Because the left atrium (LA) lies just anterior to the esophagus in most patients, the LA can be seen in the near field (ie, at the top) of most midesophageal (ME) images of the heart (probe tip is approximately 35 cm from the teeth and anteriorly oriented). Evaluation of the LA usually starts from an ME 4-chamber view (Fig. 31-3A; multiplane angle at 0 to 20 degrees with transducer slightly retroflexed from the neutral position). It can be evaluated further as the multiplane angle sweeps from 0 to 120 degrees. Within the LA, a tissue ridge ("Coumadin ridge") separates the LAA and left upper pulmonary vein (Fig. 31-3B, 31-3C, and 31-3D). This atrial tissue can accumulate fat, creating a mass-like appearance. Because the majority of LA thrombi are located within the LAA, this structure should always be interrogated. The normal LAA is lined with ridges of pectinate muscle, which may be difficult to differentiate from small thrombi. Thrombi are generally more rounded and often fill the appendage.
A. Standard midesophageal 4-chamber view. B. Midesophageal 4-chamber view with an atrial myxoma (arrow). C. Midesophageal 2-chamber view with left atrial appendage (LAA) and Coumadin ridge (arrow). D. Three-dimensional transesophageal echocardiography zoom of the LAA adjacent to the ligamentum of Marshall and the left superior pulmonary vein (LSPV). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
LA thrombus usually is associated with high-risk structural and functional heart disease, most commonly atrial fibrillation, mitral stenosis, MV prosthesis, or LA enlargement resulting from LV dysfunction. These structural and functional cardiac abnormalities tend to be associated with blood stasis within the LA, which facilitates thrombus formation. Mitral regurgitation (MR) may decrease LA stasis and protect against LA thrombus formation. Aortic stenosis (AS) or an AV prosthesis usually does not result in significant LA stasis unless accompanied by LV dysfunction. Thrombus usually is homogeneous in appearance, more echogenic than the underlying myocardium, appears in multiple imaging planes, and moves in concert with the underlying myocardium.
TEE is considered the gold standard imaging modality for detection of LA and LAA thrombi. This is partly because of the large percentage of LA thrombi that are found in the LAA, which can be well delineated by TEE. The LAA can be evaluated by keeping the LAA centered in the image and rotating the multiplane angle from 0 to 180 degrees. Spontaneous echo contrast (SEC), seen as a slowly swirling "smoke" pattern, indicates low-flow velocities that are strongly associated with LA thrombus. Doppler interrogation of the LA appendage also may be helpful because lower blood flow velocities identify patients at higher risk. Despite a relatively high specificity, 2D TEE imaging may overestimate the incidence of thrombi partly because of the complex 3D morphology of multilobed LAA.31 This complex structure of the LAA lends itself well to 3D assessment. Recent reports using RT 3D TTE or reconstruction 3D TEE showed that 3D assessment enables excellent visualization of the LAA anatomy and function.32-34 Furthermore, RT 3D TEE provides excellent visualization of the LAA orifice, which may optimize the guidance for the placement of LAA occlusion devices.35 Successful application of RT 3D TEE to confirm stable catheter position along the entire length of the ligament of Marshall during LA catheter ablation for atrial fibrillation has also been described. RT 3D TEE could potentially enhance lesion delivery during LA catheter ablation for atrial fibrillation to improve efficacy and safety.36 Furthermore, RT 3D TEE might become the method of choice to more accurately evaluate the LAA, especially to distinguish thrombi from anatomical variants and might alter the course of therapy in patients with atrial fibrillation, including the placement of a LAA occlusion device.37 The LAA can be best visualized by using the 3D zoom mode, obtaining the en face view of the LAA with the adjacent ligament of Marshall (Fig. 31-3D).
Evaluation of the right atrium (RA) can be approached from the ME 4-chamber view, ME bicaval view (Fig. 31-4A; probe turned to the patient's right with a multiplane angle of 110-120 degrees), ME RV inflow–outflow view (Fig. 31-4B; 40-60 degrees), and transgastric (TG) RV inflow view (rotating the angle to 90 degrees and turning the probe to the right from the TG short-axis [SAX] view). The RA is a thin-walled structure. The superior vena cava (SVC) and inferior vena cava (IVC) enter the RA posteriorly and medially, respectively. The coronary sinus (CS) can be imaged echocardiographically as a small tubular sonolucency in the posterior atrioventricular (AV) groove. Remnant embryonic structures should be distinguished from thrombi and other masses. The eustachian valve is an elongated, membranous projection at the junction of the RA and IVC. The Chiari network, a delicate, mobile structure often arising from the eustachian valve and stretching to the interatrial septum (IAS), may be misdiagnosed as an atrial mass. The crista terminalis is a vertical ridge of muscle originating at the junction of the RA and SVC. It runs toward the IVC and has also been misinterpreted as an intracardiac mass. Central venous catheters, pulmonary artery catheters, and pacing wires often can be seen as they course through the right heart and should not be confused as pathologic masses. RA thrombi typically are associated with indwelling catheters or pacemaker leads.
A. Standard midesophageal bicaval view with crista terminalis (arrow) visualized. B. Standard midesophageal right ventricular inflow–outflow view in a patient with a large aortic valve. Down arrow indicates tricuspid valve; uparrow indicates pulmonic valve. AV, aortic valve; LA, left atrium; PA, pulmonary artery; RA, right atrium; RV, right ventricle; SVC, superior vena cava.
The IAS consists of the thin fossa ovalis centrally and thicker limbus regions anteriorly and posteriorly. The IAS should be examined with both 2D and CFD, which adds to the detection of interatrial shunts. Three-dimensional TEE imaging provides excellent RT images of the IAS and atrial septum defects and aids in guiding percutaneous placement of IAS closure devices (Fig. 31-5A).38
A. Three-dimensional (3D) transesophageal echocardiography (TEE) image of the left atrial disk of an Amplatzer atrial septal defect (ASD) occluder. B. Rims of a secundum ASD as image with 3D TEE from the left atrial aspect of a secundum ASD (asterisk).
Structural atrial septal defects (ASDs) can be divided anatomically into defects at the fossa ovalis (ostium secundum type), defects occurring inferior to the fossa ovalis (ostium primum type), and defects occurring superior to the fossa ovalis (sinus venosus type). The most common defect is the ostium secundum type, in which the posterior atrial wall may be totally absent (Fig. 31-5B). The ostium primum type usually can be seen inferior to the fossa ovalis in the ME 4-chamber view. It is associated with other endocardial cushion defects, such as ventricular septal defects, AV canal defects, and TV or MV abnormalities. The sinus venous type of ASD lies superior to the fossa ovalis close to the opening of the SVC. It may be best seen from an ME bicaval view.
A patent foramen ovale (PFO) is a flaplike opening between the atrial septa primum and secundum at the location of the fossa ovalis that persists after age 1 year. In utero, the foramen ovale serves as a physiologic conduit for right-to-left shunting. PFO is a common functional secundum ASD that results from failure of the septa primum and secundum to completely fuse (Fig. 31-6A), allowing an interatrial shunt to occur under certain hemodynamic conditions. TEE is the diagnostic standard for detecting PFO, which is present in approximately 20% of adults. The ME bicaval view often is best for detecting this lesion. CFD interrogations of the IAS and contrast echocardiography both have high sensitivity and specificity for detecting PFO. Intravenous injection of agitated saline often is used intraoperatively to produce a contrast effect (Fig. 31-6C), a maneuver that can be monitored with either 2D or 3D TEE. Simultaneous release of a breath-holding maneuver will increase RA pressures relative to LA pressures and may open a functionally closed PFO.
A. Turbulent flow through a patent foramen ovale between the septum primum (SP) and septum secundum portion of the interatrial septum (arrow). B. Midesophageal bicaval view (with imaging depth reduced) with color-flow Doppler interrogation of the interatrial septum in a patient with a patent foramen ovale (not clearly demonstrated in this frame) and lipomatous hypertrophy of the SP portion of the interatrial septum. C. Contrast echocardiography ("bubble study") showing bubbles (long yellow arrow) that have crossed through a patent foramen ovale (short yellow arrow). D. Three-dimensional transesophageal echocardiography zoom en face view demonstrating a left atrial myxoma attached to the interatrial septum above the mitral valve with the anterior mitral leaflet (AML) on the top and the posterior mitral leaflet (PML) on the bottom (asterisk denotes the aortic valve). LA, left atrium; RA, right atrium.
In the presence of an ASD with left-to-right shunting, the LA usually appears normal, and the RA and RV enlarge from volume overload. As pulmonary hypertension occurs, the RV wall becomes hypertrophied. With an ASD, the pulmonary vasculature dilates and can be as wide as the aorta.
Lipomatous hypertrophy of the atrial septum is a peripherally thickened septum surrounding the thin fossa ovalis (Fig. 31-6B). It results from fat deposits in the atrial septum and should not be confused with intra-atrial masses such as myxomas.
An atrial septal aneurysm is an outpouching of thin, mobile, redundant tissue in the region of the fossa ovalis. The atrial septum is considered to be aneurysmal when a portion at least 15 mm wide has an interatrial excursion of at least 15 mm. Atrial septal aneurysm formation may be secondary to increased interatrial pressure gradients, producing a bulging septal shift toward the low-pressure side, and has been associated with the occurrence of a PFO.39 An atrial septum aneurysm must be considered in the differential diagnosis of atrial cysts and tumors and has been related to atrial arrhythmias, systemic and pulmonary embolism, MV prolapse, and ASD.
Metastatic cardiac tumors are more common than primary cardiac tumors. Metastatic disease may result from contiguous extension, lymphangitic spread, or hematogenous spread from the primary tumor. It tends to involve the pericardium and myocardium rather than the valves and endocardium. Extension of tumor thrombus via the IVC into the RA is a well-recognized complication of advanced renal cell carcinoma.
Myxomas, the most common primary cardiac tumors, account for approximately 50% of all primary cardiac tumors. Myxomas can cause obstruction and embolization, making prompt surgical removal mandatory. Myxomas usually are solitary and are found most commonly within the LA (Figs. 31-3B and 31-6D), originating from the IAS (often the fossa ovalis). Myxomas characteristically have hemorrhagic cystic spaces and possibly areas of calcification.
Assessment of regional and global systolic LV function often is the primary indication for perioperative echocardiography. TEE is well suited to providing accurate evaluation and monitoring of ventricular filling and systolic function during hemodynamic instability. For purposes of identifying wall motion abnormalities, the ASE divides the LV into 17 segments (Fig. 31-7).40 The basal and midlevels of the LV each have inferior, inferolateral (formerly termed posterior), anterolateral, anterior, anteroseptal, and inferoseptal segments. The apical level has inferior, lateral, anterior, and septal segments. The apical cap is the final segment. All segments (except the apical cap) can be visualized from either an ME or TG probe location. If wall motion abnormalities are observed, the typical blood supply patterns (or actual blood supply patterns from a previous angiogram) to these segments can help identify the compromised coronary artery or graft.
