Transesophageal Echocardiography: Advanced Echocardiography Concepts

Narrow Sector (Live 3D)—Real Time

In this mode, a 3D volume pyramid is obtained. The image shown in this mode is real time. Just as in live 2D imaging, manipulations of the TEE probe (eg, rotation) lead to instantaneous changes in the image seen on the monitor ( Fig. 11.2 ).

Wide Sector Focused (3D Zoom)—Real Time

If only a specific region of interest (ROI) requires imaging, the “zoom mode” can be used. A typical example for this mode would be the mitral valve (MV) apparatus. The 3D zoom mode displays a small magnified pyramidal volume that may vary from 20 × 20 degrees up to 90 × 90 degrees, depending on the density setting. This small data set can be spatially orientated at the discretion of the echocardiographer. A key advantage to this mode is that the real-time 3D images are devoid of rotational artifacts, as are commonly encountered with ECG-gated 3D acquisitions ( Fig. 11.3 ).

Large Sector (Full Volume)—Gated

Because of insufficient time for sound to travel back and forth in large volumes while maintaining a frame rate greater than 20 Hz with reasonable resolution in live scanning modes, one maneuver to overcome this limitation entails stitching four to eight gates together to create a “full-volume” mode. These gated “subvolumes” represent a pyramidal 3D data set as would be acquired in the live 3D mode. This technique can generate more than 90-degree scanning volumes at frame rates greater than 30 Hz. Increasing the gates from four to eight creates smaller 3D subvolumes; this can be used to maintain frame rates and/or resolution as the volumes (pyramids) become larger ( Fig. 11.4 ).

Unfortunately, as with any conventional gating technique, patients with arrhythmias are prone to motion artifacts when the individual data sets are combined. The acquired real-time 3D data set subsequently can be cropped, analyzed, and quantified using integrated software in the 3D operating system (QLAB; Philips Healthcare, Andover, MA; Fig. 11.5 ).

Three-Dimensional Color Doppler—Gated

Because of the large amount of data that must be acquired with 3D color Doppler mode, a gating method must be utilized similar to that of the full-volume mode; however, because of the large amount of data required, 8 to 11 beats need to be combined to create an image. Jet direction, extent, and geometry easily can be recognized using this technique. The strength of this methodology lies in its ability to quantitate severity of regurgitant lesions; 3D quantification of mitral regurgitation (MR) correlates better than 2D imaging, when using angiography as the gold standard. In an experimental setting, 3D quantification was more accurate (2.6% underestimation) than 2D or M-mode methods, which had the tendency to underestimate regurgitant volumes (44.2% and 32.1%, respectively; Fig. 11.6 ). Recent guidelines from the American Society of Echocardiography for the noninvasive evaluation of native valvular regurgitation recommend 3D to locate valve pathology, calculate left ventricle (LV)/right ventricle (RV) volumes, and measure effective regurgitant orifice area (EROA) and quantitation of flow and regurgitant volume by 3D color flow Doppler (CFD).

Types of Prosthetic Valves

Current prosthetic valves are grouped as biologic or mechanical. ^, The manufacturer’s valve sizing refers to the external diameter of the sewing ring, not the actual diameter of the effective orifice space. Bioprosthetic valves do not require long-term anticoagulation ( Fig. 11.11 ) and are composed of three biologic cusps (leaflets) sewn into the outer fabric, which open to create a circular orifice with a flow pattern that is similar to the native valve when in the aortic position. Bioprosthetic valves may be stented or stentless, the former having the leaflets sewn into a fabric-covered metal supporting strut. Stentless valves are either a preparation of animal aorta or sculpted pericardial leaflets without any added strut support which was meant to overcome stress and tissue failure associated with the stent, while providing a larger effective orifice area (EOA) compared to its stented counterpart.

A variety of mechanical valves ( Fig. 11.12 ) have been implanted. The most commonly implanted mechanical valve is a bileaflet valve in which two semicircular disks rotate around supporting struts attached to the valve housing. These open to form two large lateral orifices and a smaller central orifice. Several other types of mechanical valves were implanted in the past and will uncommonly be encountered in patients. The ball-in-cage valve houses a spherical occluder contained within a metallic cage. This occluder fills the cage orifice in the closed position but rides above the orifice during antegrade flow. Single tilting disk valves contain a single circular disk controlled by a metal strut that opens at an angle to the annulus plane ( Boxes 11.1 and 11.2 ).

BOX 11.1

Causes of Prosthetic Valve Regurgitation

• Paravalve

  • Calcification

  • Abscess

  • Dehiscence

• Leaflet pathology: excess mobility

  • Abscess

  • Tears

  • Degeneration

  • Endocarditis

  • Bioprosthetic valves: leaflet perforation/destruction

  • Mechanical valves: interference with valve opening/closing

• Leaflet pathology: restriction/distortion

  • Suture

  • Thrombus

  • Pannus

  • Preserved leaflet valve apparatus interfering with closure of mechanical leaflets

  • Stuck leaflet

BOX 11.2

Causes of Prosthetic Valve Stenosis/Obstruction

• Prosthetic valve stenosis

  • Stuck leaflet

  • Thrombus

  • Pannus

• Nonvalvular obstruction

  • Dehiscence

  • Obstructing retained native tissue

  • Suture causing restriction of leaflet

  • Subvalvular obstruction (aortic and pulmonary valves)

  • Systolic anterior motion (aortic and pulmonary valves)

  • Supraannular narrowing (aortic and pulmonary valves)

• Doppler issues/artifacts/errors: normal prosthetic valve function

  • Sampling of other flow (ie, sample mitral regurgitation during assessment of the aortic valve)

  • Subvalvular obstruction

  • High cardiac output

  • Significant aortic valve insufficiency

• Patient-prosthesis mismatch

• Compliance issues (net changes) affecting pressure half-time

Doppler Echocardiography for Prosthetic Valves

Compared with a normal native valve, normally functioning prosthetic and repaired valves in the same space have a smaller EOA and higher antegrade pressure gradients. Knowledge of manufacturers’ publish data on the flow characteristics of each specific prosthetic valve and its various sizes is useful to discern normal from abnormal function ( Table 11.3 ).

