development. Initially, the sinus venosus receives venous blood from left and right sinus horns (Figure 3–1A and B). In time, the veins to the left sinus horn are obliterated and the remnants become the coronary sinus. The right sinus horn, on the other hand, enlarges and forms the smooth-walled part of the right atrium (RA), known as the sinus venarum. As the RA expands, the sinus venarum displaces the trabeculated tissue of the primitive RA into the periphery and into the right atrial appendage (which may have prominent pectinate muscles). Right and left venous valves mark the junction of the original sinus venarum and the primitive RA. The left venous valve disappears as it fuses with the developing atrial septum. The right venous valve of the right sinus venosus horn develops inferiorly into (1) the valve of the inferior vena cava (IVC) or the eustachian valve, which directs fetal blood flow from the IVC across the foramen ovale, and (2) the valve to the coronary sinus or the thebesian valve (Figure 3–2). Superiorly, the convergence of the smooth sinus venarum and the trabeculated RA is the crista terminalis. Concurrently, the atrial septum forms with migration of the septum primum to obliterate the ostium primum, followed by the migration of the septum secundum to cover the ostium secundum. This migration leads to the characteristic thin-walled appearance of the foramen ovale, with incomplete septation leading to the possibility of a patent foramen ovale.3

In the left atrium (LA), the smooth tissue of the pulmonary veins is incorporated into the wall of the left atrium and it displaces the primitive atrial trabeculated tissue almost entirely into the left atrial appendage. The ridge of tissue at the junction of the smooth left superior pulmonary vein and the trabeculated left atrial appendage is called the ligament of Marshall or, more colloquially, the coumadin ridge (since this structure was initially misinterpreted as a thrombus requiring anticoagulation). During the 8th week of embryonic development, the distal end of the left common cardinal vein degenerates, and the proximal portion connects via the left brachiocephalic vein to the right brachiocephalic vein, forming the superior vena cava (SVC). The left posterior cardinal vein also degenerates and the remnants of the left sinus horn, receiving venous drainage from the heart, become the coronary sinus. Failure of the left posterior cardinal vein to resorb results in a persistent left superior vena cava (PLSVC) that drains into and dilates the coronary sinus.

The anatomic variants are best classified by location, although some variant structures can appear in more than one cardiac chamber.

Right Atrium

Crista Terminalis

The crista terminalis is seen at the junction of the SVC and the RA, forming a structure that may appear to protrude longitudinally into the RA towards the IVC. This structure is often visualized in the midesophageal (ME) bicaval view and should not be mistaken for thrombus or tumor (Figure 3–3). Of note, the crista terminalis is thought to be a location where atrial tachydysrhythmias originate due to the high density of adrenergic nerve fibers, and thus may be a site for ablation therapy.4

Eustachian Valve

The eustachian valve can be found in multiple views including the ME bicaval view and right ventricular (RV) inflow-outflow views (Figure 3–4). It is seen at the junction of the IVC and RA in approximately 25% of individuals and appears as an elongated, membranous, sometimes undulating structure that can extend from the IVC to the border of the fossa ovalis. Usually it is of no physiological consequence, but it can be confused with an intracardiac thrombus, cause turbulent atrial blood flow, complicate IVC cannulation, or serve as a site for endocarditis or thrombus formation.5 Occasionally it may also appear to bisect the right atrium, simulating cor triatriatum dexter, but a eustachian valve is distinguished by a lack of flow disturbance on color-flow Doppler examination.6

Thebesian Valve

The thebesian valve is a structure that can be seen as a thin piece of tissue guarding the entrance to the coronary sinus in the ME four-chamber view with the probe slightly advanced towards the tricuspid valve. It can also be seen in a modified bicaval view inferior to the left atrium in the atrioventricular groove (Figure 3–5). This valve serves to prevent retrograde flow into the coronary sinus during atrial contraction and is inconsequential unless it inhibits cannulation of the coronary sinus for retrograde cardioplegia catheter placement or biventricular pacing wire advancement.7