Depiction of the American Society of Echocardiography's 17 left ventricular wall segments, with color coding according to normal variations of coronary blood flow. 1, Basal anteroseptal; 2, basal anterior; 3, basal anterolateral; 4, basal inferolateral; 5, basal inferior; 6, basal inferoseptal; 7, mid anteroseptal; 8, mid anterior; 9, mid anterolateral; 10, mid inferolateral; 11, mid inferior; 12, mid inferoseptal; 13, apical anterior; 14, apical lateral; 15, apical inferior; 16, apical septal; 17, apical cap (apex). LAD, left anterior descending coronary artery; LCX, left circumflex artery; RCA, right coronary artery.
A wall motion description should be assigned for each segment. Mild hypokinesis refers to a decrease in inward wall movement and a 10% to 30% increase in endocardial systolic thickening (normal is >30%). Severe hypokinesis refers to only slight wall movement and less than 10% thickening. Akinesis refers to lack of both movement and endocardial thickening (indicating severe ischemia or infarct). Dyskinesis refers to outward wall movement and endocardial thinning during systole (indicating old infarct). Movement may be passive because of contraction of adjacent segments or translational movement of the heart, so thickening is believed to be more reliable than wall movement in determining wall motion abnormalities. If scaled scores are assigned to each type of wall motion abnormality, the average of those scores from each segment provides a semiquantitative assessment of global ventricular function, termed the wall motion index. The wall motion index can be converted to estimate ejection fraction (EF) and results in good agreement with other measures of EF.41
Many other measures of global ventricular function can be made; only the most common are discussed here. Fractional area change (FAC) can be obtained from the TG SAX view ("donut view"). It is simply the proportion of diastolic area of the LV chamber in the midpapillary SAX view (Fig. 31-8A and 31-8B) that is reduced during systole:
A. Basal transgastric short-axis view showing open mitral valve. Posterior (up arrow) and anterior (down arrow) mitral leaflets. B. Midpapillary transgastric short-axis view. Posteromedial papillary muscle (up arrow) and anterolateral papillary muscle (down arrow).
Although FAC often is estimated visually, the chamber circumference can be traced in both systole and diastole to provide the areas for more accurate calculation. Because FAC is measured in only 1 plane, it may miss significant wall motion abnormalities outside that plane and therefore has limited accuracy in the assessment of overall ventricular function. Oblique planes of view also may reduce accuracy.
The LV EF, which includes the volume change of the whole ventricle rather than the area change of a change.
Generating accurate 3D volumes from 2D echocardiography can be a source of error. Multiple geometric methods have been developed that assume that the ventricle fits a stereotypical ellipsoidal shape. They include the single-plane ellipsoid method, cylinder–hemi-ellipsoid method, and area–length method; all of these methods estimate volume from diameter and length measurements in 1 or 2 planes. These geometric assumptions limit the accuracy of EF estimation when segmental wall motion abnormalities or unusual ventricular shapes are present. If the plane of measurement does not include the true apex, termed a foreshortened view, then the volumes and EF will be unreliable.
The modified Simpson method, also known as the disk summation method, is considered the best method for deriving ventricular volumes and EF from 2D echocardiography. For this method, the endocardial border is traced in 2 orthogonal planes (eg, ME 4-chamber and 2-chamber views). Computer software then models the ventricle as a series of 20 or more stacked elliptical disks (Fig. 31-9). The volume of each disk then is calculated from the thickness of the disk and the diameters of each ellipsoid disk (Fig. 31-9C), and all of the individual disk volumes are summed to yield the total volume of the ventricle. Similar cylindrical disks or rotating ellipsoid models can be generated from a single tomographic view but with reduced accuracy. This biplane disk summation method allows for variably shaped ventricles. It also can account for significant regional wall motion abnormalities but still may be limited by image quality or foreshortened views. To reduce foreshortening errors, the 2 orthogonal views should not be combined if the chamber lengths appear to differ by more than 20%.
Ejection fraction calculated using the disk summation method from 4-chamber end diastole (A), 2-chamber end diastole (B), 4-chamber end-systole (C), and 2-chamber end systole (D) tracings. E. Depiction of a single Simpson disk with elliptical diameters measured from midesophageal 4-chamber and 2-chamber views. Using the software package of the transesophageal echocardiography machines, the volume of each theoretical disk is automatically calculated separately in this way and then summed together to obtain the left ventricular volume in both end diastole and end systole, allowing for calculation of ejection fraction.
In clinical practice, the assessment of the LVEF is routinely performed by "eye-balling," which relies on the echocardiographer's experience and ability to visually integrate spatial information. Further limitations of 2D TEE assessment of the LVEF are attributed to the use of foreshortened views of the LV and the reliance on geometric assumptions to calculate volumetric parameters. However, the reliability of visual estimation of EF by an experienced echocardiographer appears to be similar to wall motion index and EF calculations using the Simpson rule.41
The advent of 3D echocardiography along with built-in quantification software, which is based on semiautomated endocardial border detection, allows obtaining fast and accurate measurements of global and regional LV function.42-44 Studies comparing magnetic resonance imaging (MRI) with 3D echocardiography for the assessment of LV mass and function show very good correlation and agreement that is superior to 2D echocardiography.45 This also holds true for RT 3D TTE assessment of patients with cardiomyopathies or regional wall motion abnormalities secondary to myocardial infarction (MI) with abnormal LV geometry.46-48 A recent study suggests that LV function assessment based on 3D-TEE data offers a more reliable perioperative quantification, especially for less experienced users.49 However, further research comparing 3D TEE with a gold standard such as MRI is required to assess if 3D TEE is superior to 2D TEE in assessing the LV function.
The best mode to assess global and regional LV function by 3D TEE is the full-volume mode, which is acquired based on the ME 4-chamber view. Using built-in software, data for both global LV function as well as regional wall motion abnormalities are obtained in a semiautomatic fashion. The software relies on automatic endocardial border detection and border-tracking algorithms, which can be edited manually. Global LV function is assessed by analysis of end-systolic and end-diastolic volumes, stroke volumes, and EF. Upon completion of the analysis, as many as 17 regional waveforms are displayed simultaneously, thus enabling objective wall motion comparisons. This requires a manually performed definition of the septal, lateral, anterior, inferior, and apical endocardial borders of the LV in the end-systolic and the end-diastolic frames followed by an automatic border-tracking algorithm (Fig. 31-10A). The system will then calculate end-systolic as well as the end-diastolic volumes by summation of the voxels enclosed by the endocardial borders. Thereafter, global stroke volume and EF are derived. The obtained shell view (Fig. 31-10D) is subdivided into 17 regions, which are analyzed separately by performing the "segment analysis," and 17 segmental time-volume waveforms are displayed simultaneously offering the possibility for objective wall motion comparisons (Fig. 31-10A). Activation of "show reference mesh" displays the end-diastolic surface mesh as a diastolic reference point (Fig. 31-10C). Other viewing modes include the "iSlice" view (Fig. 31-10B), which displays 4 and up to 16 simultaneously moving SAX views of the LV and allows verifying appropriate endocardial border detection as well as the "Slice Plane" view, which shows a moving LV surface mesh within 3 orthogonal axis planes (Fig. 31-10C).
A. Three-dimensional (3D) transesophageal echocardiography (TEE) full volume of the entire heart displayed in 3 multiplanar reconstruction planes (MPRs, green = 4-chamber view; red = 2-chamber view; and blue = midpapillary short axis view). Manual definition of septal, lateral, anterior, inferior, and apical endocardial border points of the left ventricle (LV) in end systole and end diastole followed by an automatic border-tracking algorithm and segmental analysis will display the LV shell in 17 segments (rightlower quadrant) along with the corresponding segmental time-volume waveforms. The iSlice view (13C) (B). the slice plane view with end-diastolic reference mesh (C), and the LV shell views (D) are alternative options for display of the data.
Neither FAC nor EF is a pure index of myocardial contractility because both depend on loading conditions, especially at the extremes of preload and afterload. Attempts have been made to measure load-independent indices of ventricular function. Generation of pressure–volume loops at different loading conditions results in a linear end-systolic relationship, the slope of which is termed end-systolic elastance. The area within pressure–volume loops is stroke work, which can be plotted against the corresponding end-diastolic volumes to obtain preload-recruitable work. These measures are much more complex and include measuring intraventricular pressures or their surrogates and thus are principally used for research purposes at this time.
Less load-dependent measures that are easier to obtain, although rarely reported, include the peak systolic pressure-end systolic volume ratio and cardiac power. Mean cardiac power is the product of stroke volume, mean arterial pressure, and heart rate. Peak instantaneous power also can be calculated. These measures can be corrected for end-diastolic volume to make them load independent. If MR is present, dP/dt of the MR jet is a relatively load-independent measure of contractility, which is otherwise difficult to assess when ventricular work is lost into the lower-pressure LA. The myocardial performance index is the sum of isovolumic contraction time and isovolumic relaxation time divided by ejection time. It combines systolic and diastolic function into one easily obtainable and reproducible index that has good prognostic value.50 All of these measures have the benefit of being independent of ventricular geometry and the subjective determination of endocardial borders.
Diastole is divided into 4 distinct phases: isovolumic relaxation, early rapid filling, diastasis, and atrial contraction (Fig. 31-11). Isovolumic relaxation begins with closure of the AV. The LV chamber relaxes, and the pressure within the LV decreases. When the pressure falls below the pressure in the LA, the MV opens, ending the period of isovolumic relaxation. Isovolumic relaxation is an active, energy-dependent process; therefore, abnormalities in systolic function usually are accompanied by abnormalities in isovolumic relaxation. Blood flowing through the MV initiates the early rapid filling phase. The rapid filling of the chamber (early diastole) depends on both LV relaxation (an active process) and chamber compliance (a passive property). As volume fills the ventricle, the pressures between the atrium and the ventricle equalize and the flow begins to slow. This period is referred to as diastasis because there is little blood flow between the chambers. The MV leaflets remain in an open position, and the duration of diastasis depends on heart rate and chamber compliance. With the onset of atrial contraction, atrial pressures become greater than ventricular pressures, so again there is a net flow of blood into the ventricle. In normal individuals, atrial contraction contributes approximately 20% to the end-diastolic ventricular volume. The atrial contraction phase depends on the chamber compliance, LA function, and the electrical conduction system.