TABLE 11.3

Expected Ranges of Areas and Pressure Gradients for Prosthetic Valves in the Aortic and Mitral Positions

Diameter (mm)	Peak Gradient (mm Hg)	Mean Gradient (mm Hg)	Effective Orifice Area (cm 2 )
Stented Bioprosthetic Aortic Valve
19	32–44	24–26	0.8–1.2
21	25–28	17–21	1.1–1.5
23	21–29	12–16	1.3–1.7
25	16–24	9–13	1.9
27	19–22	6–12	2.2
29	18–22	10–12	2.8
Stentless Aortic Valve
19		12–13	1.2–1.3
21	17–40	7.5–18	1.2–1.6
23	18–29	7–18	1.6–2.2
25	14–28	5–17	1.6–2.3
27	26	4.7–18	1.9–2.7
29	24	4	2.4
Bileaflet Mechanical Aortic Valve
16	40–50	25–30	0.6
17	30–40	20–25	0.9–1.0
19	30–40	15–20	0.9–1.2
21	25–30	13–20	1.2–1.4
23	19–25	11–20	1.4–1.8
25	17–23	9–12	1.9–2.2
27	14–20	8–11	2.3–2.5
29	10–20	6–9	2.8–3.1
31	10–15	5–10	3.1
Bileaflet Mechanical Mitral Valve
25	10	4	1.8–2.7
27	8–11	3–4	1.8–2.9
29	8–10	5	1.8–2.3
31	8–12	4–5	2.0–2.8
33	8–9	4–5	3.0
Stented Bioprosthetic Mitral Valve
25	10–15	5.9–6.3	2.0–2.4
27	9.5–16	5.4–6.2	2.0–2.6
29	5–13	3.6–4.6	2.4–2.6
31	4–13.5	2.0–5.0	2.3–2.4
33	12.8	3.8	3.4

The data highlight the variability of reported data reflecting a host of operator variables and assumptions of physical principles. The data also provide practitioners with a reference to determine which prosthetic valve size is most appropriate for the individual patient to avoid patient-prosthesis mismatch. Similar data are applied when right-sided valves are being replaced as similar valves are employed; however, clinical echocardiographic data are not similarly available.

Whereas Doppler flow profiles across normal native, most repaired, and bioprosthetic valves are consistent for flow moving through a single orifice, flow profiles across multiple orificed mechanical valves and some repaired valves (eg, Alfieri repair, MitraClip repair) are more complex ( Figs. 11.13 and 11.14 ). Flow and pressure gradient through each orifice are dependent on orifice size, geometry, and stroke volume (SV).

The bileaflet prosthetic valve has two semicircular disks which opens to form two larger semicircular lateral orifices and a smaller slit-like central orifice ( Figs. 11.13–11.15 ) ^{, ,} In the open position, CFD shows antegrade flow through two larger lateral orifices and a small central orifice. A higher velocity, less dense, outer flow profile (outer envelope) may reflect due to local acceleration forces through the central orifice. In the mitral position, this flow velocity has also been thought to represent distal flow accelerations or artifact. For the bileaflet mechanical mitral prosthesis, the denser, lower velocity, inner flow profile better represents valve function. ^{, ,}

Given that pressure gradients vary depending on SV and orifice size and are specific for native, prosthetic, and repaired valves, determining the valve EOA adds useful information regarding function. Indexing the valve areas to individual body surface area (BSA) allows an assessment of the valve relative to the patient’s size. A relatively small valve area (relative to the BSA) is called patient-prosthesis mismatch (PPM). PPM is more commonly described and discussed in the context of AV surgery, and is associated with short- and long-term adverse outcomes. A recent investigation into intraoperative Doppler interrogation of surgical AV replacements demonstrated that intraoperative gradients are less valuable than the type and size of a prosthetic valve in predicting postoperative PPM. Elevated gradients therefore are important in identifying valve disfunction as opposed to identifying PPM.

Color Flow Doppler

Mechanical valves have normal washing jets engineered into their design ( Fig. 11.16 ). ^{, ,} These flows occur within the annulus and are thought to prevent the formation of thrombi at sites of blood flow stasis. These jets are small (vena contracta [VC] <3 mm) and low velocity, typically have a uniform color pattern (minimal aliasing), and do not extend far from the valve plane. Bioprosthetic valves tend to have small central regurgitant jets. All paravalvular regurgitant jets are considered abnormal. However, regurgitant jets less than 3 mm in width are not likely to pose a long-term problem, especially in the absence of clear disease. Ideally, a repaired valve will have no regurgitant jet, however, due to multiple variables, the postrepair examination should yield mild or less regurgitation.

Antegrade flow across a single tilting disk prosthetic valve is characterized by a major and a minor orifice. CFD indicates nonlaminar and asymmetric flow as blood accelerates along the tilted surface of the open disk. In the closed position, a single tilting disk normally demonstrates a regurgitation jet directed away from the sewing ring starting at the edge of the major orifice. When a bileaflet mechanical valve is imaged in the closed position, multiple washing jets of regurgitation are normally seen in the plane parallel to the leaflet-opening plane. All the regurgitant jets are located inside the sewing ring, with two jets originating from where the leaflets meet the housing apparatus, and a third central jet originating where the leaflets meet each other.

Three-dimensional imaging with CFD highlights why simpler 2D assessments may not be accurate ( Figs. 11.17–11.19 ). Specifically, geometric assumptions required for several of the equations and principles are not always accurate. Visualizing the flow profile on three levels—pre-valve, valve, and post-valve—displays the characteristics of the valve orifice and flow through it. The recent advancements in 3D imaging allow a more accurate area measurement using planimetry (see Fig. 11.19 ).