Chiari Network

The Chiari network is a thin, mobile, membranous structure seen within the RA in multiple imaging views (Figure 3–6) that is thought to be a remnant of sinus venosus–derived structures. It is similar to but usually more extensively attached to intracardiac structures than the eustachian valve. The Chiari network is typically perforated and associated with the IVC orifice; however, the primary site of origin can vary to include the RA wall, interatrial septum, or the coronary sinus. The Chiari network moves toward the tricuspid valve during atrial contraction followed by a rapid posterior motion at the onset of ventricular systole. It has little clinical significance except that it has been associated with a patent foramen ovale, interatrial septal aneurysm, and paradoxical embolization. It is seen in 2% to 3% of all patients at autopsy and by TEE.8

Persistent Left Superior Vena Cava (PLSVC)

The coronary sinus is best seen with slight probe advancement in the ME four-chamber view as an echolucency in the RA, just superior to the tricuspid valve (Figure 3–7). Since it courses in the atrioventricular groove superior to the mitral valve annulus,9 it can also be seen in a modified ME bicaval view as it curves around the atrium in the atrioventricular groove (see Figure 3–5), or in cross-section in the ME two-chamber view (Figure 3–8). It is a useful structure to identify in order to assist with the placement of coronary sinus catheters for retrograde cardioplegia delivery and pacing wires for biventricular pacing. Despite echocardiographic guidance, injury to the coronary sinus during these procedures is not uncommon.10 Understanding the normal anatomy of the coronary sinus is also important for identification of an inferior sinus venosus defect. The coronary sinus is normally less than 1 cm wide and approximately 3 cm long, but can dilate as a consequence of right heart volume or pressure overload.11 Coronary sinus dilation can result from atrial hypertension, tricuspid regurgitation, or a PLSVC that drains into the coronary sinus (Figure 3–9).12 A PLSVC can also be seen between the left upper pulmonary vein and the left atrial appendage in the ME four-chamber view (Figure 3–10). Diagnosis of a PLSVC is suggested by a dilated coronary sinus (> 1.1 cm) and confirmed by injection of agitated saline into a left upper extremity vein resulting in opacification of the coronary sinus as the PLSVC flow enters the coronary sinus (see Figure 3–10) and then into the RA.

Patent Foramen Ovale

The normal foramen ovale is seen best in a ME bicaval view; it appears as a thin slice of tissue bound by thicker ridges of tissue, one of which appears as a “flap.” Up to 30% of the population may have a probe patent foramen ovale (PFO), with the possibility of right to left intracardiac shunting (Figure 3–11) when right atrial pressure exceeds that of the left atrium.13 TEE evaluation of the foramen ovale should include 2D assessment for flap movement and color-flow Doppler assessment, optimized for measurement of lower velocity flow. Injection of agitated saline (a “bubble study”) along with a Valsalva maneuver is typically used to provoke right to left shunting. In such a study, the bubbles should be injected after the Valsalva maneuver produces a decrease in RA volume, and the Valsalva should be released (so as to transiently increase RA pressure over LA pressure) when the microbubbles are first seen to enter the RA. Admixture of agitated saline with small quantities of blood has been reported to improve the acoustic signal of the microbubbles. The bubble study is positive if bubbles appear in the left atrium within five cardiac cycles (Figure 3–12).

Atrial Septal Aneurysm

This condition may be idiopathic or may develop as the result of right heart dysfunction and elevated right-sided pressures.13 The interatrial septum is enlarged and seen to be undulating between each atrium during the cardiac cycle (Figure 3–13). An interatrial septal aneurysm is defined as constituting more than 1.5 cm of the atrial septum and extending 1.5 cm into either atrial chamber (Figure 3–14). The grading system for these aneurysms is largely based on the extent of excursion into the left and right atrium (see Appendix H). Atrial septal aneurysms have been associated with PFO and Chiari network and may predispose to thrombus formation, resulting in potential paradoxical embolism and stroke.14 Percutaneously inserted closure devices for PFOs may be efficacious in patients with paradoxical emboli.15

Lipomatous Hypertrophy of the Atrial Septum

Lipomatous thickening of the interatrial septum is often quite striking, and may mimic an infiltrative process. This benign process creates a dumbbell-like appearance of the superior and inferior atrial septum, and is characterized by the lack of involvement of the fossa ovalis (Figure 3–15). The echogenic fat may also involve the right atrial wall, a finding that is associated with coronary artery disease and obesity.16

Trabeculations

Trabeculations seen on echocardiographic examinations represent the muscle bundles on the endocardial surface of the heart and are more characteristic of the RA, right atrial appendage, and right ventricle than the left atrium and ventricle. Right ventricular hypertrophy may accentuate these trabeculations.

