The mitral valve (MV) is ideally suited to examination with transesophageal echocardiography (TEE) because it lies close to the esophagus and is separated from the transducer by the blood-filled left atrium, which acts as a superb acoustic window. The valvular structures can be positioned easily in the center of the sector scan, permitting the plane of the scan to be rotated 180 degrees through the midpoint of the valve and allowing full visualization of the leaflets. In systole, the leaflets lie perpendicular to the ultrasound beam, enhancing the quality of the two-dimensional (2-D) image. Flow through the valve is nearly parallel to the ultrasound beam, creating excellent conditions for Doppler analysis. These factors, combined with the importance of mitral pathology in cardiac surgical patients, have contributed substantially to the greatly increased use of perioperative TEE over the last decade.
One of the most important developments in echocardiography in the last few years has been the introduction of real-time 3-D imaging into clinical practice (see Chapter 4 ). The MV is ideally suited to 3-D imaging with TEE, and assessing MV pathology is the most common indication for 3-D TEE during the perioperative period.
Mitral anatomy
The MV and subvalvular apparatus include the fibrous skeleton, annulus, leaflets, papillary muscles, and chordae tendineae, as well as the adjacent LV myocardium ( Figure 9-1 ).
Fibrous skeleton, annulus, and leaflets
The fibrous skeleton of the heart provides the structural framework for the four heart valves and is based on three U-shaped cords that form the aortic annulus. Extensions of these cords form the left and right trigones, which together form the mitral annulus. The mitral annulus is weakest posteriorly, where the extensions of the two trigones join.
The mitral annulus is a 3-D, saddle-shaped, ellipsoid fibrous ring ( Figure 9-2 ), which alters shape and decreases in area as it descends during systole; the reduction in diameter of the annulus contributes to valve closure. The “lower” (more apical) and longer axis is along the intercommissural line (seen in the midesophageal commissural view). The “higher” (more basal) and shorter axis is along the anterior–posterior line (seen in the midesophageal long-axis view). Note that the “shorter axis” of the mitral annulus is imaged in the long-axis view. The mitral annulus should be measured at end systole in both the midesophageal commissural and the midesophageal long-axis views.
The diagnosis of MV prolapse should be made only with reference to the “high” axis (midesophageal long-axis view, 120 to 150 degrees), as the presence of leaflet prolapse will be overdiagnosed if the “low” axis (midesophageal commissural view) is used.
The MV is bileaflet, consisting of an anterior and a posterior cusp ( Figure 9-3 ). Each leaflet inserts at its base into the mitral annulus. The leaflets do not lie in a strictly anterior–posterior orientation; the anterior mitral leaflet lies somewhat medially and the posterior mitral leaflet somewhat laterally. The posterior leaflet has twice the annular attachment but only half the base-to-tip length of the anterior leaflet (i.e., the posterior leaflet is longer and thinner), but each leaflet has approximately the same surface area.
The valve leaflets join at two commissures: the anterolateral and the posteromedial. During systole, when the leaflet tips are opposed, a curved coaptation line forms between the two commissures. There is normally 3 to 5 mm of overlap between the leaflets along the coaptation line during systole. The anterior leaflet is in fibrous continuity with the noncoronary leaflet and, to a lesser extent, the left cusp of the AV.
The posterior leaflet is divided into three distinct anatomic scallops or segments: the anterolateral, middle, and posteromedial. Small scallops may be identified in the region of the commissures. Carpentier and Duran have each developed systems of classification of the mitral leaflets ( Figure 9-4 ). The ASE/SCA guidelines use the Carpentier nomenclature, and this approach has been adopted throughout this chapter: A1, A2, and A3 represent the anterior leaflet’s anterolateral, middle, and posteromedial segments, respectively, and P1, P2, and P3 represent the posterior leaflet’s anterolateral, middle, and posteromedial scallops, respectively.