Normal Anatomic and Functional Features of the Native Valve

The anatomic and functional features of MV have been reviewed extensively (see Chapter 10 ) and understanding of MV function and failure has contributed to the success of MV repair. ^, The normal MV is a thin bileaflet (each < 2 mm thick) valve, of which the anterior and posterior leaflets insert into their respective annuli. Each of the leaflets is divided into segments or scallops, which have been defined by Carpentier and Duran ( Fig. 11.20 ). Both investigators describe the posterior leaflet as having three scallops or segments: anterolateral and superior (P ₁ ), middle (P ₂ ), and posteromedial and inferior (P ₃ ). Duran divides the anterior leaflet into two larger segments (anterior [A ₁ ] and posterior [A ₂ ]) and two smaller commissural segments (C ₁ and C ₂ ). By contrast, Carpentier describes the anterior leaflet with relation to the posterior leaflet; A ₁ , A ₂ , and A ₃ lying in the same respective planes. Although the posterior annulus covers two-thirds of the annular circumference, the posterior leaflet covers only one-third of the valve area. By contrast, the anterior leaflet is responsible for two-thirds of the valve area (see Fig. 11.20 ). Functionally, it appears that the posterior leaflet provides a coapting surface for the larger anterior leaflet. During coaptation the leaflets overlap by at least 6 mm and the base of the coaptation point lies within 6 mm of the annular plane but not above it. The importance of the leaflet heights or lengths and coaptation point is seen in their effect on blood flow direction into and out of the LV. ^, During ventricular diastole, the anterior leaflet is concave to the left atrium, directing blood flow toward the ventricular apex along the posterolateral wall ( Fig. 11.21 ). Subsequently, before and during ventricular contraction, blood flow is directed toward the left ventricular outflow tract (LVOT) along the anteroseptal wall. During this latter time period, the anterior leaflet is convex toward the left atrium enlarging the LVOT just before and during systolic ejection. This pattern of blood flow sets up a vortex with energy that drives flow up and toward the AV with minimal interference and maximum efficiency (see Fig. 11.21 ). Other anatomies and flow directions are less efficient.

The chordae connect the mitral leaflets to the two papillary muscles (anterolateral and posteromedial) and ventricular walls, and create important interactions between the mitral apparatus and the ventricular myocardium ( Fig. 11.22 ). The anterolateral papillary muscles connect to the more anterior and lateral portions of each leaflet and the posteromedial papillary muscle connects to the more posterior and medial portions. The primary purpose is to prevent leaflet prolapse or flail by creating tension during papillary muscle contraction (i.e., ventricular systole). There are multiple types of chordae. While the primary chordae prevent prolapse, other secondary, tertiary, and quaternary chords connect areas of the mitral leaflets to the ventricular walls. These chordae help maintain both function and shape of the ventricle.

The normal mitral annulus is a 3D saddle-shaped dynamic structure ( Fig. 11.23 ). Its shape and position change throughout the cardiac cycle to optimize forward flow into the ventricle, prevent regurgitant flow, and accommodate ventricular systolic outflow. During diastole the mitral annulus is more planar and forward toward the ventricular cavity opening up wide and directing flow toward the posterolateral ventricular wall creating a vortex and vortical forces, resulting in flow toward the apex and then anteroseptal toward the LVOT prior to systolic ejection. In conjunction with the end of diastole and onset of systole, the mitral annulus contracts posterolaterally toward the membranous portion and superiorly toward the atrium, both actions increasing size of the LVOT, increasing its reservoir capacity prior to ejection, and minimizing interactions between systolic outflow and the mitral leaflets.

Prosthetic or Repaired Mitral Valve

It is important to know the details of the surgical procedure including what kind of valve (bioprosthetic vs mechanical) was placed or how the valve was repaired. For valve repairs, information regarding annulus type (flat vs saddle-shaped, full vs partial), and leaflet resection, repair, or augmentation helps echocardiographers understand what they see during imaging. ^{, , ,}

The repaired valve relies mostly on a normally mobile anterior leaflet that is adequate in size to cover the coapting area, while the posterior leaflets provide a coapting surface ( Figs. 11.24 and 11.25 ). ^, The anterior leaflet is generally preserved or, when necessary, repaired, while the abnormal posterior leaflet scallops are either resected or repaired. Variations of the latter include repair (neochordae) or folding of the posterior leaflet to provide a larger coapting surface and a larger valve area (see Figs. 11.24 and 11.25 ). The Alfieri repair is currently a much less common alternative repair procedure that reduces or prevents prolapse. ^, It is classically performed centrally, resulting in a figure-of-eight opening; however, it may also be performed peripherally along the commissures to form a dual figure-of-eight orifice in diastole ( Fig. 11.26 ). The relatively recent application and expanding role of the MitraClip procedure, a percutaneous “Alfieri” procedure, in which a metal clip apposing two opposing leaflet edges provides options for high-risk cases as a solution for high-risk surgical cases ( Fig. 11.27 ). For all echocardiographic assessments, recording of the patient’s hemodynamic status improves the perspective at the time of evaluation.

The Echocardiographic Examination

The 2D and Doppler examinations are accomplished from a number of echocardiographic windows, with emphasis on midesophageal (ME) windows (0–150 degrees), to analyze the native valve before surgery, and the repaired or prosthetic valve after ( Figs. 11.26 , 11.28–11.30 ). ^{, , ,} Transgastric (TG) views complement imaging of the valve, allowing a short-axis perspective, and are also useful to visualize and interrogate, using Doppler, the LVOT ( Figs. 11.30–11.32 ).

Evaluation includes assessment of thickness, and any associated mobile structures, the latter of which may include chordae, masses, fractured calcium deposits, and suture materials. Imaging of the subvalvular apparatus identifies thickening, calcifications, mobile or flail of the chordae and/or papillary muscles. The valve should appear stable (i.e., no rocking) and secured in the surrounding tissues. Hypoechoic spaces or lucency of the surrounding tissues may suggest infection or abscess, dehiscence, or rupture ( Fig. 11.33 ).