Pectinate Muscles

A series of parallel ridges known as pectinate muscles course across the anterior endocardial surfaces of the left and right atria, including both appendages. Pectinate muscles are more apparent in the RA than in the left atrium (Figure 3–16). Prominent pectinate muscles can be distinguished from a mass or thrombus by their movement in synchrony with cardiac tissue, whereas a thrombus is often asynchronous with cardiac motion and is associated with arrhythmias such as atrial fibrillation or low flow states such as mitral stenosis.17

Right Atrial Appendage (RAA)

The RAA is most commonly seen in a ME bicaval view where the crista terminalis separates the SVC and RAA. Occasionally, the prominent trabeculations or pectinate muscles can also be seen. The RAA can also appear as an echo-free space anterior to the ascending aorta and near the right ventricular outflow tract in the ME aortic valve long-axis view.

Left Atrium

Ligament of Marshall

The atrial tissue separating the entrance of the left upper pulmonary vein (LUPV) from the left atrial appendage (LAA) commonly has multiple appearances, including a globular fatty appearance, often resembling a “Q-tip” (Figures 3–17 and 3–18). It is commonly referred to as the “warfarin” or “coumadin ridge” because it has historically been misinterpreted as a thrombus leading to treatment with anticoagulants. The ligament of Marshall is an important landmark for electrophysiological ablation procedures as it is thought to contribute to the maintenance of atrial fibrillation.18

Left Atrial Appendage (LAA)

The LAA is best seen in an ME two-chamber view where it is separated from the left superior pulmonary vein by the ligament of Marshall (Figure 3–19). Trabeculations and pectinate muscles in the LAA can be distinguished from thrombus by their synchronous movement and similar density to other cardiac tissue. Transesophageal echocardiography (TEE) is superior to transthoracic echocardiography (TTE) for identification of a cardiac embolic source in patients with a history of transient ischemic attack (TIA) or stroke.19 In addition to 2D imaging, color-flow Doppler, pulsed-wave Doppler, tissue Doppler, power Doppler, contrast echo, and 3D imaging can enhance the diagnostic process for thrombi.20,21 Pulsed Doppler is the most commonly applied technique and is performed by placing the pulsed-wave Doppler sample at the mouth of the LAA. A velocity greater than 40 cm/s in the LAA decreases the likelihood of a thrombus (Figure 3–20). Thirty to fifty percent of people also have a bilobed or multilobed left atrial appendage (Figure 3–21).22 These are often characterized by a round circle of normal-appearing tissue within the LAA which represents one lobe of the LAA that is angulated relative to the other lobe.

Right Ventricle

Moderator Band

The moderator band is the most prominent muscle band that lies in the apical third of the right ventricle (RV) and is associated with the anterior papillary muscle of the RV.23 It can be seen in long- (LAX) or short-axis (SAX) views (Figure 3–22) and can be confused with a tumor or thrombus. The moderator band is involved with the conduction system as Purkinje fibers may course through it. The left ventricle (LV) does not usually have a moderator band.

Left Ventricle

False Tendons and LV Bands

“False tendons” are finer, usually filamentous structures compared to the RV moderator band and have also been called false chordae tendineae (Figure 3–23). They usually occur between the ventricular septum and the free wall, and have an association with murmurs and arrhythmias, but they are usually of little clinical significance, other than the potential for misinterpretation as a thrombus.24 Occasionally, larger bands can occur in the LV, but unlike the RV moderator band, they are not usually associated with the conduction system (Figure 3–24).

Lambl's Excrescences

Lambl's excrescences are small filamentous structures arising from the aortic valve leaflets, usually on the aortic side of the leaflets (Figure 3–25). They occur along the line of leaflet coaptation and are usually multiple. A clinical history is usually required to distinguish these from thrombi, vegetations, and cardiac neoplasms. Distinguishing Lambl's excrescences from papillary fibroelastomas is a common clinical challenge. Papillary fibroelastomas are less likely to be filamentous and more likely to have multiple fronds. On pathological examination, they are also rich in an acid mucopolysaccharide matrix and smooth muscle cells. Lambl's excrescences do not have a clearly defined clinical significance, but have been thought to be associated with stroke. The decision to excise these when noted as an incidental finding is variable and largely dictated by a history of embolic events.25

Nodule of Arantius

This nodule-like appearance at the coaptation point of the three aortic cusps results from thickening in the middle of the free edge of the aortic valve cusps from the wear and tear of valvular opening and closing.26 The nodule can become calcified and appear as a mass on the aortic valve leaflets, or can hypertrophy and lead to aortic regurgitation.