Pressure tracings from a normal cardiac cycle. Pressure differences (which cannot be measured directly by transesophageal echocardiography [TEE]) between chambers drive the corresponding flow velocities (which are measured with TEE to calculate pressure differences). A, atrial contraction; D, diastasis; ERF, early rapid filling; IVRT, isovolumic relaxation time; LA, left atrium; LV, left ventricle.
From the preceding discussion, one can conclude that flow is driven primarily by pressure gradients between the atrium and the ventricle. For a given pressure, if LV relaxation is brisk, the result is a large, early pressure gradient (often even a suction effect) that drives filling during early diastole. This results in less filling in late diastole. On the other hand, if ventricular relaxation is sluggish, early diastolic filling declines and a greater proportion of diastolic filling is seen in late diastole. In the latter situation, there is a greater dependence on atrial contraction for filling.
It follows then that a decrease in LV relaxation or compliance will lead to a compensatory increase in LA pressures to maintain end-diastolic ventricular volume. Because the rate of LV relaxation and increase in LA pressures is a continuum, many different transmitral pressure gradients and LV filling patterns are possible. This leads to a challenge in quantifying diastolic dysfunction over the continuum of varying patient conditions.
Doppler echocardiography, by virtue of its ability to evaluate flow patterns across valves and in large blood vessels, allows the clinician to diagnose diastolic dysfunction. Two-dimensional echocardiographic inspection of the ventricular systolic function may provide an alternative cause for a patient's heart failure or suggest that diastolic dysfunction is likely. For example, if a patient with the clinical picture of heart failure is found to have normal ventricular systolic function and volumes but LV hypertrophy (end-diastolic wall thickness >1.1 cm) is present, diastolic heart failure is likely. Combined systolic and diastolic failure may be present or a patient may have ventricular hypertrophy without measurable diastolic abnormalities. Therefore, 2D findings are neither sensitive nor specific for diastolic dysfunction, and further investigation is warranted. Therefore, two-dimensional echocardiography is most useful in helping to quantify systolic function and to differentiate isolated diastolic dysfunction from combined systolic–diastolic dysfunction. To fully assess diastolic function, use of Doppler echocardiography techniques is necessary.
The period required for isovolumic relaxation (first phase of diastole) is the isovolumic relaxation time (IVRT). IVRT is measured as the time interval from closure of the AV to opening of the MV. IVRT can be obtained from the deep TG long-axis (LAX) view (multiplane angle at 90 degrees) with a PWD sample at (or CWD through) the junction of the MV inflow and the LV outflow tract (LVOT). Normally, IVRT lasts 60 to 90 milliseconds and reflects the rate of myocardial relaxation. Impaired relaxation delays the decrease in ventricular pressure below that of the atrium, resulting in prolonged IVRT. It probably is the most sensitive Doppler index for detecting impaired relaxation because it is the first to become abnormal, but it is dependent on afterload and heart rate.
If a PWD sample is acquired near the coaptation point of the MV leaflets, transmitral flow velocities can be mapped and measured, corresponding to early diastolic filling. Flow at this time is directed away from the transducer (below the baseline). This wave is the early or E wave. The time required for the flow velocity to return to zero (from the peak of the E wave back to the baseline) is the deceleration time. For a brief time, there is no flow across the MV, and the velocities remain zero (diastasis). Soon after, the LA contracts, and flow again begins. Plotting these velocities versus time will yield the atrial or A wave. The total duration of the A wave (from the end of diastasis to the return of zero flow) is termed A-wave duration (Adur).
Normally, most diastolic filling occurs in early diastole so that the E/A ratio is greater than 1 (Fig. 31-12A). However, mitral flow velocity curves vary with loading conditions, age, and heart rate. In healthy young patients, the E/A ratio may be as high as 2. As people get older, LV relaxation slows; there is a gradual decrease in the peak E-wave velocity and an increase in the A-wave component. In most individuals, E and A become approximately equal in the sixth decade of life. Because relaxation is impaired beyond what is "normal" for age, early diastolic filling decreases.
A. Normal transmitral flow velocities. B. Pseudonormal transmitral flow velocities in a patient with regurgitant mitral flow. C. Restrictive diastolic dysfunction in a patient with mitral regurgitation. A, A wave of atrial contraction; E, E wave of early diastolic filling; MR, regurgitant mitral flow velocities (aliasing, a limitation of pulsed-wave Doppler, is also demonstrated, with some mitral regurgitation velocities incorrectly displayed below the baseline as forward velocity).
With diastolic dysfunction, the volume that remains in the atrium at the end of the early filling phase increases, and a progressively vigorous compensatory atrial contraction ("atrial kick") occurs. This results in a reversed E/A ratio (E/A <0.75; delayed relaxation pattern). In this case, the deceleration time is increased (>220 milliseconds) and IVRT is increased (>100 milliseconds).
With further diastolic dysfunction, LV compliance is even lower, and filling pressures begin to increase. This leads to a compensatory increase in LA atrial pressure, resulting in increased early filling velocities despite impaired relaxation. The filling pattern appears relatively normal (termed pseudonormalization), and the E/A ratio returns to approximately 1 (Fig. 31-12B). Pseudonormalization represents abnormalities of both relaxation and compliance and can be distinguished from normal filling by a shortened deceleration time.
In patients with severely decreased LV compliance, LA pressure is markedly elevated and drives vigorous early diastolic filling velocities despite impaired relaxation. This restrictive filling pattern (E/A >1.5) is consistent with an abnormal increase in LV diastolic pressure and an abrupt deceleration of early diastolic flow (deceleration time <150 milliseconds) with little additional filling during mid-diastole and atrial contraction (Fig. 31-12C). In the extreme case, the change in pressure in the ventricle exceeds LA pressure so that MR in mid-diastole may occur.
Analysis of pulmonary venous filling patterns provides additional information about LV diastolic function. PWD is used to sample pulmonary venous flow approximately 1.5 to 2.0 cm within the left upper pulmonary vein (or alternatively the right upper pulmonary vein). Flow from the pulmonary veins into the LA occurs in 3 phases: systolic phase (S wave), diastolic phase (D wave), and retrograde flow with atrial contraction (A wave). Under normal conditions (LA pressure is normal and the MV is competent), most of the flow into the atrium occurs during ventricular systole (S-wave velocity > D-wave velocity) as the MV annulus is pulled downward (Fig. 31-13A). During diastole, additional blood flows from the pulmonary veins into the LA, which is simultaneously emptying into the LV. During atrial contraction, blood is ejected into the LV, with a small amount of retrograde flow into the pulmonary veins. The smaller A wave is in the opposite direction to the S and D waves.
A. Normal pulmonary venous flow velocities (S wave > D wave). B. Abnormal pulmonary venous flow velocities (D wave > S wave) from diastolic dysfunction. A, retrograde atrial flow wave; D, diastolic phase wave; S, systolic phase wave.
As pressure in the LA increases (compensating for advancing diastolic dysfunction), systolic flow decreases (decreased S-wave velocity) and flow occurs predominantly in diastole (increased D-wave velocity; Fig. 31-13B). The absolute values of the S and D waves do not necessarily provide any additional information. Because they depend on the volume status of the patient, the absolute values of the S and D waves can vary significantly even under normal conditions.
Pulmonary venous flow patterns help to differentiate normal transmitral filling patterns from pseudonormal patterns. In the pseudonormal pattern, the atrium contracts against an increased afterload in the LV because of an elevated diastolic filling pressure and a stiff LV. More blood is ejected along the "path of least resistance" back into the pulmonary veins. As a result, the A wave in pseudonormal diastolic dysfunction is tall (often >0.35 milliseconds) and prolonged.
Both transmitral and pulmonary venous flow patterns are affected by the patient's volume status. Color M-mode Doppler echocardiography is a relatively new modality that can be used to assess diastolic function in a preload-independent manner. When using color M-mode, an "ice pick" scan line is used to display color Doppler velocity information versus time. By placing the scan line through the mitral inflow jet of the LV, 2 distinct flow profiles are obtained. The displayed profiles correspond to the E and A waves from PWD. The slope of the first (E) wave's aliasing velocity is the propagation velocity (Vp), which is an indication of the velocity at which blood travels from the mitral annulus to the apex during early ventricular filling (Fig. 31-14). Vp correlates to the degree of diastolic dysfunction and is independent of preload and heart rate. Another advantage of color M-mode Doppler echocardiography is that it provides a superior combination of temporal, spatial, and velocity resolution. Propagation velocities less than 45 cm/s are consistent with diastolic dysfunction in people who are older than 30 years of age, but Vp less than 55 cm/s is abnormal in younger patients.
Normal propagation velocity measured using color M-mode Doppler. Yellow arrow indicates closed mitral valve. Green arrow indicates the beginning of transmitral early diastolic flow as the mitral valve opens.
Doppler tissue imaging is another relatively new ultrasound imaging modality that measures the velocity of the actual myocardium during the cardiac cycle. Myocardial tissue Doppler shifts typically are higher in amplitude and lower in frequency than the traditional blood flow measurements. PWD tissue imaging provides the capability of recording the low velocities of a moving wall structure with a relatively high sampling rate. A PWD sample is taken at the lateral MV annulus, and the peak early diastolic myocardial velocity (E') is measured. In contrast to blood flow velocity profiles that are below the baseline (away from the TEE transducer), Doppler tissue imaging profiles are above the baseline as the MV annulus recoils toward the transducer in diastole.
During diastole, motion of the mitral annulus shows 2 distinct movements toward the atrial side in patients with sinus rhythm (Fig. 31-15A). During the early diastolic period, the onset of E coincides with the beginning of mitral inflow. The E' peak velocity precedes the peak velocity of the transmitral E wave. Unlike transmitral inflow velocities, in which measured parameters are preload dependent, E' is a good index of LV relaxation and appears to be less sensitive to alterations in preload.
A. Normal mitral valve annulus tissue Doppler velocities. A′, atrial contraction myocardial velocity; E′, early diastolic myocardial velocity. B. Mitral valve tissue Doppler showing restrictive diastolic dysfunction. A′, atrial contraction (late diastolic) myocardial velocity; E′, early diastolic myocardial velocity.
E' below 8 cm/s is consistent with diastolic dysfunction (Fig. 31-15B). In addition, a peak early transmitral inflow velocity to peak early diastolic myocardial velocity ratio (E/E') greater than 10 is consistent with diastolic dysfunction. E/E' then can be used to differentiate normal from pseudonormal transmitral flow pattern. Whereas E/E' greater than 15 has been shown to be highly specific for elevated LA pressures, E/E' less than 8 is highly sensitive for normal LA pressures (Fig. 31-16 and Table 31-4).