For mechanical prosthetic valves, imaging perpendicular to the leaflets allows seeing the opening and closing of the leaflet edges while parallel imaging facilitates viewing of signature regurgitant jets ( Figs. 11.13, 11.16, 11.34–11.37 ). Specific concerns regarding bioprosthetic valves include positioning of the struts in the LVOT potentially causing obstruction to systolic outflow ( Fig. 11.38 ).

The Doppler examination assesses, both qualitatively and quantitatively, the presence, direction, and width of normal and abnormal blood flows of the native, prosthetic, and repaired valves. In general, abnormal flows may appear ‘turbulent’ in that they exceed the Nyquist limit or aliasing velocity. The ME windows offer the best proximity of the valve to the transducer aligning blood flow and the ultrasound beam. Although qualitative CFD assessments may suggest elevated velocities based on the presence of aliasing, this may or may not indicate abnormal flow. Further quantitative analysis should be performed to clarify the flow.

Different prosthetic valves have signature flow profiles. Bioprosthetic valves allow a large central forward flow and, for some prostheses, a small central regurgitant jet (see Figs. 11.34–11.37 ). Mechanical valves consist of two or three forward jets and one or two small regurgitant jets (see Fig. 11.37 ).

Flow across the repaired valve depends on the repair technique. Typically, a large singular jet directed toward the posterior and lateral walls toward the apex followed by flow toward the LVOT along the anterior and septal wall is seen, which is not dissimilar to the normal native valve (see Fig. 11.21 ). ^, Alternatively, a central Alfieri repair results in a figure-of-eight orifice and provides two forward moving jets of flow (see Fig. 11.26 ).

Mitral Regurgitation

MR occurs as a result of dysfunction of one or more of the components of the mitral apparatus ( Table 11.4 ). MR can be grouped into three types: those with normal leaflet mobility (type 1) (see Fig. 10.79 ; Video 10.60 ), those with excessive leaflet mobility (type 2) (see Fig. 10.75 ; Video 10.57 ), or those with restrictive leaflet mobility (type 3). ^, The latter group can be further distinguished based on the timing of the cardiac cycle to which leaflet mobility is impaired. Type 3a involves restriction during the diastolic phase or during both systole and diastole as seen in rheumatic disease with involvement of leaflet and chordae (see Fig. 10.76 ; Video 10.58 ). Type 3b involves restriction during the systolic phase of the cardiac cycle as seen in patients with functional MR as a result of either myocardial ischemia/infarction or cardiomyopathy during which tethering and/or remodeling has occurred (see Fig. 10.77 ; Video 10.59 ). The types of MR are summarized in Fig. 10.78 .

Type 1 MR can be seen in the presence of annular dilation or leaflet perforation. In the former, the annulus is more likely to dilate along the posterior and lateral annular areas as these are mostly muscle and membranous tissues. As the annulus dilates, it becomes more circular and flatter. The regurgitant jet may be centrally or eccentrically directed. The greater the amount of annular dilation (diameter >5 cm) and dysfunction, the less likely that valve repair will provide long-term freedom from valve replacement. Leaflet perforation occurs in the presence of endocarditis and is more commonly found on the anterior leaflet.

For type 2 MR, the leaflets are described by their systolic excursion relative to the annular plane. Prolapse is defined, during two-dimensional imaging from the long-axis widow, as a greater than 2-mm excursion above the annular plane with the leaflet tip pointing down. ^, Flail is similarly described except with the leaflet tip/edge pointing above the annular plane. Excessive leaflet mobility is often accompanied by redundant or torn chordae or, in the case of myocardial infarction (MI) or trauma, a torn or ruptured papillary muscle. Regurgitation caused by degenerative or myxomatous mitral disease is associated with either prolapse or flail of an isolated scallop or multiple scallops involving one or both leaflets. Most commonly, the posterior leaflet is involved with the middle scallop (P ₂ ) being involved in more than 40% to 50% of the cases. ^{, ,} Next in incidence, the middle scallop of the anterior leaflet (A ₂ ) is involved. Both leaflets are involved in up to 40% of cases. The delineation of the scallops is important in determining the appropriate surgical procedure and whether a repair is feasible.

Type 3b MR seen with dilated cardiomyopathy (DCM) and/or ischemic cardiomyopathy may include normal appearing leaflets; however, reduced systolic return is decreased as a result of tethering. Quantitative assessments help to determine the presence and extent of tethering and may predict outcome after valve repair. These assessments include tethering height and area, and angles of coaptation ( Figs. 11.39 and 11.40 ). Tethering heights greater than 1 cm or tethering areas greater than 1.6 cm ² are suggestive of severe long-standing changes with greater left ventricular dysfunction, dilation, and remodeling ( Figs. 11.40 and 11.41 ). With greater chronicity, leaflet compliance and mobility decline as well.

Restriction of abnormal leaflets (type 3a) is seen with rheumatic valves or after radiation therapy. In these cases, the valve leaflets, with or without subvalvular tissues, may be thickened and/or shortened. Although rheumatic leaflets (anterior leaflet) may appear like a hockey stick during diastole, this finding is not necessary for the diagnosis to be considered.

Prosthetic valves are associated with a normal signature of expected regurgitant jets and should be differentiated from abnormal flows (see Figs. 11.16, 11.31, 11.35–11.37 ). Normal or nonproblematic regurgitant jets are less than 3 mm in width and do not extend far from the valve. All paravalvular regurgitant jets are considered abnormal. However, regurgitant jets less than 3 mm in width are not likely to pose a long-term problem, especially in the absence of clear disease ( Fig. 11.42 ). Regurgitant jets greater than 3 mm in width and/or eccentrically directed away from the middle of the valve carry a greater risk of MR progression and/or reintervention ( Fig. 11.43 ). These abnormal flows can result from a number of causes, including leaflet restriction or excess mobility, endocarditis, or annular dehiscence ( Figs. 11.44–11.46 ).