Extracardiac Spaces

Pericardial Effusion

The normal pericardial sac contains about 15 to 30 mL of pericardial fluid that is not typically seen with TEE. However, a larger effusion separates the myocardium from the pericardium and creates an echo-free space that is easily visualized (Figure 3–26). The clinical significance of an effusion depends upon the degree of ventricular and atrial compression and the rate of fluid accumulation, and can be identified by signs such as diastolic right ventricular collapse (see Chapter 15).27 The pericardial sac may also be calcified or thickened, leading to constrictive pericarditis. Of note, pericardial fat is often confused with a pericardial effusion.28

Transverse and Oblique Sinuses

The transverse sinus is formed by a reflection of pericardium between the posterior wall of the ascending aorta, the anterior left atrium, and the posterior pulmonary artery (Figure 3–27). It may be misinterpreted as a cyst or abscess cavity, and has even been reported to contain a hemagioma.29 The transverse sinus should not have color flow in it, but can contain fibrinous material, fat, or fluid. The oblique sinus is another, more inferior pericardial reflection located posteriorly between the entry of the four pulmonary veins into the left atrium (Figure 3–28). The oblique sinus is not well visualized with TEE, but may be seen on transthoracic echo posterior to the left atrium in the parasternal long-axis view.

Pleural Effusion

Pleural effusions, lateral to the heart, can easily be identified by TEE. Left pleural effusions can be seen lateral and posterior, near the descending thoracic aorta (Figure 3–29). Right pleural effusions can be seen lateral to the heart, superior to the liver. TEE has been shown to be accurate in the identification of pleural fluid in the cardiac surgical patient, with the ability to detect a median of 125 mL of fluid on the left and 225 mL on the right.1

An artifact is any structure in an ultrasound image that does not have a corresponding anatomic tissue structure. Although artifacts are largely related to the physics of ultrasound, they can also result from operator fault or equipment failure. Artifacts can be broadly categorized as (1) missing structures, (2) degraded images, (3) falsely perceived objects, and (4) misregistered locations.30

Missing Structures

Missing structures are related to the resolution of the ultrasound beam or to shadowing from a structure that reflects ultrasound so strongly that distal structures are not imaged or are “shadowed.”

Resolution

Resolution is a property of ultrasound that allows one to differentiate two separate structures that are closely approximated.1 Lateral resolution allows one to distinguish objects in a horizontal plane and is determined by the bandwidth of the ultrasound probe. With lateral resolution artifact, two structures that are closer together than the width of the ultrasound beam will appear as a single merged structure. Thus, a small reflector such as an air bubble may also be displayed as a wide line rather than a round point. Longitudinal resolution allows one to distinguish objects in a longitudinal plane and is related to spatial pulse length. Longitudinal resolution artifact occurs when one reflection is created from two structures that are closer than one-half the spatial pulse length. Higher frequency transducers have better longitudinal resolution while lateral resolution is optimal in the focal zone where the ultrasound beam width is narrowest (Figure 3–30). Therefore, resolution (lateral and longitudinal) can be improved by increasing frequency, placing the area of interest in the focal zone, and decreasing the overall gain to better visualize distinct objects.

Acoustic Shadowing

High-density structures with high acoustic impedance can prevent the ultrasound beam from penetrating beyond them, causing an echolucent shadow deep to the dense object. Prosthetic valves, patches, or implants are common examples of such structures (Figure 3–31).31 Similarly, heavily calcified structures such as valves, mitral valve annuli, or chordae tendineae can also cause shadowing. Large shadows can be problematic as they can obstruct the evaluation of important cardiac structures (Figure 3–32),32 and alternate views may be required (Figure 3–33). For example, a prosthetic valve in the aortic position is best evaluated in the transgastric long-axis or deep transgastic views so that acoustic shadowing from the prosthesis does not obscure perivalvular leaks or other valve dysfunction. An edge shadow is a special type of shadowing that results from the refraction and divergence of sound along the edge of a curved structure.