Transesophageal evaluation of diastolic dysfunction. A, peak late diastolic transmitral flow velocity; A′, peak late diastolic tissue velocity; Ar, peak pulmonary venous (PV) atrial reversal flow velocity; D, peak diastolic PV flow velocity; E, peak early diastolic transmitral flow velocity; E′, peak early diastolic myocardial velocity; S, peak systolic PV flow velocity; Vp, flow propagation velocity.
Table 31-4 Normal Doppler Values ||Download (.pdf)
Table 31-4 Normal Doppler Values
|Parameters||Adults Younger Than 41 Years of Age||Adults Older Than 55 Years of Age|
Peak mitral flow velocity
|76 ± 13||63 ± 11|
Peak mitral filling rate
|38 ± 8||52 ± 9|
|Mitral E/A||2.1 ± 0.6||1.3 ± 0.3|
|Mitral E deceleration time||184 ± 24|
|Isovolumetric relaxation time (ms)||74 ± 26|
Peak pulmonary venous
AR wave (cm/s)
|18 ± 3||25 ± 5|
Peak pulmonary venous
S wave (cm/s)
|41 ± 10||60 ± 10|
Peak pulmonary venous
D wave (cm/s)
|53 ± 10||38 ± 10|
The MV with its complex saddle-shaped configuration presents one of the most challenging structures to be assessed with 2D TEE. Two-dimensional TEE imaging of the MV requires a mental integration of several views for accurate assessment and therefore depends on observer experience and expertise. Its complex structure and interrelationship of the MV to chordae, papillary muscles, and myocardial walls make it particularly suited to 3D assessment. The MV is attached to a fibrous ring and consists of 2 leaflets, 1 anterior and 1 posterior. Although morphologically different, the surface areas of the anterior and posterior MV leaflets are nearly identical and together exceed the area of the mitral annulus in a greater than 2:1 relationship.51 The mitral annulus is a 3D, saddle-shaped, ellipsoid structure that changes shape and decreases in area as it descends during systole (Fig. 31-17). Coaptation of the 2 leaflets is curvilinear, and both leaflets join at the anterolateral and posteromedial commissures (Fig. 31-2B and 31-18).
Anatomic view of the mitral valve viewed from the base of the heart looking toward the left ventricular apex. Orientation of the leaflets and commissures is shown using the Carpentier naming system for mitral segments. The left (L), right (R), and noncoronary (NC) aortic valve leaflets are shown.
Midesophageal commissural view of a normal mitral valve. A2 segment of anterior leaflet is seen between the commissures with P1 and P3 segments lateral to commissures. LA, left atrium; LV, left ventricle.
The subvalvular apparatus consists of 2 papillary muscles and chordae tendineae. The anterolateral papillary muscle supplies chordae to the anterior aspect of both the anterior and posterior mitral leaflets; the posteromedial papillary muscle supplies chordae to the posterior aspect of both valve leaflets. Three groups of chordae exist, named in accordance with their insertion points on the MV leaflets (Figs. 31-19 and 31-20). First-order chordae attach to the free edge of the leaflets, second-order chordae attach to the body of the leaflets, and third-order chordae attach near the base of the posterior leaflet only.52 More than 120 chordal tendons subdivide as they project from each papillary muscle to attach to the free edge and body of both MV leaflets.8 The subvalvular apparatus is responsible for maintaining valve integrity during systole and plays a crucial role in preserving the overall structure–function relationship of the LV.
Carpentier classification of mitral regurgitation with normal, prolapsed, flail, and restricted mitral leaflets. The classification of chordae tendineae is also shown.
Midesophageal long-axis view showing subvalvular chordae (arrows). Ao, aorta; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RV, right ventricle.
The MV shares a close anatomic, and at times pathophysiologic, relationship with the AV. In particular, the fibrous skeleton of the heart that gives rise to the anterior MV annulus is intimately associated with both the left and noncoronary cusps of the AV.
Recent advances in 3D echocardiography provide clinicians with spectacular images of complex MV pathology. RT 3D TEE permits an accurate identification of the etiology and mechanism of MR and is more sensitive than 2D TEE in identifying the location of the pathology leading to MR, especially in patients with bileaflet and commissural defects using both reconstruction 3D TEE and RT 3D TEE.22,53,54 In addition, the severity of MR can be more accurately determined using 3D color Doppler echocardiography,55 and specific geometric shapes for different MR-pathologies can be identified.56-58 Ongoing development of dynamic analysis techniques for 3D echocardiography images allows a quantitative and systematic analysis of the MV and demonstrates increasing value of 3D imaging.
RT 3D TEE provides excellent visualization of prosthetic MVs and annuloplasty rings.59,60 Thus, it might help in identifying the location of a paravalvular leak (Fig. 31-21A and 31-21B).61 3D TEE has been shown to provide complementary information in patients with an Alfieri stitch and may aid in long-term follow-up.62 3D TEE provides additional information in patients with a postoperative MV dehiscence and thus may help planning an optimal surgical intervention.60 Prosthetic valve endocarditis remains a challenging diagnosis, especially for TEE. However, initial experiences suggest that 3D TTE might improve the sensitivity of detecting endocarditis.63
A. Live three-dimensional (3D) image of a repaired mitral valve demonstrating a posterior-medial defect outside the annuloplasty ring (yellow arrow). B. Corresponding 3D color imaging nicely illustrating the paravalvular leak outside the ring structure.
A comprehensive 3D assessment of the MV involves the acquisition of an en face view, a full-volume, and a 3D color full-volume image. The en face view refers to a view of the MV with the patient in the supine position through a surgical left atriotomy. The anatomical identification of structures is based on Carpentier's classification. This view is routinely generated using the live 3D zoom mode based on the ME 4-chamber view and by rotating the obtained image to display the AV at the 12 o' clock position as the midpoint of the anterior annulus and the posterior leaflet at the bottom of the image (Fig 31-2B). Three-dimensional zoom MV images may then be manipulated such that the MV may be viewed from either atrial or ventricular perspectives, which is another unique feature of 3D imaging. The full-volume data set allows assessing the intimate interrelationship among the MV, the papillary muscles, the myocardial walls, and the LV outflow tract. Using 3D color, the size and geometry of regurgitant jets can be visualized, and exact quantification of effective regurgitant orifice areas (EROA) can be obtained (Fig. 31-22A). These images can be supplemented by 3D quantitative assessment of the MV using built-in software (MVQ). The MVQ offers a semiautomated analysis package for accurate modeling of the mitral annulus, valve commissures, leaflet coaptation, leaflet topography, aortic orifice to MV angle, and so on (Fig. 31-22B). Reconstructive approaches to assess the MV with 3D TEE (Siemens, Mountainview, CA) paired with offline computer software (TomTec Imaging Systems, Unterschleissheim, Munich, Germany) allow for similar quantification of the MV.64
A. Three-dimensional (3D) transesophageal echocardiography color full volume of a mitral valve (MV) with severe mitral regurgitation displayed in 3 multiplanar reconstruction planes (green, red, and blue MPRs). The left lower quadrant (blue MPR) depicts the 3D vena contracta (3D-VC) and reflects the effective regurgitant orifice area. This was achieved by carefully cutting the MV at the annular plane. B. 3D model of a MV demonstrating the options for quantitative assessment of the MV using built-in software (MV Quantification, QLAB 7.0, Philips Medical Systems, Andover, MA). A, anterior; AL, anterolateral commissure; P, posterior; PM, posteromedial commissure.
To accurately diagnose MV pathology, it is crucial to be able to relate TEE images of this valve to specific anatomic regions. Three approaches to 2D examination of the MV by TEE have been published. Although these approaches all have strengths and limitations, they all emphasize the importance of concise, systematic 2D evaluation of the MV in multiple scan planes and from multiple points of view.
In the early 1980s, Carpentier introduced a functional classification of mitral insufficiency (Fig. 31-19).65 Type I MR has normal motion of the leaflets with MR caused by leaflet perforation, usually from endocarditis, or annular dilation, often accompanying LV dysfunction. Type II MR has increased leaflet motion, typically from myxomatous change, leading to either leaflet prolapse or a flail leaflet. Leaflet prolapse, a result of leaflet redundancy and chordal elongation, is defined as doming of the leaflet body above the level of the mitral annulus in systole with the leaflet tip still directed toward the LV. With myxomatous change, the annulus often is significantly dilated in addition to the defect in leaflet tip coaptation. This regurgitant lesion usually evolves slowly and ranges in scale from trivial to severe. A flail leaflet has a leaflet tip directed toward the LA throughout systole. This regurgitant lesion usually is severe with an abrupt onset and is poorly tolerated by the patient. Type III MR is characterized by restricted leaflet motion. Type IIIa dysfunction involves restricted leaflet motion during diastole and systole because of rheumatic changes. Type IIIb dysfunction correlates to restricted leaflet motion during systole secondary to papillary muscle displacement in ischemic or dilated cardiomyopathy.
Mitral insufficiency caused by global LV dysfunction appears to result from a distorted geometric relationship between the MV leaflets and the papillary muscles. At the gross level, the LV is seen to transform from its usual ellipsoid shape into that of a sphere, causing widening of the interpapillary angle and restriction or tethering of leaflet motion.66 The valve may appear morphologically normal on 2D imaging but with loss of the usual systolic leaflet overlap or with a visible coaptation defect. With dilated cardiomyopathy, the regurgitant jet usually is central (Fig. 31-23). Dilation of the annulus may contribute to regurgitation, most notably in the region of the P2 segment, but in most cases is not the major mechanism of regurgitation.
A. Midesophageal 2-chamber view with color-flow Doppler (CFD) showing mild mitral regurgitation from left ventricular dilation. B. Midesophageal long-axis view with CFD showing moderate mitral regurgitation. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.
With ischemic MR, dilation of specific areas of myocardium may lead to asymmetric tethering and an eccentric regurgitant jet. Papillary muscle rupture, which most frequently affects the posteromedial muscle, is an occasional complication of MI and can result in severe bileaflet regurgitation. The papillary muscle and chordae tips can often be seen flinging into and out of the LA. In hypertrophic obstructive cardiomyopathy, the MR jet usually occurs in mid to late systole and is directed posteriorly as the anterior leaflet is pulled into the LVOT (systolic anterior motion of the anterior leaflet), resulting in a coaptation defect (Fig. 31-24).
Midesophageal long-axis view with color-flow Doppler revealing mitral regurgitation caused by hypertrophic obstructive cardiomyopathy. Ao, aorta; IVS, interventricular septum (hypertrophied); LA, left atrium; LV, left ventricle; RV, right ventricle.