Repair of the MV generally is applied to regurgitant valves. ^, Although the goal is to eliminate regurgitation, mild or less is acceptable, while more than mild increases the risk of MR progression and reoperation (see Fig. 11.46 ). The location and direction of the regurgitant jet depends on the pre-repair dysfunction and the repair technique. Determining the cause of MR after repair is important to decide whether additional repair is feasible or if replacement is warranted.

MR is also described by its acuity, which is related to the level of compensation or decompensation and clinical presentation. In the acute setting, LA and LV compliances have not adapted, resulting in elevated chamber pressures, pulmonary hypertension, and pulmonary edema. RV dysfunction follows as a result. Chronic MR is initially compensated for and includes ventricular hypertrophy and increased EF to maintain forward flow. The increased left ventricular ejection fraction (LVEF) is the result of a lower total resistance as a result of the backward ejection into the pulmonary vascular bed. A normal LVEF in the presence of severe MR is greater than 60%. With continued or worsening MR, ventricular dilation, contractile dysfunction, and increased chamber pressures coincide with clinical decompensation. LA dysfunction, pulmonary hypertension, and, finally, right heart dysfunction occur. Arrhythmias reflect these cardiac changes and decompensation.

Two-dimensional analysis of the native valve helps determine feasibility and technique to repair the valve. For stenotic valves, the examination helps the practitioner determine whether valvuloplasty is a viable option.

Measurements guiding valve repair of the regurgitant valve include annular dimensions, leaflet lengths (anterior leaflet, posterior leaflet), coaptation height (tenting height or area), various angles of coaptation, and relations between the leaflets (coaptation) and the ventricular cavity, or specifically, the ventricular septum (see Figs. 11.39–11.41, and 11.47 ). ^, Data may help the practitioner predict risk of postrepair complications such as SAM and LVOT obstruction (see Fig. 11.47 ).

Predictors of repair failure differ for patients with functional or ischemic MR versus those with degenerative disease. ^{, ,} For all patient types, severe annular dilation (>50 mm) represents prolonged MV dysfunction (i.e., end-stage disease) and a greater risk of repair failure. For functional or ischemic MR, the greater the amount of pre-repair tethering such as a tenting height >1.0 cm or area >1.62 cm ² , and/or a posterolateral coaptation angle greater than 45 degrees is predictive of greater recurrence of moderate or greater MR after 6 months ( Figs. 11.40, 11.41, 11.48 ). Adverse ventricular remodeling predicts repair failure and is indicated by inferior and lateral wall motion abnormalities, dilated LV (LV end-diastolic diameter >65 mm; LV end-systolic diameter >50 mm, or LV end-systolic volume >75 mL/m ² ), and/or a sphericity index higher than 0.7. Although repair of papillary muscle rupture has been reported, such cases are generally managed with valve replacement.

Predictors of a more complicated repair and failure for degenerative valve dysfunction include involvement of multiple scallops, anterior leaflet disease, bileaflet disease, and endocarditis with leaflet destruction. ^, In addition, severe MR in the presence of a normal annular diameter, or short anterior (<26 mm) and posterior (<10 mm) leaflets present a risk of repair failure and post-repair stenosis. These latter predictors reflect the importance of identifying something repairable and of having adequate leaflet heights prior to and after the repair.

Other predictors of difficult repair or adverse outcome include MR due to rheumatic valvitis, radiation therapy; severe calcification of either the valve, the annulus, and/or the subvalvular apparatus; and atrialization of the coaptation points ( Figs. 11.49 and 11.50 ). ^{, ,} The former three reflect restricted tissues, an absence of repairable tissues, or the lack of adequate leaflet lengths. The latter reflects an end-stage degenerative state.

Mitral Stenosis

The normal mitral valve area (MVA) ranges from 4 to 6 cm ² and transmitral flow velocities are less than 1 m/s ( Table 11.5 ). The more common causes of mitral stenosis (MS; MVA <2.0 cm ² ) include rheumatic stenosis, calcific MS, and, less commonly, congenital MS. The echocardiographic examination incorporates 2D and Doppler technologies to diagnose and assess for the presence and severity of MS (see Figs. 11.54 and 11.55 ).

Rheumatic valvitis causes commissural fusion, chordal shortening/fusion, and leaflet thickening, all complicated by calcification of the structures. The leaflet tips become fused. While stenosis is more common in the rheumatic MV, the leaflet and chordal abnormalities can also be associated with significant MR (Carpentier type IIIa). In addition, involvement of other cardiac tissues and valves is not uncommon, including AV insufficiency and tricuspid regurgitation (TR). Calcific mitral degeneration mainly affects the mitral annulus followed by leaflet base calcification and uncommonly results in stenosis unless associated with leaflet thickening.

Patients with MS may be asymptomatic or may have varying degrees of LV and RV failure depending on the severity and chronicity of the disease. With greater decompensation, forward flow across the valve and into the LV declines, while LA pressure size and function deteriorates. With time, the pulmonary vascular pressures rise, pulmonary edema occurs, and significant right-sided heart afterload, dilation, and dysfunction follow. Patients experience fatigue, hemoptysis, and right-sided heart failure. TR may result either from primary rheumatic involvement and/or secondary to pulmonary hypertension. Atrial fibrillation and stroke may be initial presenting signs, the latter, in part, resulting from development of atrial thrombus, 90% of which occur in the left atrial appendage (LAA).

The assessment of the stenotic MV assesses etiology, severity, and the need for and timing of invasive procedures, the latter being either valvuloplasty or valve replacement. The Wilkins score was proposed and now used to predict outcome after valvuloplasty. The score includes assessment of leaflet thickening, mobility, and calcification, as well as subvalvular thickening, each of which is scored from 1 to 14. A score less than 8 suggests that the valve is more amenable to valvuloplasty as compared to a score higher than 8. Variations on this score as well as others have been proposed, including one based on 3D imaging. Findings consistently show that the greater the amount of thickening, calcification, and immobility, the worse the outcome after valvuloplasty.