Papillary muscles and chordae tendineae
The MV is supported by two papillary muscles: the anterolateral and the posteromedial. Their orientation is similar to that of the commissures of the same names (see Figure 9-3 ). The larger, anterolateral papillary muscle usually consists of a single trunk, whereas the smaller posteromedial papillary muscle often consists of two or three distinct pillars.
The papillary muscles attach to the valve leaflets via thin fibrous structures, the chordae tendineae. Primary chordae attach to the leaflet tip, and secondary chordae attach to the undersurface of the leaflet (see Figure 9-1 ). A substantial volume of blood normally passes through the interchordal space during diastole; therefore, chordal fusion may contribute to mitral stenosis by causing subvalvular obstruction.
The anterolateral papillary muscle supports the anterolateral segments of each leaflet (A1/P1 and part of A2/P2), and the posteromedial papillary muscle supports the posteromedial segments of each leaflet (A3/P3 and part of A2/P2). The anterolateral papillary muscle has a dual blood supply, from branches of the left anterior descending and circumflex coronary arteries, whereas the posteromedial papillary muscle is usually supplied entirely by the right coronary artery. For this reason, the posteromedial muscle is more prone to infarction and subsequent rupture. The chordae tether the ventricle, as well as the leaflets, and if this function is lost, ventricular wall stress increases and LV function may deteriorate. This is the principle behind preserving the subvalvular apparatus during MV replacement.
Orientation of the mitral valve
Orientation of the MV can be confusing. Three views may be used ( Figure 9-5 ).
Anatomic view
The valve is viewed from the base of the heart (i.e., the LA side of the valve) with the atria cut away. This is the most intuitive of the views, as the patient’s left and right correspond to the observer’s left and right, and the anterior and posterior leaflets appear in their appropriate positions. The lateral aspect of the valve is on the left, and the medial (or septal) aspect is on the right.
The anatomic orientation is used in line drawings throughout this chapter.
TEE view
Rotation of the anatomic view through 180 degrees produces the TEE view, in which the observer’s left and right are reversed relative to the patient. This corresponds to the orientation of the MV as it appears in the transgastric basal short-axis view.
Surgeon’s view
The view the surgeon has, standing on the patient’s right, results when examining the valve through the opened left atrium. The AV and the base of the anterior MV leaflet are viewed at the 12 o’clock position, and the LA appendage is seen in the 9 o’clock position. The surgeon’s view is the orientation most commonly used when viewing 3-D datasets of the MV (see Figure 4-15 ).
Systematic examination of the mitral valve
The ability to relate TEE images of the MV to specific anatomic regions is crucial for accurate diagnosis of valvular pathology. In this section, a sequence of examination is described based on the ASE/SCA guidelines and two other reports.
The examination consists of four standard midesophageal views (four-chamber, commissural, two-chamber, and long axis) and two transgastric views (basal short axis and two-chamber). Details on how to obtain these images are provided in Chapter 3 . For assessing the MV, the sector depth should be reduced and the focus should be adjusted to concentrate on the valve, not the left ventricle. In each view, the valve should be examined with 2-D imaging. Color flow Doppler should be used in at least the midesophageal long-axis view, and more extensive color flow imaging should be performed if significant mitral pathology is detected. From a practical point of view, it is preferable to use both modalities in the midesophageal views before moving on to the transgastric views. Complete examination of the MV also involves evaluation of the transmitral and pulmonary venous Doppler waveforms.
The key echocardiographic–segmental relationships are summarized in Table 9-1 .
| Tee View | Mitral Segments Visualized (Left to Right Across the Screen) |
|---|---|
| ME four-chamber | A2/P2 |
| ME commissural | P3/A2/P1 |
| ME commissural with left turn of probe | A3/A2/A1 |
| ME commissural with right turn of probe | P3/A3/A2/A1 |
| ME long axis | P2/A2 |
| ME long axis with left turn of probe | P1/A1 |
| ME long axis with right turn of probe | P3/A3 |
Midesophageal four-chamber view (0 degrees)
Echocardiographic anatomy
The anterior leaflet is displayed on the left, and the posterior leaflet is on the right ( Figures 9-6 and 9-7 ). The scan plane typically cuts the coaptation line obliquely at A2/P2.
