The anatomic variants are best classified by location, although some variant structures can appear in more than one cardiac chamber.
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
The crista terminalis is shown at the arrow.
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
The eustachian valve is shown at the arrow. A pulmonary artery catheter is also seen inferior to the eustachian valve as a round structure in the right atrium creating an acoustic shadow.
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
The thebesian valve (arrow) is shown at the mouth of the coronary sinus.
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
The Chiari network is shown at the arrow.
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.
Dilated coronary sinus (CS) is shown just superior to the tricuspid valve (TV). A pulmonary artery catheter is visible in the right atrium. (RV, right ventricle; LV, left ventricle.)
A normal coronary sinus is shown at the arrow. The circular echolucency on the right side of the image (near the asterisk) may be the coronary sinus or the circumflex artery.
A drawing of a persistent left superior vena cava.
Opacification of the coronary sinus (arrow) after injection of agitated saline into a left arm vein. The bubbles have coursed into the right atrium and ventricle as well.
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).
A drawing of persistent foramen ovale.
Positive bubble study in a patient with a patent foramen ovale (PFO). The arrow points to the PFO through which bubbles (left of arrow) have entered the left atrium (LA). (RA, right atrium.)
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
An interatrial septal aneurysm is demonstrated at the arrow. (LA, left atrium; RA, right atrium.)
The image demonstrates the use of M-mode to measure the excursion of an interatrial septal aneurysm.
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
Lipomatous hypertrophy of the interatrial septum (arrows). The thin flap of the fossa ovalis is seen in between the hypertrophied sections of the atrial septum.
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.
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
Pectinate muscles are demonstrated in the periphery of the right atrium as small round echo densities—like “pearls on a string.”
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.
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
Ligament of Marshall or “coumadin ridge” is shown at the arrow. It often looks like a Q-tip and separates the left upper pulmonary vein and the left atrial appendage.
Three-dimensional image of the ligament of Marshall (arrow). (LAA, left atrial appendage; LUPV, left upper pulmonary vein.)
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.
A normal left atrial appendage is shown. (LAA, left atrial appendage.)
Pulsed Doppler flow in the left atrial appendage from a patient with atrial fibrillation demonstrating flow greater than 40 cm/s.
A bilobed left atrial appendage is demonstrated at the arrows. Note the ligament of Marshall is located posteriorly, appearing as a “Q tip.”
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.
A moderator band in the right ventricle is demonstrated in short-axis at the arrow.
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).
A false tendon in the left ventricle is shown at the arrow. The linear echo density in the right ventricle is a side lobe artifact from the pulmonary artery catheter.
A large left ventricular band is shown at the arrow.
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
Lambl's excrescence is shown at the arrow.
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.
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
A pericardial effusion is demonstrated at the arrow.
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.
The transverse sinus is shown at the arrow. It is a pericardial reflection noted between the left atrium, the pulmonary artery, and the aorta.
A drawing of the oblique pericardial sinus, located posterior to the left atrium (LA), between the entry of the four pulmonary veins into the LA. (SVC, superior vena cava; IVC, inferior vena cava; LUPV, left upper pulmonary vein; LLPV, left lower pulmonary vein; RUPV, right upper pulmonary vein; RLPV, right lower pulmonary vein.)
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
A pleural effusion adjacent to the descending thoracic aorta (AO) is seen at the arrow.