Assessing forward flow across the prosthetic MV is similar to that for the native valve. As described earlier, different prostheses have different signature forward flow profiles. It is expected that normal transvalvular velocities and calculated gradients will be higher than that normal native valve in the same position. The more information known about specific prosthesis, the easier it is to distinguish between normal and abnormal. Prosthetic valve stenosis is caused by leaflet restriction, thickening, and/or thrombosis (see Figs. 11.56 and 11.57 ).

The American Society of Echocardiography level 1 recommendations for assessing MV patency include peak transvalvular jet velocity, pressure gradients, and MVA calculated from the pressure half-time (PHT) or measured by planimetry (see Figs. 11.54 and 11.55 ). ^{, ,} The most direct measurement for tissue valves is planimetry made possible by 2D or, more recently, 3D imaging, the latter by using a multiplanar reconstruction (MPR) analysis. Whereas 2D planimetry is performed from TG MV short-axis imaging, 3D planimetry is obtained using volumetric data from ME windows.

Peak pressure gradients are calculated from the peak transvalvular jet velocity using the simplified Bernoulli equation. Mean pressure gradients are obtained by tracing the TVI across the MV to integrate the various jet velocities allowing calculation of the mean gradient. Since the peak gradient is influenced more by the net compliance between the left atrium and LV, the mean gradient is of greater importance.

The Doppler data are affected by changes in cardiac loading conditions, cardiac output (CO), and net compliances, coexisting valvular or congenital lesions, specifically including MR, AV dysfunction, and an atrial septal defect (ASD). The calculation of the MVA from the PHT is done by applying an empirically derived value (see Fig. 10.73 ).

Variables that increase the LA pressure or reduce LV pressure increase gradient and may overestimate MS severity. Doppler measures of MVA, including the PHT, are affected by these variables. ^, Variables that reduce LA pressure or increase LV pressure do the opposite. For example, an ASD with left to right flow, moderate or greater AI, or net positive change in the LV-LA compliance causes an overestimation of MVA by shortening the PHT.

The deceleration time (DT) is an extension of the PHT and is the time from the peak velocity to zero velocity across the orifice. Using the DT to calculate MVA requires knowing that PHT is 29% of the DT.

The transmitral TVI may be bimodal with a more rapid initial deceleration followed by a slower decline in gradient. It is recommended to measure the PHT from the slower decline as it better reflects the contribution of the MVA.

Degrees of MS follow similar charts for native and prosthetic valves. Significant (more than mild) MS is considered with a peak velocity greater than 1.8 m/s, a mean transvalvular gradient greater than 5 mm Hg, and a peak gradient greater than 12 mm Hg. An MVA less than 1.5 to 2.0 cm ² is considered stenotic. PPM has been described for prosthetic MVs and considered for an indexed effective orifice area (EOAi; cm ² /BSA [m ² ]) less than 1.25 cm ² /m ² .

Different methods are used to assess the EOA, including the PHT, the continuity equation, and the flow convergence method. The continuity equation can be simply described by the following equation ( Fig. 11.58 ):

The SV can be measured from a reference site using Doppler echocardiography (e.g., pulmonary artery [PA] or LVOT), a noninvasive method (e.g., arterial waveform), or using thermodilution CO if a PA catheter were present.

PISA or flow convergence method has been described to measure MVA and assumes geometric assumptions that variably exist for native valves and less so for prosthetic valves (see Fig. 11.55 ). Qualitatively, the presence of a flow convergence area supports the diagnosis of mitral stenosis.

To avoid geometric assumptions and other variables listed, a Doppler velocity index (DVI) also may be used to assess prosthetic MV patency.

For cases in which imaging is difficult, a modified Gorlin equation can be employed. In this equation, the CO is divided by the square root of the peak transmitral pressure.

Prosthetic or Repaired Aortic Valve

Prior to the evaluation of the prosthetic or repaired AV, it is important to know the details of the surgical procedure and the normal hemodynamic functions that are expected for the replaced or repaired valve. ^{, ,} Surgically aortic valve replacement (SAVR) involves prosthetic valves with annular sizes 19, 21, 23, and 25 mm being most commonly placed. In general, 19, 21, and 23 mm valves result in EOAs of 1.1, 1.4, and 1.6 cm ² , respectively (see Table 11.3 ). ^{, , ,} While stentless bioprosthetic valves are anticipated to have respectively larger EOA, initially the hemodynamic profile may appear inferior due to geometric changes in the presence of perivalvular aortic edema and hematoma, which resolve within 6 months of surgery.

Transcatheter aortic valve implantation (TAVI) includes prosthetic valves sized 20 to 31 mm in diameter with estimated aortic valve area (AVA) ranging from 2.4 to 6.6 cm ² . While the SAVR bioprosthetic valve has three defined struts, the TAVI valve has a curtain that surrounds the leaflets.

While AV repairs are mostly performed for regurgitant valves, repair of congenital AV stenosis has been reported. The appearance of the repaired valve depends on the repair, but by and large results in a singular orifice with a flow profile similar to a normal native valve. While delineation of the pre-repair dysfunction helps guide the repair, the postrepair evaluation predicts long-term function. This includes assessment of length (>4 mm) and level (above annulus) of leaflet coaptation, presence of residual AI, and the size of the annulus.

Echocardiographic Examination

The 2D examination of the AV includes assessments of the supravalvular and subvalvular tissues. Although a comprehensive examination is necessary, particular echocardiographic windows of importance include ME short-axis and ME long-axis windows to image the AV and the tissues above and below in short- and long-axis views. TG windows are useful for quantitative Doppler as the Doppler beam can be best aligned with blood flow across the aortic root.