Additional views
Slightly withdrawing (or anteflexing) the probe moves the sector scan farther toward the anterolateral commissure and cuts through the (LVOT) (midesophageal five-chamber view). Slightly advancing (or retroflexing) the probe moves the sector scan toward the posteromedial commissure.
Main utility
The midesophageal four-chamber view is a convenient starting place for examining the MV and gives a general idea of leaflet pathology. However, as the coaptation line is cut obliquely, it is not the ideal view for measuring leaflet length or the width of the vena contracta. Also, as the probe is advanced and withdrawn, it is not easy to be sure which segments are visualized.
Midesophageal commissural view (60 degrees)
Echocardiographic anatomy
This view is transitional between views in which the anterior leaflet appears on the left (<60 degrees) and those in which it appears on the right (>60 degrees) ( Figure 9-8 ; see also Figure 9-7 ). The scan passes through the intercommissural line and therefore cuts the (curved) coaptation line twice: P3/A3 on the left and A1/P1 on the right. The body of A2 appears to flick in and out of the center of the annulus as the MV opens and closes. The LA appendage is not usually seen, but both papillary muscles are usually visible. This is also known as the “seagull view.”
Additional views
Turning the probe to the left (anticlockwise) sweeps the sector scan through the body of the posterior leaflet (P3, P2, and P1). Turning to the right (clockwise) sweeps the sector scan through the body of the anterior leaflet (A3, A2, and A1).
Main utility
The commissural view is useful for assessing which segments are regurgitant. On color flow Doppler, regurgitation arising from the left coaptation point indicates involvement of the posteromedial segments (P3/A3); regurgitation arising from the right coaptation point implies involvement of the anterolateral segments (A1/P1).
This view is not useful for assessing which leaflet is involved or for evaluating the vena contracta. Because the scan plane runs parallel to the coaptation line, jet width is overestimated. Also, the coaptation line may be cut twice, resulting in two jets (see Figure 9-7 ). This can give the erroneous impression of a mitral cleft or, if the jets merge, greatly overestimate the severity of the mitral regurgitation.
Midesophageal two-chamber view (90 degrees)
Echocardiographic anatomy
The sector scan cuts through P3 on the left and all three segments of the anterior leaflet on the right (A3, A2, and A1) ( Figure 9-9 ). The coaptation line is cut at P3/A3. The coronary sinus is seen on the left, and the LA appendage is on the right. The posteromedial papillary muscle is usually visible on the left. The segmental anatomy is similar to that seen when the probe is turned to the right from the commissural view.
Main utility
This view is useful for assessing the coaptation line at the level of the posteromedial segments (P3/A3) and gives a good view of the entire anterior leaflet. This is usually the best view in which to see the LA appendage.
Midesophageal long-axis view (120 to 150 degrees)
Echocardiographic anatomy
The midesophageal long-axis view is identified by visualizing both the MV and the AV but neither papillary muscle ( Figure 9-10 ; see also Figure 9-7 ). In most patients, this occurs with the sector scan between 120 and 150 degrees. This view cuts the coaptation line perpendicularly through P2/A2.
Additional views
Turning the probe sweeps the sector scan perpendicularly along the coaptation line. Turning to the left (counterclockwise) sweeps the image plane toward the anterolateral commissure (P1/A1). Turning to the right (clockwise) sweeps the image plane toward the posteromedial commissure (P3/A3). The anterolateral commissure may be identified from the LA appendage (not always seen); the posteromedial commissure may be identified by visualizing the coronary sinus or the right atrium. During this maneuver, to maintain a true long-axis orientation, it may also be necessary to advance the probe when turning to the right and to withdraw it when turning to the left.