Degraded Images

Reverberations

Reverberations typically occur when the sound wave bounces back and forth between two strong reflectors (eg, calcified structures, metallic objects, catheters, and air/fluid interfaces). Successive reflections returning to the transducer result in repeated, equally spaced images extending from the object, away from the transducer—the first two reflections closest to the transducer being real. Less commonly, reverberations can occur when a strong ultrasound signal returns to the transducer from a single reflector and is reflected back to the tissues. Once again, repeated images of the structure appear on the screen, but this time at distances that are multiples of the actual object's distance from the transducer (Figure 3–34). Reverberations are commonly seen in the descending thoracic aorta (Figure 3–35). Diagnostic criteria for reverberant images in the descending aorta include displacement parallel to aortic walls (as opposed to free movement of a flap, for example), blood flow superimposed on the artifact during color-flow Doppler imaging, and similar blood velocities on both sides of the image.33 When closely spaced reverberations merge to form a single line deep to the echo-dense object, they are known as a comet tail or ring down artifact.

Acoustic Noise/Near Field Clutter

Structures too close to the transducer can be obscured by high-amplitude oscillations of its piezoelectric elements in a phased array system.1 This is often observed in the LA and the descending aorta when imaging with a TEE probe, and can be improved by adjusting the gain settings. It is very noticeable with epiaortic and epicardial scanning, and can be minimized by physically separating the transducer from the tissue of interest with fluid or gel.

Electrical Noise

This artifact often occurs in the operating room from electrical interference and appears as “snow” on an image display. Newer transducer and ultrasound systems have incorporated electrocautery suppression software to limit this artifact.

Enhancement

Enhancement occurs when a deeper object appears more reflective (brighter) than it should because the ultrasound beam has traveled through a region with abnormally low attenuation. It is commonly seen with the anterior pericardium in a transgastric view. Adjusting the ultrasound time-gain compensation can minimize enhancement.

Falsely Perceived Objects

Refraction Artifact

When sound waves travel through relatively homogeneous media, they are propagated in essentially straight lines. However, when an ultrasound beam crosses an interface of tissues or fluid with different propagation speeds, the ultrasound beam changes direction.1 The ultrasound system, however, assumes that sound travels in a straight line from the transducer and will therefore place a second copy of an object seen in the path of the refracted wave, side by side with (at the same depth as) the true image of the object (Figure 3–36).

Mirror Images

Mirror image artifacts are produced when a strong reflector redirects the ultrasound beam, resulting in a second copy being placed deeper to the real structure. The structure that acts as a mirror lies on a direct line between the transducer and the artifact, and the true reflector and artifact are equal distances from the mirror (Figure 3–37). Mirror images that occur commonly in the descending aorta and in the aortic arch are sometimes referred to as a reverberation, but if there is only one copy, it is more aptly described as a mirror. Mirror artifacts can appear in any image plane, often causing confusion about the identity, nature, and pathology of the mirror image.34

Misregistered Locations

Side Lobes

The lateral edges of the ultrasound transducer can generate extraneous but weaker beams of ultrasound that diverge from the direction of the main ultrasound beam. Reflected signals from such extraneous beams are, however, interpreted as if they resulted from the direction of the main beam. The energy in these extraneous beams is typically much less than the main beam and often no erroneous image is created. However, when the extraneous ultrasound beams contact very reflective structures, a side lobe artifact appears as a curvilinear object at a uniform distance from the transducer (Figure 3–38).1 Side lobe artifacts create uncertainty when they appear as an unexpected object or linear structure in a cardiac chamber35 (Figure 3–39) or when imaging for the presence of aortic dissection.33 Unlike true dissections (Figure 3–40), side lobe artifacts tend to be displaced parallel to aortic walls and have similar blood flow velocities on both sides of the artifact. Imaging with multiple planes can also aid in distinguishing the true reflector from the artifact.

Speed Errors

A speed error artifact occurs when the sound wave travels through an object that has a propagation speed different from that of soft tissue. If the propagation speed is slower than that in soft tissue, reflectors are placed deeper on the image than they really are because sound is traveling slower than the ultrasound system assumes. Similarly, if the propagation speed is faster, the reflector will be shallower.