Leaflet number, thickness, and mobility, and the presence of masses, the latter of which may represent fibrinous strands, endocarditis, tumor, or fractured calcium deposits, are key to determining the etiology of dysfunction and determining whether or not the valve can be repaired or should be replaced. Any evidence of instability and/or hypoechoic planes within the aortic wall or between the valve and the aortic wall suggest valve dehiscence and/or root infection or abscess ( Figs. 11.61 and 11.62 ). ^, The comprehensive examination defines whether or not AI is due to a primary valve dysfunction or secondary to aortic root pathology (e.g., aortic dissection or root dilation). Secondary cardiac effects of AS or AI, including LVH, left heart dilation, and dysfunction, allude to the severity of dysfunction and timing of invasive treatment.

The Doppler (color, PW, CW) examination allows both qualitative and quantitative evaluations of patency and competence, including presence, direction, and width of normal and abnormal blood flow in and around the native, the repaired, and prosthetic valves. ^,

The post cardiopulmonary bypass examination is similar to the pre-examination ( Fig. 11.63 ). The stented and stentless bioprosthetic valves can be differentiated by the presence or absence of both the stent and the supportive struts with the stent ( Fig. 11.64 ). Defined normal forward and regurgitant flows are described for prosthetic valves. It is important to recognize the presence of periprosthetic thickening due to edema or hematoma which begins to resolve in the early postoperative period. For patients with stentless or repaired valves, this may result in a smaller EOA and elevated transvalvular gradients in the immediate postoperative period followed by a significant increase in EOA over the first 3 to 6 months associated with resolution of the perivalvular swelling (see Fig. 11.64 ).

Aortic Regurgitation

AV regurgitation results from either primary aortic leaflet or valve abnormalities or secondarily from ascending aortic pathology. ^{, , ,} Trace or mild AI may be seen in the absence of significant pathology; however, this occurs in the minority of cases (<20%). Similar to other valves, regurgitation can be divided based either on mobility and/or leaflet pathology. Type I dysfunction includes AI due to aortic root dilation ( Fig. 11.65 ). Root dilation includes those tissues extending to the STJ, but not beyond (ie, the ascending aorta). Type II dysfunction reflects excess leaflet mobility noted by either leaflet prolapse or flail ( Figs. 11.66 and 11.67 ). The presence of fenestrations, seen with fibroelastic deficiency, is suggested by multiple areas of regurgitation and may hinder successful repair. Type III dysfunction also reflects restricting leaflet motion ( Fig. 11.68 ). Repair should be considered for type I and type II dysfunctions.

Primary valve pathologies include bicuspid AV, quadricuspid AV, myxomatous degeneration (fibroelastic disease), fenestrations, endocarditis, calcification (often associated with AS), radiation therapy, rheumatic disease, and trauma ( Figs. 11.66–11.69 and Table 11.6 ). The AV also can be involved in association with a subvalvular membrane or a ventricular septal defect (VSD) ( Fig. 11.70 ). Type II dysfunction includes prolapsing or flail leaflets. Multiple color Doppler regurgitant jets are consistent with leaflet fenestrations. Masses, calcification, rheumatic disease, or radiation therapy reduces leaflet mobility. Secondary causes include aortic root pathology such as dilation, dissection, and infection in which the aortic leaflets may be involved or appear normal (see Figs. 11.61 and 11.65 ). Determining the cause of AI is important to determine the best mode and timing of therapy, and whether the valve can be repaired or requires replacement.

Aortic Stenosis

Changes in the native AV architecture occur with age including leaflet thickening found in more than 20% of patients older than 65 years. There is a 4% incidence of AS found in patients older than 85 years. The vast majority of fixed native AS is due to elderly (or senile) calcific trileaflet pathology. ^, This is followed by bicuspid AS and rheumatic AS (see Figs. 10.56 and 10.57 ; Video 10.49 ; Table 11.7 ). Less common outflow obstructions are due to unicuspid valve, supravalvular stenosis (e.g., Williams syndrome), and subvalvular obstruction, such as a subvalvular membrane (see Fig. 11.70 ). Hypertrophic obstructive cardiomyopathy is a dynamic form of obstruction that should be distinguished from fixed forms of obstruction as management is different (see Chapter 18 ). There can be coexistence of obstruction at different levels.

Trileaflet calcific AS is characterized by calcium collection on the leaflet mostly at the leaflet tips and proximal. Rheumatic stenosis involves commissural fusion and thickening of the trileaflet valve with a central triangular orifice. Rheumatic AV disease most often occurs in conjunction with MV disease. Bicuspid AS results from fusion of the commissures with or without calcification. The most common configuration of a bicuspid AV is fusion of the right and left commissures with or without a raphe seen. Fusion of the left and noncoronary cusps is least common. A subvalvular membrane may be a simple protrusion of tissue or a circumferential narrowing of the subvalvular space. Supravalvular stenosis appears as an hourglass-shaped deformity in the supravalvular space with or without irregularities of the coronary arteries. Delineating where the obstruction occurs is extremely important to therapy decision-making.

Miscellaneous Issues

Analyses should be performed at a time when patient hemodynamics (CO/SV) are optimized or at least known. This is especially important for the condition known as low-gradient AV stenosis:

Low-gradient AV stenosis is seen in patients with a reduced SV across the valve, which occurs as a result of reduced LVEF (<40%), CO or SV, arrhythmias, and significant MR. For such cases, calculation of AVA is necessary. If the AVA is less than 1.0 cm ² , a stress echocardiogram (either exercise or dobutamine) should be considered to differentiate between true AS and pseudo-AV stenosis, the latter being the result of reduced opening forces. Hemodynamic goals of the stress test include an increase in the heart rate of either 10 to 20 beats per minute, an increase of more than 100 beats per minute, and/or an increase in SV or EF of 15% to 20%. True AS is characterized by a rise in the mean gradient greater than 40 mm Hg with a persistent AVA less than 1.0 cm ² . An increase in the AVA greater than 1.0 cm ² supports pseudo-AV stenosis. An absence of a hemodynamic response to stress (ie, no change in LVEF) suggests a lack of contractile reserve, which is associated with increased morbidity and mortality with surgery.