Main utility
The midesophageal long-axis view is useful for assessing mitral pathology for the following reasons:
- •
Since the image plane cuts the coaptation line perpendicularly, the observed base-to-tip leaflet length accurately reflects the true leaflet length. For the same reason, it is the appropriate view for assessing the width of the vena contracta (as described later).
- •
The image plane passes through the “high” (more basal) axis of the mitral annulus and is therefore the appropriate view for assessing leaflet prolapse.
- •
The scan cuts the posterior leaflet through the P2 scallop, which is the mitral segment most likely to be affected in myxomatous degeneration, annular dilatation, and regurgitation.
- •
The image plane can be swept along the coaptation line by turning the shaft of the probe, allowing a detailed assessment of all segments of each leaflet.
Transgastric basal short-axis view (0 degrees)
Echocardiographic anatomy
This view shows the MV en face and allows visualization of all six mitral segments ( Figures 9-11 and 9-12 ). P3 is closest to the apex of the sector scan, the posteromedial commissure is in the upper left, and the anterolateral commissure is in the lower right of the image. It is also called the “fish mouth” view.
Additional views
The transgastric mid-short-axis view should also be obtained to assess the papillary muscles and adjacent myocardium.
Main utility
Using color flow Doppler, this view is, in theory, useful for assessing where along the coaptation line regurgitation is occurring. A loop can be saved in memory and slowly scrolled through to assess where the systolic color disturbance is taking place. This principle is demonstrated in Figure 9-12 , where the regurgitant jet is seen in the region of A2/P2. However, in practice, it is frequently difficult to localize the origin of the jet. This is partly because the image plane is perpendicular to the direction of regurgitation, making color flow Doppler difficult to interpret.
In the mid-short-axis view, it is important to look for SWMAs and ventricular dilatation, which may contribute to MV dysfunction.
Transgastric two-chamber view (90 degrees)
Echocardiographic anatomy and main utility
The posterior mitral leaflet appears in the near field, and the anterior mitral leaflet is in the far field ( Figure 9-13 ). It can be difficult to be sure of segmental leaflet anatomy in this view, but a clear view of the papillary muscles and chordae is usually obtained because the ultrasound beam is perpendicular to these structures.
Mitral regurgitation
Table 9-2 lists some common causes, mechanisms, and typical jet directions of native MV regurgitation. Trivial or physiologic mitral regurgitation can occur in structurally normal MVs.
| Pathology | Lesion | Mechanism | Direction of Jet |
|---|---|---|---|
| Rheumatic disease | Stenosis with or without regurgitation | Leaflet restriction, chordal shortening | Eccentric toward the side of the lesion. Central if both leaflets are equally affected. |
| Myxomatous degeneration | Regurgitation | Prolapse, flail, annular dilatation | Eccentric away from the side of the lesion. |
| Ventricular dysfunction | Regurgitation | LV sphericity, ventricular dysfunction, papillary muscle dysfunction or rupture, annular dilatation, SAM (hypertrophic cardiomyopathy) | Usually central if global LV dysfunction. Eccentric (toward side of lesion) if leaflet restriction is unequal, as with focal LV dysfunction. |
| Endocarditis | Regurgitation | Leaflet destruction and perforation | Multiple jets, variable direction. |
| SAM | Regurgitation | Prolapse of anterior mitral leaflet into LVOT | Posteriorly directed. |
The following points should be addressed during echocardiographic assessment of mitral regurgitation:
- •
The pathologic process underlying the regurgitation (myxomatous degeneration, rheumatic disease, endocarditis, or ventricular dysfunction)
- •
The mechanism of regurgitation (prolapse, flail, restriction, perforation, or cleft)
- •
The location and extent of the lesion (which segments are involved and whether the lesion involves the commissures)
- •
Associated features
Despite the important role of color flow Doppler in assessing mitral regurgitation, most of this information is gained from careful 2-D imaging. Mitral regurgitation, particularly if secondary to ischemia, altered geometry of the left ventricle, or (SAM), is particularly sensitive to loading conditions, so severity is better assessed on the preoperative echocardiogram rather than with TEE under the effects of anesthesia or sedation. Sometimes severe dynamic mitral regurgitation is only recognized during stress echocardiography. Thus, the absence of significant mitral regurgitation on intraoperative examination should not necessarily be considered reassuring.