MV endocarditis can affect native valves and result in regurgitation because of perforation or deformation of the valve leaflets (Fig. 31-25). Vegetations commonly arise on the upstream side of a valve, which are generally areas of slower flow and therefore are usually seen in the LA. The finding of MV endocarditis mandates careful inspection of the other heart valves to rule out their involvement. Leaflet perforation is identified by the appearance of 1 or more regurgitant jets that do not seem to arise from the coaptation line. A clue to this particular pathology is the presence of multiple convergence zones on color Doppler. A recent study showed that 3D TTE may improve the sensitivity of TTE in detecting endocarditis involving prosthetic valves.63 3D imaging may also be useful for assessing complications associated with endocarditis.67 Studies using 3D-TEE in the diagnosis of IE are very limited but suggest an incremental benefit when used in addition to 2D TEE.68,69
Midesophageal 4-chamber view with color-flow Doppler demonstrating mitral regurgitation caused by mitral valve endocarditis (arrow). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Echocardiographic examination of the insufficient MV should involve inspection of other structures in the heart that may be altered as a result of the regurgitant process. LA dilation is commonly found in chronic MR of at least moderate severity but is not a feature of acute MR. Left-to-right bowing of the IAS caused by elevated LA pressure often can be appreciated in the ME 4-chamber or ME bicaval view. Signs of pulmonary hypertension, such as RV and RA enlargement, often accompany progressive MR.
Because a significant portion of the systolic volume is unloaded into the LA with severe MR, normal systolic function should appear like a hypercontractile LV. Therefore, an LV with apparently normal systolic function may actually have significant systolic dysfunction. Spherical enlargement of the LV with eccentric hypertrophy signifies long-standing MR in which the compensatory processes of the ventricle are failing.
Echocardiographic grading of MR severity is based on a number of qualitative and quantitative parameters.70 Among these, the width of the 2D vena contracta (VC) as visualized by color Doppler has been widely considered to accurately reflect MR severity.71 However, although this may be true for simple MR orifices, there is a significant overlap between of 2D VC measurements and angiographic severity grades because orifices are multiple and asymmetric. A VC of 6 mm or larger identifies angiographically severe MR with a sensitivity of 95% and a specificity 98%. Eccentric regurgitant jets imaged by CFD commonly appear to occupy less overall area than jets of similar flow rates directed centrally within the LA.72 An eccentric jet has a different observed morphology compared with free jets secondary to limited expansion because of impingement of the jet along the atrial wall. Consideration of jet morphology in the CFD assessment is important to avoid underestimating the degree of regurgitation. Illustrating variable MV pathology with 3D color imaging and using the additional information to obtain an EROA by cropping into the 3D MR jet takes advantage of the new 3D technology.
A proximal isovelocity surface area (PISA) may be seen on the LV side of the MV during systole as blood flow accelerates toward the regurgitant orifice, causing aliasing with CFD. The product of PISA and the aliasing velocity provides the flow rate through the valve during the measurement. According to the continuity principle, dividing the peak flow rate by the peak regurgitant velocity, as measured by CWD, provides quantitative assessment of the effective regurgitant orifice (ERO):
where PISAMR = 2Pi*r2, and r = radius of semicircular shell of color change at the set Nyquist limit.
The continuity principle also can be used to derive regurgitant fractions by determining stroke volumes through various other sites in the heart (notably the LVOT, AV, and pulmonic valve). Stroke volume is calculated as the product of the velocity–time integral (VTI) through an orifice and the calculated orifice area at the same location.
Alterations in the pulmonary venous Doppler profile are useful in quantifying the severity of MR. Trivial or mild regurgitation is generally associated with a normal flow velocity pattern (Peak S wave > Peak D wave), moderate regurgitation is associated with systolic blunting (Peak S wave < Peak D wave), and severe regurgitation is associated with S-wave reversal (S wave directed away from transducer as regurgitant blood flows retrograde into the pulmonary vein).73 It is advisable to interrogate at least 1 pulmonary vein from each side of the LA because regurgitant jets may preferentially affect the pulmonary venous profile of one side over the other.
Peak E-wave velocity is another parameter that can be used to qualitatively assess the degree of MR. When the degree of MR increases, the added regurgitant volume across the MV increases the pressure gradient between the LA and the LV. This increase in pressure gradient subsequently increases early mitral inflow velocity. E-wave velocity greater than 1.2 milliseconds identifies patients with severe MR with a sensitivity of 86%, specificity of 86%, positive predictive value of 75%, and negative predictive value of 92%.
One caveat that must be emphasized is that MR severity often can be difficult to interpret in the intraoperative period because of the relatively deranged hemodynamic profile of the patient undergoing general anesthesia. Altered loading conditions and cardiac contractility can lead to varying degrees of MR that may be different from those seen in the awake, physiologically normal state. Furthermore, application of severity estimation methods depends on the technical expertise of the imaging staff, the complexity involved with the measurement technique, associated limitations with the individual method, and time constraints.
Most cases of hemodynamically significant native MV stenoses are caused by rheumatic heart disease. Uncommon causes include severe mitral annular calcification, obstructing lesions such as LA tumors and endocarditis vegetations (Fig. 31-26), and congenital deformities such as parachute MV or cor triatriatum. Surgical correction can involve either open commissurotomy or valve replacement. In addition to confirming the severity of the stenosis, it is equally if not more important to evaluate the heart for evidence of LA thrombus (particularly within the LA appendage), RV and LV function, presence and severity of tricuspid regurgitation (TR), and degree of residual stenosis or regurgitation after valve repair or replacement.
Midesophageal 4-chamber view with color-flow Doppler demonstrating mitral stenosis from mitral valve endocarditis (arrow). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Common echocardiographic findings of rheumatic MV stenosis (Fig. 31-27A) include leaflet thickening and calcification, leaflet restriction, and subvalvular involvement (shortening, tethering, and calcification of the chordae). The resulting failure of leaflet coaptation causes a regurgitant jet that is directed toward the side of the lesion (Fig. 31-27B). These leaflet changes are best seen in the ME 4-chamber and LAX views. Subvalvular involvement usually is best visualized from the TG 2-chamber view. The TG basal SAX view may reveal calcification in the region of the commissures. Rheumatic heart disease also may involve the pericardium, myocardium, and other heart valves.
A. Midesophageal 4-chamber view with turbulent flow through a stenotic rheumatic mitral valve. B. Midesophageal 4-chamber view with color-flow Doppler demonstrating mitral regurgitation in a patient with rheumatic heart disease. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Associated findings in mitral stenosis include atrial dilation, pronounced left-to-right bowing of the IAS, SEC in the LA (with or without atrial thrombus), and signs of pulmonary hypertension (right-heart dysfunction).
A number of methods are available to echocardiographers for assessing the severity of mitral stenosis. Mean transmitral pressure gradients are easily estimated from the transmitral CWD profiles using the simplified Bernoulli equation:
Severe MV stenosis is associated with mean transvalvular gradients greater than 12 mm Hg.
The pressure halftime (PHT) denotes the rate of diastolic pressure decline across the MV, specifically the time required to reach 50% of the peak pressure gradient. Normally, the diastolic E wave undergoes rapid deceleration because of the abrupt decrease in transmitral pressure gradient as the LV fills during early systole. However, in mitral stenosis, the pressure gradient is sustained much later in diastole, giving rise to a greatly prolonged E-wave deceleration and thus longer PHT. Angiographic experiments have shown that an MV area of 1 cm2 corresponds to a PHT of 220 milliseconds; thus, the area of the stenotic orifice can be estimated by dividing 220 by the PHT in milliseconds.74
The continuity equation can be used in conjunction with the peak transmitral E-wave velocity and PISA measurements to estimate the stenotic orifice area. Providing there is no significant aortic or pulmonary regurgitation or interventricular shunts, the continuity equation also can use stroke volumes of the LVOT, AV or pulmonary valve, and the measured VTI of transmitral inflow to estimate the area of the stenotic mitral orifice.
Assessment of the MV area with 3D planimetry is an alternative approach to grading MS severity and correlates well with catheter-based techniques.75 RT 3D TEE helps identifying MV commissural fusion and limited MV opening. Furthermore, RT 3D TEE has successfully been used for guidance during percutaneous mitral valvuloplasty and has been shown to be a suitable technique for monitoring its efficacy and complications.76,77
High-resolution images of the AV are provided by TEE because the valve and probe are separated by the LA, which acts as an excellent acoustic window. The AV is composed of 3 leaflets or cusps that are suspended from the aortic wall along 3 crescent-shaped lines. The junctions of the free edges of the cusps are called the aortic commissures. Behind each leaflet is the respective sinus of Valsalva, a pouchlike dilation of the aortic root. The leaflets and sinuses are named according to the adjacent coronary artery (ie, left, right, and noncoronary cusps and sinuses).
Four standard views allow examination of the AV and LVOT. Beginning with the imaging depth set at 10 to 12 cm, the ME AV SAX view is obtained by advancing or withdrawing the probe with a multiplane angle of 30 to 50 degrees until the AV appears in the center of the screen (Fig. 31-28). All 3 cusps should be seen symmetrically by rotating the multiplane angle and slightly anteflexing the probe. The general morphology of the AV (bicuspid, tricuspid) is noted as well as the thickness and mobility of the leaflets. CFD is applied to detect flow disturbances indicating aortic regurgitation or stenosis. The AV orifice may be traced to measure valve area.
A. Midesophageal aortic valve short-axis view with color-flow Doppler (CFD) showing central aortic insufficiency in a dilated aortic valve. B. Midesophageal aortic valve long-axis view with CFD demonstrating aortic insufficiency. Ao, aorta; IVS, hypertrophied interventricular septum; LA, left atrium, LC, left aortic valve cusp; LV, left ventricle, NCC, noncoronary aortic valve cusp, PA, pulmonary artery, RA, right atrium, RC, right aortic valve cusp, RV, right ventricle, RVOT, right ventricular outflow tract.
The ME AV LAX view is obtained by rotating the multiplane angle forward 90 degrees from the ME AV SAX to visualize the LVOT, AV, and proximal ascending aorta in the LAX view (Fig. 31-29). The AV leaflets appear as 2 thin lines opening parallel to the aortic walls. The right coronary cusp, being farthest from the probe, is visualized toward the bottom of the display. The left or noncoronary cusp (depending on the imaging plane), located closer to the probe, is seen toward the top of the display. The diameters of the LVOT, aortic annulus, sinotubular junction, and ascending aorta can be measured in this view. The annulus is measured where the leaflets insert into the aorta. The proximal ascending aorta should be evaluated for calcification, atheroma, intimal flap or dissection, and aneurysmal dilation. CFD is again applied to detect the flow pattern through the LVOT, AV, and ascending aorta. Turbulent LVOT flow in this view should prompt further evaluation for hypertrophic obstructive cardiomyopathy or another obstruction to LVOT flow. Systolic anterior motion of the MV (often a fluttering motion into the LVOT but sometimes apparently occluding the LVOT), associated MR, premature AV closure or fluttering of the AV cusps, and thickened interventricular septum (>1.4 cm, disproportionate from the free wall) confirm hypertrophic obstructive cardiomyopathy.