Other conditions that affect the echocardiographic-derived gradient include poor alignment of the ultrasound beam with blood flow, which may underestimate the true flow velocity and subsequently calculated gradient.

Increased transvalvular velocities can be seen in the presence of AI and/or a high-flow state. A higher jet velocity may be recorded and overestimate the severity of AV obstruction. Given the proximity of the MV during TG Doppler interrogation of the LVOT and AV, erroneous measurement of the mitral regurgitant jet will cause overestimation of the true transaortic valve velocity. The two flow profiles can be differentiated in that MR is a holosystolic jet compared to a decrescendo-crescendo flow profile of AS (see Fig. 11.76 ). Finally, sequential narrowings (subvalvular or supravalvular stenoses or obstructions) affect detection of the gradient across the AV (see Fig. 11.77 ).

Another issue regarding Doppler assessment of transvalvular gradients is poor alignment between the Doppler ultrasound beam and blood flow, which causes an underestimation of flow velocity and calculation of pressure gradients.

The peak gradient during echocardiography is an instantaneous peak gradient and is larger than that measured during catheterization, which is the gradient between the peak transvalvular pressure and the peak LV pressure. During catheterization, the two peaks occur at different times.

A phenomenon called pressure recovery results in differences between gradients measured during Doppler echocardiography and cardiac catheterization. When flow crosses the stenotic AV, potential energy is converted to kinetic energy and a high pressure gradient is recorded. ^, However, downstream from the stenotic valve, energy is lost to turbulence and viscous forces. Energy may be converted back to potential energy, causing a rise in pressure or pressure recovery. The amount of pressure recovery is related to the differences in the cross-sectional area (CSA) of the ascending aorta.

Pressure recovery is related to the ratio of the EOA/AoA or the EOA of the AV and the CSA of the ascending aorta. Pressure recovery is most significant for patients with an ascending aortic diameter less than 3.0 cm.

Although not often discussed for SAVR, the location of the coronary ostia is a critical part of the evaluation prior to TAVI. During SAVR, the surgeon can identify the coronary ostia and position the prosthetic valve and struts to avoid any obstruction. This is not the case during the insertion of the TAVI valve for which a circumferential supporting curtain, the height of which ranges from 5 to 10 mm, can cause immediate or delayed coronary ostial obstruction. Approximately 90% to 94% of the time, the left and right coronary ostia take off below the STJ, and 10% of the time (L > R), the ostia take off within 10 mm of the AV annulus, increasing the risk of ostial obstruction. Additional risk of coronary ostial occlusion includes a small sinus of Valsalva (diameter <30 mm). Identifying the location of the coronary ostia and the root size are important to define coronary risk for TAVI, but are also important to define the same risk during SAVR.

Surgical or Procedural Intervention

Surgical or transcutaneous AVR is indicated for symptomatic severe AS ( Fig. 11.78 ). Surgical AVR also should be considered for asymptomatic patients with severe AS, or patients with moderate AS with a likely rapid progression (>0.1 cm ² /year), while undergoing other cardiac or aortic procedures. Elective AVR for asymptomatic patients with severe AS is considered to prevent irreversible myocardial changes. AVR for low-gradient (mean <40 mm Hg) severe AS may require assessment of reserve function, ie, viability studies. The decision to perform SAVR or TAVI is an evolving discussion that balances age risk and longevity of the patient, risk of coronary obstruction and future need for coronary intervention, and the durability of the prosthetic valve ( Fig. 11.79 ). ^,

The risk of coronary artery obstruction is significant for both SAVR and TAVI, perhaps more for TAVI given the circumferential curtain. Nevertheless, assessment of coronary height (annulus to ostia) is important to predict and prepare prior to AVR.

Normal Anatomic and Functional Features

The normal TV area is 4 to 6 cm ² and the normal annular diameter is less than 28 mm. The TV has three unequal-sized leaflets (septal, anterior, and posterior) surrounded by a 3D saddle-shaped ellipsoid annulus that contracts and changes its shape and area during the cardiac cycle. ^,

The septal leaflet is attached to the medial or septal wall, which is in continuity with the fibrous trigone of the heart. The posterior leaflet is the smallest of the three leaflets. The anterior leaflet is the largest. The leaflets are attached via chordae to three respective papillary muscles and each papillary muscle gives off chords to at least two leaflets. Congenital variations range from two to nine papillary muscles and as many as six leaflets.

The function, shape, size, and planarity of the annulus are affected by changes in right atrial (RA) and RV size, shape, and function. As the annulus dilates, it becomes more planar, circular, and less contractile. The septal region is attached to the fibrous trigone, it stays relatively stable, however, while the antero-lateral annular regions dilate away from the fibrous skeleton, and is associated with the development of TR.

Prosthetic or Repaired Tricuspid Valve

The importance of TV function and its impact on right-sided heart function and patient outcome is increasingly appreciated. As a result, TV surgery has increased either alone or in association with surgical procedures on the left side of the heart. The vast majority of TV surgery is for regurgitant valves; however, both severely regurgitant and stenotic valves result in clinically relevant right heart failure and warrant surgical consideration. ^, Moderate TV dysfunction should receive consideration for surgery when patients are undergoing cardiac surgical procedures for the left side of the heart.

The majority of cases are due to functional or secondary TR, and more than 80% are repaired. Valve replacement may be considered for cases with high risk of repair failure. Valve replacement is performed for TV stenosis, primary valve disorders (endocarditis, rheumatic valvitis, carcinoid syndrome, traumatic rupture), nonrepairable regurgitant valves, or for clinically relevant recurrent regurgitation after repair. ^, Details of the surgical procedure complement the postcardiopulmonary bypass echocardiographic evaluation.