Carpentier classification of mitral regurgitation
Carpentier has classified mitral regurgitation on the basis of leaflet motion.
Type 1
Leaflet motion is normal. Mitral regurgitation results from annular dilatation, leaflet clefts, leaflet perforation, or leaflet destruction (e.g., due to endocarditis). Mitral regurgitation is typically central.
Type 2
Leaflet motion is excessive and may be classified as prolapse or flail. The most common cause is myxomatous degeneration with or without chordal rupture. Regurgitation is usually eccentric and directed away from the diseased leaflet.
Type 3
Leaflet motion is restricted. Type 3 may be further subdivided into structural (Type 3a), in which leaflets are diseased, and functional (Type 3b), in which leaflets are structurally normal but tethered by the papillary muscles or underlying myocardium. The most common cause of structural restriction is rheumatic disease; the most common cause of functional restriction is LV dysfunction. Regurgitation may be central (both leaflets equally restricted) or eccentric (directed toward the diseased leaflet).
Etiology and mechanism of mitral regurgitation
The competence of the MV relies on coordinated interaction among the leaflets, annulus, subvalvular apparatus, and left ventricle. Mitral regurgitation can be attributed to dysfunction of one or more of the following:
- •
Annulus
- •
Valve leaflets
- •
Chordae
- •
Papillary muscles
- •
Geometry of the left ventricle
The annulus
Dilation of the mitral annulus reduces the degree of overlap between the leaflets along the coaptation line during systole and thus contributes to mitral regurgitation. Annular dilatation may occur because of dilation of the ventricle or because of myocardial ischemia or infarction. Annular dilatation also occurs with myxomatous degeneration of the MV. However, annular dilatation is rarely the primary mechanism of mitral regurgitation, whatever the underlying pathology.
In the midesophageal long-axis view, the upper limit of normal for the annular dimension is 3.6 cm, and values above 4 cm indicate significant dilatation.
Mitral annular calcification is a relatively common degenerative process but rarely causes significant valvular dysfunction. The major implication of this condition is that it can create technical difficulties in removing the valve or suturing in a mitral prosthesis or annuloplasty ring. In addition, on TEE examination, the calcification may cause shadowing and echo dropout, which obscures the far field.
The leaflets
Congenital disorders
Conditions associated with disorders of the atrioventricular canal endocardial tissue (which gives rise to the septum primum, ventricular septum, and atrioventricular valves), may be associated with mitral regurgitation. Atrioventricular canal defects include a primum (ASD), an inlet (VSD), and varying degrees of abnormality of the (TV) and MV (see Chapter 14 ). Severe atrioventricular canal defects, in which there are major structural defects of the MV and TV (and severe regurgitation of the atrioventricular valves), are usually identified and repaired in childhood. Occasionally, an isolated primum ASD is discovered as an incidental finding perioperatively. Primum ASDs are associated with a cleft in the anterior mitral leaflet and regurgitation (see Figure 14-11B ). Thus, mitral regurgitation should always be sought if a primum ASD is identified.
Myxomatous degeneration
The most frequent cause of native mitral regurgitation in industrialized nations is myxomatous degeneration. Rarely, myxomatous degeneration is associated with systemic diseases such as Marfan and Ehlers-Danlos syndromes.
Myxomatous degeneration is a process in which the valve leaflets become thickened and elongated. Redundant leaflet tissue and stretching of the chordae lead to excessive leaflet motion, which creates a characteristic appearance on 2-D imaging ( Figure 9-14 ). Regurgitation develops from either leaflet prolapse or leaflet flail. The mitral annulus is usually significantly dilated.