Midesophageal aortic valve long-axis view. Arrow indicates sinotubular junction. Asc Ao, ascending aorta; LA, left atrium; LVOT, left ventricular outflow tract; RCS, right coronary sinus behind right cusp of aortic valve; RVOT, right ventricular outflow tract.
The deep TG LAX view can be obtained by advancing the probe tip deep into the stomach and then anteflexing to create an imaging plane originating from the LV apex with the AV appearing in the far field. Alternatively, the TG LAX view is obtained from the TG midpapillary SAX view by rotating the angle forward to 90 to 110 degrees until the AV comes into view in the far field to the right side of the image. Both of these TG views allow for parallel alignment of the ultrasound beam through the AV, making them most useful for measuring Doppler flow velocities through the LVOT and AV rather than visualizing anatomy. Positioning the PWD sample volume in the center of the LVOT allows Doppler flow measurement in the outflow tract. Flow velocity through the AV is measured with CWD. Either or both of these TG views may be difficult to obtain in some patients, and a severely stenotic AV may make Doppler interrogation difficult. CFD may be helpful in detecting flow through the stenotic orifice, facilitating appropriate placement of the Doppler beam.
The 3D assessment of the native AV is more difficult compared with 3D imaging of the MV. The AV can be optimally visualized only in 18% when using RT 3D TEE, most likely because the AV is an anterior structure with a longer distance to the transducer, is associated with a less favorable angle of insonation and has thin pliable cusps compared with the MV leafets.59
Three-dimensional echocardiographic imaging of the AV appears to be most successful when using the live 3D mode (Fig. 31-30A and 31-30B). Occasionally, the 3D full-volume mode might offer more detailed information based on higher frame rates, and this mode also permits assessing both AV valves and the AV simultaneously. Thickening and calcification of the AV cusps mostly facilitates RT 3D TEE imaging of the AV, but significant calcification results in similar drop-out (shadowing) as seen with 2D TEE. Cropping of a 3D TEE image assists in the planimetric assessment of the AV area, and RT 3D TEE potentially helps differentiating bicuspid from tricuspid anatomy of the AV and helps identify the exact location of an aortic dissection (Fig. 31-30C and 31-30D).
A. Midesophageal live three-dimensional (3D) transesophageal echocardiography (TEE) image of a normal open aortic valve acquired in short axis. B. Midesophageal live 3D TEE image of a normal closed aortic valve orientated in long axis. C. 3D image showing the elliptical opening of a bicuspid aortic valve. Arrow indicates calcification along raphe where right and left aortic valve cusps appear fused into a single cusp. D. Type A dissection of the ascending aorta originating very close to the AV, obtained in AV long-axis orientation. AML, anterior mitral valve leaflet; LA, left atrium; LCC, left coronary cusp; NCC, noncoronary cusp; RCC, right coronary cusp.
Acute or chronic regurgitation may result from abnormalities of the AV and the aortic root. Aging, rheumatic heart disease, endocarditis, and congenital bicuspid or unicuspid AV all may lead to aortic regurgitation. Dilation of the aorta resulting from connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome), sinus Valsalva aneurysm, aortic root abscess, and hypertension are other causes of aortic insufficiency (AI).
Two-dimensional TEE imaging should be applied in the ME AV SAX and LAX views to detect congenital abnormalities or acquired defects such as myxomatous degeneration and vegetations. The aortic root should be assessed for dilation, and measurements of the LVOT, AV annulus, sinotubular junction, and ascending aorta should be obtained. The area of the end-diastolic gap between the aortic cusps, measured by planimetry, correlates with the severity of AI (mild, <0.2 cm2; moderate, 0.2-0.4 cm2; severe, >0.4 cm2).
The VC should be measured by CFD in the ME LAX view with the imaging depth reduced. A VC less than 0.3 cm indicates mild AI, and a value greater than 0.6 cm signifies severe AI. The ratio of the regurgitant jet area to the LVOT area also can be measured by CFD in the ME LAX view. Similarly, the width of the regurgitant jet can be compared with the width of the LVOT. Values greater than 60% for area and greater than 65% for width indicate severe AI.
The PHT, described previously to grade mitral stenosis, can be applied to grade the severity of AI. The more severe the AI, the shorter the PHT because the aortic diastolic pressure gradient declines more rapidly. Whereas PHT is best obtained in the TG LAX or deep TG LAX views with CWD. PHT greater than 500 milliseconds indicates mild AI, PHT less than 200 milliseconds is compatible with severe AI. PHT measurements can be misleading in patients with elevated LV end-diastolic pressure (diastolic dysfunction). In these instances, the gradient will dissipate rapidly, and the true severity of regurgitation may be overestimated.
Early diastolic flow reversal in the descending aorta, measured with PWD, may be a normal finding. However, holodiastolic flow reversal in the proximal abdominal aorta or distal thoracic aorta indicates severe AI.
The echocardiographic assessment of AS is based on a detailed description of cusp morphology, AV function, and the grading of AS severity. Calcific degeneration of the AV, the most common cause of AS, is characterized by restricted leaflet motion and calcification along the free edges of the leaflets. Patients with calcific degeneration usually become symptomatic in their sixth to seventh decades of life.
Rheumatic AS typically is seen in middle-aged immigrants. The tips of the leaflets are thickened and calcified, and the commissures are fused, producing a characteristic "doming" during systole. The orifice may become circular instead of the normal triangular shape. Rheumatic AS almost always is associated with rheumatic involvement of the MV.
Congenital abnormalities of the AV may lead to AS. Bicuspid AV is the most common form, occurring in approximately 2% of the normal population, and symptoms usually occur in the fourth to sixth decades of life. The bicuspid AV orifice is elliptical, and a calcified raphe is often present on one of the leaflets, giving the false impression of a trileaflet valve (Figs. 31-30C and 31-31).
A. Midesophageal aortic valve short-axis view showing the elliptical opening of a bicuspid aortic valve. Arrow indicates calcification along the raphe, where the right and left aortic valve cusps appear fused into a single cusp. B. Midesophageal aortic valve long-axis view showing bowing of the restricted bicuspid aortic valve leaflet (arrow). Ao, aorta; LA, left atrium; LVOT, left ventricular outflow tract; NCC, noncoronary aortic valve cusp; PA, pulmonary artery; RA, right atrium.
TEE interrogation should start with 2D imaging in the ME AV SAX and LAX views. Thin and mobile AV leaflets without calcification usually exclude severe AS. Thickening, calcification, and restricted leaflet motion are seen in all cases of AS. Commissural fusion is seen in rheumatic valvulitis. Poststenotic dilation of the aortic root and the proximal ascending aorta may be present. The AV area can be measured by planimetry in the ME AV SAX view using the zoom mode to magnify the frozen image. The inner edges of the distal leaflets should be traced in systole during their greatest excursion. Severe thickening and calcification of the leaflets, shadowing, accentuated cardiac motion, and the inability to obtain a true SAX view near the leaflet tips all may make planimetry difficult and inaccurate. In the ME AV LAX view, leaflet morphology, mobility, calcification, and thickening also can be evaluated. The LVOT can be examined for subaortic pathology.
Turbulent, high-velocity flow can be seen in the proximal ascending aorta with severe AS. Pressure gradients and transvalvular velocity should be measured. To accomplish this, the CWD beam is positioned across the AV in the TG LAX or deep TG LAX views (Fig. 31-32), and the edge of the spectrum is traced to obtain the peak and mean pressure gradients and flow velocities. Severe AS corresponds to a peak velocity greater than 4 milliseconds (Fig. 31-33A). The VTI of the traced spectrum is calculated and corresponds to the distance traveled by a column of blood during the stroke cycle. This allows use of the continuity principle to calculate the effective AV cross-sectional area (CSAAV). The continuity principle is based on the conservation of flow over time between 2 conduits within a closed circuit (AV and LVOT in this example). Because flow is the product of the cross-sectional area of the conduit and the VTI through the conduit:
where CSA = πr2, and r = radius of the respective conduit.
Deep transgastric long-axis view with aortic valve leaflets (arrow) seen on the left. LA, left atrium; LVOT, left ventricular outflow tract.
A. Continuous-wave Doppler through deep transgastric long-axis view of the aortic valve showing severe aortic stenosis (velocity >4 milliseconds). B. Continuous-wave Doppler through deep transgastric long-axis view of the aortic valve in a patient with hypertrophic obstructive cardiomyopathy (note the sharp "ice pick" contour). C. Continuous-wave Doppler through the aortic valve with velocity–time interval measured at the left ventricular outflow tract (inside tracing) and aortic valve (outside tracing) simultaneously.
The radius or diameter of the LVOT can be measured in the ME LAX view. VTILVOT can be obtained in the TG LAX or deep TG LAX views using PWD. VTIAV can be directly measured with CWD from the deep TG view. Alternatively, a "double-envelope" technique can be used to simultaneously measure LVOT and AV VTIs by CWD in the TG LAX or deep TG LAX views (Fig. 31-33C). Because the velocity of flow through the smaller AV must accelerate from that of the larger diameter LVOT, the larger envelope must correspond to the VTI of the AV, and the smaller but denser envelope represents the VTI of the LVOT. Demonstration of the noncircular shape of the LVOT by RT 3D TEE has raised questions of the accuracy of this method. However, accuracy in the AV area calculation can be improved by direct volumetric measurement of the LV stroke volume using a 3D full-volume data set.78
The role of intraoperative TEE in guiding percutaneous AV implantation for patients with symptomatic AS is evolving. TEE can help to confirm the diagnosis, provides accurate measurements of the AV annulus for appropriate sizing, guides the transcatheter positioning of the prosthetic valve, and permits immediate evaluation of the deployed prothesis.79 RT 3D TEE modes and biplane imaging provide valuable complementary information to fluoroscopy in guiding these procedures.80
The aorta is the largest artery in the body with a normal diameter up to 3.5 cm. It is divided anatomically into 4 segments: the ascending aorta, transverse aortic arch, descending thoracic aorta, and abdominal aorta. The ascending aorta begins at the level of the aortic annulus and the AV. Just distal to the aortic annulus, the ascending aorta dilates to form a segment known as the aortic sinus of Valsalva, which includes the respective left coronary, right coronary, and noncoronary sinuses. Distal to the aortic sinuses, the aorta has a brief segment with a reduced diameter called the sinotubular junction.