Aliasing

Aliasing of Doppler flow can introduce confusion regarding the direction of blood flow and can prevent measurement of a peak velocity. Aliasing is produced when the Doppler frequency shift exceeds one-half the pulse repetition frequency (PRF), also known as the Nyquist limit. The PRF determines the maximal Doppler shift, or maximum velocity, that is reliably measured by the transducer. When the velocity of the sound wave in question is greater than the Nyquist limit, the system cannot sample frequently enough to accurately detect the velocity. As a result, the signal is displayed as starting correctly, but once it reaches the Nyquist limit it “wraps around” the scale, appearing to come from the opposite side of the baseline (Figure 3–41). Aliasing does not occur with continuous-wave Doppler, as with this modality the system is continuously sending and receiving ultrasound; thus, it can accurately measure all velocities. The aliasing artifact can be overcome by increasing the velocity scale to the maximum, using a lower-frequency transducer (lower Doppler shifts), selecting a shallower depth (increased PRF), using continuous-wave Doppler, or shifting the baseline. As color-flow Doppler is a pulsed ultrasound technique, it can alias as well (Figure 3–42). In this situation, when the blood flow velocity exceeds the Nyquist limit, the flow is assigned the color on the opposite end of the color bar—giving the impression (if one was only to look at the color) that the blood flow had turned around to flow in the opposite direction (Figure 3–43). However, this is just the color Doppler version of “wrap around.”

Ghosting and Clutter

Movement of heart muscle or vessel walls produces very low-frequency Doppler shifts that can be detected by ultrasound systems. In spectral Doppler, these low-frequency shifts are known as clutter, while in color-flow Doppler, they are known as a ghosting artifact.

Three-Dimensional Echocardiography

Just as 2D echocardiography reveals normal anatomic variants and is subject to artifacts, so is 3D echocardiography. The anatomic variants are the same as seen in 2D imaging, but must be identified as such with 3D imaging. Similarly, many of the artifacts seen with 2D echocardiography are also seen with 3D echocardiography, including side lobe generation and attenuation of beam intensity, leading to blurry images in the far field.36,37 Two other artifacts are particularly relevant to 3D imaging. First, a “stitch” artifact may occur with the acquisition of a full-volume image during a disturbance of cardiac rhythm, patient movement, or operator movement. This is because a full-volume image is acquired from several sub-volume images, which are “stitched” together to create a full-volume image. If any one of the sub-volume images does not match the other sub-volumes with respect to cardiac cycle or position, then a jagged or blurred interface occurs in the image (Figure 3–44). This 3D imaging artifact does not occur with real-time 3D imaging where sub-volumes are not melded together; real-time full-volume imaging would, however, still be subject to a “stitch” artifact.38 A dropout artifact can also occur when the z-axis is not monitored properly, the gain setting is too low (no image acquired), or the gain setting is too high (leading to masking).36,37

Artifacts of Display

The interpretation of a 2D or 3D image can be confused by inappropriate use of spectral gain, color-flow sector size, image depth, and/or changes in the color-flow velocity scale or color-flow gain.

Appropriate interpretation of ultrasound images is necessary to diagnose both pathological and normal conditions, thereby leading to suitable interventions. Thus, it is important to be familiar with the common variants and artifacts as well as the common pathological conditions that variants and artifacts may be confused with.

A few key questions or observations may assist in determining if a structure is pathologic or is simply a normal anatomic variant or ultrasound artifact:

1. Is the density and texture of the structure the same as the rest of the heart? If yes, then the structure is likely to be a variant.

2. Does the structure move synchronously with the rest of the heart? If yes, then the structure is likely to be a variant.

3. Does the structure appear in multiple planes and views? If yes, then the structure is not likely to be an artifact.

4. Does the structure cross anatomic boundaries? If yes, then it is likely to be an artifact.

5. Look for secondary signs and clues. For example, if the patient has poor left ventricular function and/or is in atrial fibrillation, then a thrombus in either atrial appendage or the LV is likely.

6. Use various views to reduce the impact of artifacts; for example, use a deep transgastric view to assess prosthetic aortic valves to avoid acoustic shadow interference.

7. Use agitated saline injections to identify shunts, persistent left superior vena cavae, or distinguish intracardiac spaces from extracardiac spaces.