Prolapse is said to occur when the body of a leaflet domes above the level of the mitral annulus in systole (by more than 2 mm, using TTE criteria ). With TEE, prolapse should be assessed in the midesophageal long-axis view at end systole. The leaflet tip is directed toward the left ventricle, and a coaptation defect may be visible ( Figures 9-15 and 9-16 ). Prolapse occurs as a consequence of leaflet redundancy and chordal stretch; significant myxomatous change is usually evident. Regurgitation usually develops slowly and ranges from trivial to severe.
Mild prolapse in the presence of normal leaflet morphology is a variation of normal and is usually associated with trivial regurgitation.
A flail leaflet results in a visible coaptation defect with the leaflet tip directed toward the left atrium throughout systole ( Figure 9-17 ; see also Figure 9-15 ). The cause is usually torn chordae in association with myxomatous change. However, torn chordae and leaflet flail can also occur on an otherwise structurally normal valve. The freeze and scroll modes can be helpful in visualizing the ruptured chordae flicking into the left atrium during systole. In general, regurgitation due to a flail leaflet is more severe and develops more rapidly than that associated with leaflet prolapse. A ruptured papillary muscle also causes leaflet flail (as described later).
Leaflet prolapse and flail most commonly develop in the posterior leaflet, particularly in the P2 segment. With either prolapse or flail, the direction of the regurgitant jet is away from the side of the lesion (see Figure 9-17 ); since it is rare for both leaflets to be affected equally, these jets are usually eccentric and appear to hug the wall of the left atrium ( Figure 9-18 ).
Patients with chronic stable mitral regurgitation secondary to leaflet prolapse often present for surgery following an acute deterioration in their symptoms as a consequence of chordal rupture.
Rheumatic heart disease
Until recently, the most common lesion affecting the native MV was rheumatic heart disease, and in many developing countries this is still the case. Rheumatic heart disease is primarily a disease of the MV, and it may or may not involve other valves. The predominant lesion is usually mitral stenosis; mitral regurgitation frequently occurs as well but is less often the hemodynamically significant lesion.
Rheumatic MV disease can be either acute or chronic. In acute valvulitis, the leaflets remain mobile but are mildly thickened. Regurgitation is usually central and related to a generalized failure of coaptation along the length of the coaptation line. There may be inflammation of the annulus. In stable chronic valvulitis, the leaflets are more thickened with limited excursion (this can cause a degree of mitral stenosis, even in the absence of overt reduction in MV area). Retraction occurs, usually of the posterior leaflet with override of the anterior leaflet, giving rise to an eccentric posteriorly directed regurgitant jet. There is fibrosis of the leaflet tips with rolling of edges and distortion of the coaptation plane. There can be overt failure of coaptation giving rise to central regurgitation, which is more typical of chronic rheumatic mitral disease.
If rheumatic MV disease is identified, the other valves should also be inspected for involvement.
Native valve endocarditis
Endocarditis may cause mitral regurgitation of the valve leaflets by destruction, perforation, deformity, or a combination of these. Typically, vegetations develop on the upstream, or low pressure, side of a valve; thus, in mitral endocarditis, lesions are most commonly seen on the LA surface of the valve ( Figure 9-19 ). Mitral stenosis is rare.
If there is evidence of mitral endocarditis, a careful search for vegetations on the other heart valves must be undertaken. The leaflets and paravalvular tissues must be scrutinized for evidence of abscess formation.
Leaflet perforation is characterized by the presence of one or more regurgitant jets that do not appear to arise from the coaptation line. The presence of two separate proximal convergence zones should alert the echocardiographer to the possibility of perforation.