In adults, the ascending aorta is approximately 5 cm in length. After originating from the AV annulus, the ascending aorta extends rightward around the main pulmonary trunk and crosses the right pulmonary artery anteriorly. It then ascends rightward and anteriorly until it meets the aortic arch at the origin of the innominate artery (at the level of the second intercostal space). The proximal or near aortic arch is poorly visualized with TEE because of the anatomic interposition of the trachea between the esophagus and the aorta at this level. Whereas the innominate and left common carotid arteries are in close proximity to the trachea, the left subclavian artery lies to the left of the trachea and can be visualized more easily with TEE.
The descending thoracic aorta begins distal to the left subclavian artery at the level of the ligamentum arteriosus. This is an area of narrowing referred to as the aortic isthmus. The ligamentum arteriosus is a fibrous connection between the pulmonary artery and the aorta, a remnant of the ductus arteriosus during fetal life. Inferior to the isthmus, the descending aorta courses to the left lateral side of the body of the fourth thoracic vertebrae. The descending aorta is relatively transfixed to the vertebral column here. Therefore, deceleration injuries often occur at the level of the isthmus. The descending aorta continues along a slightly anterior and rightward path as it approaches the diaphragm, where it lies directly posterior to the esophagus. Therefore, at the level of the lower esophageal sphincter, the heart and the aorta are on opposite sides of the esophagus.
The SCA and the ASE have defined 6 2D views for interrogating the thoracic aorta by TEE.7 Multiple imaging planes from within similar views may be necessary to accurately define aortic pathology.
The ME ascending aorta SAX view is obtained in the 0- to 30-degree imaging plane with the probe approximately 25 cm from the lips. In this view, a SAX view of the ascending aorta along with the main pulmonary artery, right pulmonary artery, and SVC is obtained. Qualitative analysis of the aortic anatomy and wall thickness can be obtained in this view.
The ME ascending aorta LAX view is obtained between 110 and 140 degrees. This view is easily obtained after starting with the ME AV SAX view ("Mercedes Benz" view), which is easily recognized at the ME level with the multiplane angle at 20 to 50 degrees. After the "Mercedes Benz" view has been obtained, rotating the imaging plane forward an additional 90 degrees and withdrawing the probe slightly yields the ME ascending aorta LAX view (Fig. 31-34). This view is useful in defining wall thickness, aortic dimensions, and blood flow patterns in the ascending aorta.
Midesophageal ascending aorta long-axis view. Asc Ao, ascending aorta; RPA, right pulmonary artery.
From the ME ascending aorta views, turning the probe to the left with a multiplane angle of 0 degree produces a SAX image through the descending aorta. After the aorta has been visualized, the depth of the image should be optimized so the aorta is in the center of the screen. Inserting the probe to the level of the diaphragm (where the image disappears) and then slowly withdrawing the probe allows scanning of the entire descending thoracic aorta. The SAX view is useful for defining wall thickness, determining atherosclerotic severity, and measuring aortic dimensions (Fig. 31-35A).
A. Biplane view of the descending aorta illustrating a mobile atheroma (arrow) short-axis (left) and long-axis (right) views. B. Live three-dimensional image of a descending aorta with significant atheromatous disease.
From the SAX view, rotating the plane to 90 degrees produces a LAX view of the descending aorta, or alternatively, both view can be demonstrated with biplane imaging (Fig. 31-35A). These views are useful for defining spatial relationships of SAX findings, interrogating aortic flow patterns, and identifying branch vessels. Three-dimensional TEE may help to communicate the extent of atheromatous disease to the surgeon Fig. 31-35B.
With the scan plane at 0 degree, withdrawal of the probe following the aorta to an upper esophageal window with a rightward rotation produces a LAX view of the aortic arch. This view is used to define aortic dimensions, wall contour, and branch vessels. Advancing the multiplane angle to 90 degrees in the upper esophagus produces a SAX view of the arch. At the proximal arch, the main pulmonary artery and right pulmonary artery may be seen if the depth is sufficient. At the distal arch, multiple views of the arch and its branch vessels may be obtained.
Even using all of these views, TEE does not image the entire thoracic aorta. A "blind spot" in the distal ascending or proximal arch is created by the trachea. The aorta also is subject to echocardiographic artifacts and dropout caused by calcifications. With every image, the examiner should describe the morphology, dimensions, and integrity of the aortic wall. Evaluation for spontaneous echocardiographic contrast or turbulent flow also is recommended. Any fluid collection should be noted.
The aorta is a significant source of atheromatous material that can embolize to the brain, and atherosclerosis of the proximal thoracic aorta is established as an independent risk factor for cognitive dysfunction and stroke after cardiac surgery.81-83 Multiple strategies can be used to minimize embolization of atheromatous material liberated from the aortic wall to the cerebral circulation. The use of TEE and epiaortic scanning facilitates a "knowledgeable avoidance" of the atheromatous ascending aorta with respect to cannulation, clamping, and anastomosis placement.84 Hammon et al85 have recently demonstrated that avoiding manipulation of the aorta by using only a single-clamp application can significantly reduce postoperative cognitive loss. Optimal placement of the aortic cannula in an area relatively devoid of plaque, and the use of specialized cannulae with optimal hydrodynamics and less "sandblasting" effects86 can also decrease the embolization of plaque.
Most of the thoracic aorta can be routinely imaged with multiplane TEE because it is adjacent to the esophagus while moving vertically through the mediastinum. TEE offers an advantage over epiaortic ultrasound (EAU) imaging in allowing continuous monitoring without interruption of the surgical procedure. However, because the air-filled trachea is interposed between the esophagus and the distal ascending aorta and proximal aortic arch, these regions usually cannot be visualized with TEE. EAU imaging can be used to examine these areas through a median sternotomy by covering a high-frequency transducer with a sterile sheath and placing it directly on the ascending aorta in the surgical field. Recently published guidelines state that EAU imaging is a superior technique compared with TEE for the detection and localization of ascending aortic atherosclerosis compared with manual palpation and TEE.84 A comprehensive EAU examination is based on a minimum of 5 views for the evaluation of the ascending aorta from the sinotubular junction to the origin of the innominate artery and the aortic arch. An EAU examination can be performed rapidly and provides valuable information for the management of atheroma burden in patients with cardiac surgical conditions who require aortic manipulation. Further studies are warranted to determine the optimal atheroma grading scale and to delineate management strategies directed toward plaque avoidance and improving patient outcomes.
A case series using RT 3D epiaortic echocardiography showed that 3D was better in displaying diffusely dispersed plaques. Another advantage of 3D epiaortic scans might be the inclusion of discernable landmarks within the aorta like the AV to clarify the relative position of the plaque.87
Many different classification systems for aortic atheroma severity have been proposed. The most widely used system was proposed by Katz et al, consisting of a 5-grade classification system. A grade I atheroma has minimal or no intimal thickening. A grade II atheroma has severe intimal thickening without a protruding element. A grade III atheroma has intimal thickening protruding less than 5 mm into the lumen. A grade IV atheroma protrudes more than 5 mm into the lumen. A grade V lesion is any atheroma with a mobile component. Although currently there is no consensus as to the size of plaque that should warrant alteration of the surgical procedure, large atheromas and atheromas with mobile elements should warrant discussion with the surgeon.
TEE is useful for diagnosis and classification of thoracic and abdominal aneurysms (Fig. 31-36). An aneurysm of the aorta involves an increase in the luminal diameter of all 3 layers of the aorta. A pseudoaneurysm involves an interruption of the intima and media at the level of the aneurysmal sac and its communication with the native aorta. An ascending aortic diameter larger than 4 cm, descending thoracic aneurysm larger than 6 cm, or abdominal aortic aneurysm larger than 5 cm in diameter is considered an indication for surgical intervention.
Short-axis (A) and long-axis (B) views of a descending thoracic aorta aneurysm with ulcerated atheroma.
Dissection of the aorta is a process in which the intima separates from the adventitial layer. It is characterized by the presence of an intimal flap and resulting false and true lumens. Aortic dissection can result from intimal rupture followed by cleavage formation and propagation of the dissection into the media. Additionally, aortic dissection can result from intramural hemorrhage and hematoma formation in the media followed by perforation of the intima. The presence of an intimal flap is the most characteristic feature of aortic dissection. The pathogenesis of dissection is complex. Medial degeneration tends to be more extensive in older individuals and in patients with hypertension, Marfan syndrome, and bicuspid AVs.88 The true lumen diameter typically is smaller than the false lumen diameter (Fig. 31-37A), and spontaneous contrast can often be seen in the false lumen. However, PWD should be used to confirm forward flow in the presumed true lumen during systole (Fig. 31-37B).
A. Descending aorta short-axis view of an aortic dissection. B. Descending aorta long-axis view of an aortic dissection at the level of an intimal tear (arrow).
Aortic dissection is divided into acute and chronic types, depending on the duration of symptoms. Acute aortic dissection is present when the diagnosis is made within 2 weeks after the initial onset of symptoms. Approximately one-third of patients with aortic dissection fall into the chronic category in which symptom duration is longer than 2 weeks. The most common site of initiation of aortic dissection is the ascending aorta (50%) followed by aortic regions in the vicinity of the ligamentum arteriosum.
Anatomically, aortic dissection has been classified by 2 schemes. The DeBakey classification consists of the 3 types: type I includes both the ascending and the descending aorta, type II includes only the ascending aorta, and type III includes only the descending aorta. The Stanford classification consists of 2 types: type A involves the ascending aorta regardless of the entry site location, and type B involves the aorta distal to the origin of the left subclavian artery. Whereas any dissection involving the ascending aorta (DeBakey types I and II or Stanford type A) is an indication for repair, dissections confined to the descending aorta can be medically managed, at least initially.
Two-dimensional TEE is one of the most frequently used imaging modalities to diagnose aortic dissection and showed a sensitivity comparable to CT scan and MRI with a lower specificity due to false-positive findings in the ascending aorta.89,90 Several case reports have demonstrated that 3D TTE might add value to 2D TTE in identifying aortic dissection. Color Doppler 3D TEE allowed detecting an extension of the dissection into the innominate artery.91-93 The main advantage of RT 3D TEE may be the determination of the interrelationship of the dissection flap to adjacent structures (eg, if the coronary arteries are involved in the dissection) (see Fig. 31-30D). This can be best addressed by using the 3D zoom mode.
Endovascular repair of the aorta has gained popularity as a reliable alternative to conventional repair. TEE is used to supplement intraoperative angiography in guiding placement of thoracic endografts. During endovascular repair, TEE is the most sensitive imaging modality currently available for diagnosing endoleaks immediately after graft deployment. The ability to use intraoperative TEE for visualizing the thoracic and abdominal aorta and monitoring cardiac function makes it an invaluable tool during these procedures.94
The RV is often described as a crescent-shaped, thin walled, and compliant chamber. It is less contractile than the LV, and its oxygen requirements are lessened by its reduced muscle mass and lower afterload. The right coronary artery (RCA) supplies the RV free wall, the posterior descending artery supplies the inferior RV wall, and the anterior RV wall has a dual blood supply from the conus branch from the RCA and the moderator branch from the left anterior descending artery.95 The RV is a low-pressure system, with an average pressure of 20/5 mm Hg. Therefore, coronary flow to the RV from the aorta follows this favorable pressure gradient, resulting in perfusion during both diastole and systole, unlike the high-pressure LV, which is perfused mainly during diastole.96,97 RV contraction resembles peristaltic motion, which functions to prolong ejection time by ejecting blood even as proximal RV pressures decline, thus minimizing end-diastolic pressure and promoting venous return.98 RV ejection results primarily from RV free wall inward motion, with a smaller contribution from descent of the base of the heart.
The RV is highly sensitive to changes in afterload and susceptible to coronary air embolism because of the anterior location of the RCA takeoff. Furthermore, RV myocardial protection during cardiac surgery is more difficult than for the LV. Evaluation of the RV is a necessary part of a comprehensive TEE examination because RV dysfunction in cardiac surgery correlates with mortality.99 However, because of its anterior position far from the TEE probe and its geometric complexity because of its crescent shape and twisting contraction of its thin free walls, assessment of the RV with TEE is more challenging than that of the LV.
TEE examination of the RV is primarily performed qualitatively by assessing the RV in LAX with the ME 4-chamber (see Figs. 31-3B and 31-38B) and TG RV inflow views, as well as in SAX with TG mid-SAX (Fig. 31-41) and ME RV inflow–outflow views (Fig. 31-4B). The RV free wall is best viewed from the ME 4-chamber and TG mid-SAX views. When assessing RV function, RV dilation, the presence of interatrial or interventricular septal shift to the left, RV wall motion abnormalities, significant tricuspid insufficiency, and IVC engorgement indicate dysfunction.100-102RV hypertrophy is defined as end-diastolic free wall thickness larger than 0.5 cm (or greater than half the thickness of the LV).
A. Transgastric short-axis view with rightward rotation at the level of the tricuspid valve leaflets. Arrow indicates septal tricuspid leaflet poorly visualized in this plane. B. Midesophageal 4-chamber view showing severe right ventricular dilation and associated tricuspid regurgitation. AL, anterior tricuspid leaflet; LA, left atrium; LV, left ventricle; PL, posterior tricuspid leaflet; RA, right atrium; RV, right ventricle.
RV dilation is indicated by an RV diastolic diameter that exceeds the LV diastolic diameter in the TG mid-SAX view. RV dilation also can be graded from the ME 4-chamber view. The normal-sized RV will not form part of the heart apex. If the apex of the heart includes the RV apex, then moderate RV dilation is present; if the apex is entirely formed by the RV, then severe dilation is present.6
Semiquantitative assessment of RV systolic function is described by the RV fractional area of contraction in the ME 4-chamber view and the tricuspid annular plane systolic excursion (descent of the tricuspid annulus) in the ME 4-chamber view. In a retrospective study, RV fractional area of contraction below 35% was associated with poorer outcomes.103 Tricuspid annular plane systolic excursion greater than 25 mm correlates with normal RV EF.104 However, because of the complexity of the RV anatomy, these measurements may be inaccurate, so a comprehensive qualitative assessment must be performed.
In high-risk cardiac procedures, dynamic analysis of RV performance is important but has been hampered by the inability to reliably image the geometric complexity of the RV. Therefore, all 2D echocardiographic approaches to RV volumes and function are inadequate because they rely on visual estimation and geometric assumptions. With the introduction of RT 3D TTE imaging, dedicated RV quantification software has been introduced and validated in comparison with cardiac magnetic resonance and radionuclide ventriculography as gold standards.105,106 Recent work suggests that 3D echocardiography is useful for dynamic RV assessment. Three-dimensional echocardiography may be able to overcome the limitations of 2D echocardiography and has been shown to improve the accuracy and reliability of RV quantification compared with 2D.107,108 Free-standing software (TomTec Imaging software, Unterschleissheim, Munich, Germany) dedicated to RV quantification facilitates the analysis of RV volume and function and can be performed both with 3D TTE as well as 3D TEE data (Fig. 31-39).109
A. Three-dimensional (3D) transesophageal echocardiography (TEE) full volume of the right ventricle displayed in 3 short-axis and 2 long-axis reconstruction planes. B. Offline reconstruction of the right ventricular cavity using TomTec analytical software (4D RV-Function application, TomTec Imaging Systems GmbH, Unterschleissheim, Munich, Germany). Manual definition of several endocardial border points of the right ventricle in end systole and end diastole followed by an automatic border-tracking algorithm and segmental analysis will display the right ventricular shell along with an end-diastolic reference mesh (arrow) and volumetric quantification.
The TV consists of anterior, posterior, and septal leaflets; the largest is the septal leaflet (Fig. 31-32A). In the presence of normal leaflets, TR is termed functional and is commonly attributable to RV dilation or dysfunction. In contrast, TR caused by abnormalities is rare.
Similar to the RV, the TV lies in the far field, making 2D and 3D imaging difficult. In the ME 4-chamber view, the anterior (or sometimes posterior) and septal leaflets are seen. In the ME RV inflow–outflow view, the posterior and anterior leaflets are seen on the left and right of the image screen, respectively (Fig. 31-4B). In the TG RV inflow view, the posterior leaflet is in the near field, and the anterior leaflet is in the far field. Optimal visualization of the TV using RT 3D TEE is achieved only in a small percentage of patients.59 It remains to be seen if RT 3D TEE will improve the accuracy in the assessment of valvular dysfunction similar to what has been described for the MV. Early reports using 3D TTE suggest that assessment of tricuspid regurgitation is feasible in most patients and that the shape of the VC is more ovoid than that of MR regurgitant jets.110 Grading TR should consider many factors, including RA and RV size, hepatic flow patterns, VC, and jet area. Severe TR correlates well with systolic flow reversal in the hepatic veins, a VC measuring larger than 6.5 mm in the apical 4-chamber view, and TR jet area more than two-thirds of RA area.111,112 In addition, TV annulus larger than 4 cm and tricuspid inflow velocity longer than 1 millisecond by CWD is associated with severe TR.113
In the absence of pulmonic stenosis, the pulmonary artery systolic pressure can be estimated if TR is present. To accomplish this, the peak pressure gradient is calculated and added to the measured central venous pressure. To obtain the peak pressure gradient across the TV, the modified Bernoulli equation is applied to the peak TR jet velocity measured by CWD.
With regard to tricuspid stenosis, a mean inflow pressure gradient less than 2 mm Hg is considered mild, 2 to 6 mm Hg is moderate, and greater than 6 mm Hg is severe. CWD is used to measure TV inflow velocities, which are used to determine pressure gradients. Multiple views should be interrogated to obtain the best alignment with diastolic inflow and therefore more accurate measurements.
The pulmonic valve is trileaflet, consisting of anterior, left, and right leaflets. Significant pulmonic disease in an adult without congenital heart disease is rare. As with the other right-sided structures, the pulmonic valve is anterior and difficult to image with TEE. The best views for visualizing the pulmonic valve are the ME RV inflow–outflow view (Fig. 31-4B) and upper esophageal aortic arch SAX view (Fig. 31-40A).
A. Upper esophageal aortic arch short-axis view with pulmonary artery and pulmonary valve in the far field. Leftward arrow indicates pulmonic valve. The left pulmonary artery and branch point are not within this two-dimensional ultrasound plane. Ao, aorta with branch vessel (downward arrow); PA, main pulmonary artery. B. Upper esophageal ascending aorta short-axis view at level of the pulmonary artery branch point. Asc Ao, ascending aorta; IV, innominate vein; MPA, main pulmonary artery; RPA, right pulmonary artery; RVOT, right ventricular outflow tract.
In adults, pulmonic regurgitation usually is caused by pulmonary hypertension and annular dilation. The examination should include the regurgitant jet VC, jet length, RV size, and degree of CWD flow deceleration. Holodiastolic flow reversal in the main pulmonary artery (measured with PWD in the upper esophageal aortic arch SAX view) is indicative of significant pulmonic insufficiency.
Pulmonic stenosis is rare in adults and is classified as valvular, subvalvular, or supravalvular. CWD is used in the upper esophageal aortic arch SAX view to obtain a peak pressure gradient (mild stenosis, <30 mm Hg; moderate, 30-64 mm Hg; severe, >64 mm Hg).
Evaluation of the main and right pulmonary arteries is performed from the upper esophageal ascending aorta SAX view. The left pulmonary artery is difficult to image because it usually is obscured by air in the left mainstem bronchus. In adults, the main pulmonary artery is approximately 5 cm in length. The normal main and right pulmonary artery dimensions are 0.9 to 2.9 cm and 1.2 to 2.2 cm, respectively. TEE has 80% sensitivity and 100% specificity for the diagnosis of pulmonary embolus, but its low negative predictive value of 53% makes this modality unsuitable for ruling out pulmonary embolus.114
The pericardial sac is a potential space between visceral and parietal pericardium. Pericardial effusion is a syndrome in which fluid accumulates in the pericardial sac. A wide variety of disease processes can lead to pericardial effusion. Depending on the size and speed of accumulation, a pericardial effusion can compromise venous return and lead to low cardiac output. Tamponade occurs when pericardial pressure exceeds the distending pressure of the cardiac chambers, resulting in impaired diastolic cardiac filling. Echocardiography is helpful for diagnosing pericardial effusion and cardiac tamponade, but cardiac tamponade ultimately is a clinical diagnosis.
Pericardial effusions can be visualized as an echolucent space surrounding the echogenic external border of the heart chambers (Fig. 31-41). A thorough TEE examination, including ME 4-chamber, ME 2-chamber, ME LAX, and TG basal SAX views, should be performed for evaluation of pericardial cavity and surrounding structures. Effusions that separate the visceral pericardium from the parietal pericardium by less than 0.5 cm are small, and those with more than 2-cm separation are large. Three-dimensional imaging may also add to the diagnostic ability of echocardiography.115
Transgastric short-axis view revealing a significant pericardial effusion (arrow). The right ventricle (RV) is enlarged, and the D-shaped left ventricle (LV) indicates elevated right ventricular pressures.
Characteristic echocardiographic findings of cardiac tamponade are RA systolic collapse, RV diastolic collapse, abnormal ventricular septal motion, and reciprocal respiratory variation in ventricular volumes. RA systolic collapse usually develops before RV diastolic collapse. Because of the tethering effect of the pulmonary veins, LA collapse is rare and implies the presence of a large effusion. PWD of mitral inflow velocity and pulmonary vein flow velocity also shows a pronounced respiratory variation pattern in cardiac tamponade.