Systolic anterior motion of the anterior mitral leaflet
Systolic anterior motion (SAM) refers to displacement of the anterior leaflet of the MV into the LVOT during systole (see Figure 7-21 ). The consequences of SAM are twofold: (1) a systolic coaptation defect of the MV, which results in a late-peaking, posteriorly directed jet of mitral regurgitation, and (2) LVOT obstruction (see Figures 7-19 and 7-20 ). Anatomic factors that contribute to SAM include an elongated anterior mitral leaflet, hypertrophy of the basal ventricular septum, abnormal papillary muscle insertion or morphology, systolic deformation of the mitral annulus, and a nondilated left ventricle. Hemodynamic factors that contribute to SAM include hypovolemia, increased contractility (e.g., due to inotropic stimulation), and low LV afterload.
SAM typically occurs in three clinical scenarios: (1) hypertrophic cardiomyopathy, particularly when there is hypertrophy of the basal ventricular septum (see Chapter 7 ); (2) following AV replacement for aortic stenosis (see Chapter 10 ); and following MV repair (as described later). However, SAM can occur in any patient with hypertrophy of the basal ventricular septum who has a predisposing hemodynamic state, particularly hypovolemia.
The chordae
Diseases that have an impact on the integrity of the connective tissues may affect not only the valves but also the chordae, leading to laxity or rupture. Chordal rupture usually arises from intrinsic degeneration but may rarely follow infection or extrinsic trauma to the chest.
The papillary muscles
Papillary muscle rupture
Occasionally, as a complication of myocardial infarction, papillary muscle rupture occurs. This most frequently affects the posteromedial muscle (described earlier) and results in torrential bileaflet regurgitation involving A3/P3 and A2/P2. The papillary muscle and chordae can usually be seen flicking in and out of the left atrium ( Figure 9-20 ).
Papillary muscle ischemia
It is rare, but possible, for the papillary muscles to function normally under basal conditions, with little valvular regurgitation, but to become dysfunctional, with mitral regurgitation, when subjected to reversible ischemia. This may not be apparent perioperatively.
The geometry of the left ventricle
Mitral regurgitation may be the result of global dilatation from any cause of dilated cardiomyopathy.
LV dilatation and systolic dysfunction are most commonly secondary to ischemic heart disease. Depending on the severity of the underlying coronary disease, ischemia or infarction may manifest as a globally dilated cardiomyopathy or, more commonly, as a segmental wall motion abnormality.
Global left ventricular dilatation and systolic dysfunction
The mechanisms by which global LV dysfunction causes mitral regurgitation are incompletely understood but are thought primarily to involve an altered geometric relationship between the left ventricle, the papillary muscles, and the mitral leaflets. The severity of mitral regurgitation depends more on the degree of LV dilatation and increase in ventricular sphericity (and therefore loss of the normal ellipsoid shape) than the magnitude of the reduction in ejection fraction. Dilatation of the annulus may also contribute. These abnormalities result in apical and lateral displacement of the papillary muscles, widening of the interpapillary angle, and tethering or restriction of leaflets, leading to incomplete leaflet closure and regurgitation.
On 2-D imaging, the valve may appear morphologically normal but have loss of the usual systolic leaflet overlap or a visible coaptation defect. With dilated cardiomyopathy, the regurgitant jet is usually central. With milder degrees of functional mitral regurgitation, the jet occurs early in systole and then abates as the left ventricle progressively reduces in size and leaflet coaptation occurs.
Focal left ventricular dysfunction
Mitral regurgitation is often due to focal LV dilatation following myocardial infarction. If there is a reversible ischemic element to this dilatation, coronary revascularization may improve the regurgitation.
After focal myocardial infarction due to right or circumflex coronary artery occlusion without myocardial salvage, there is necrosis of myocardium with scar formation. There is local LV remodeling, often with the formation of a shallow posterobasal LV aneurysm. There is apical and lateral displacement of the papillary muscles, leading to MV tenting, incomplete mitral leaflet closure, and loss of systolic annular contraction. Typically, this results in tethering and restriction of the posterior leaflet and systolic override of the anterior leaflet, with associated eccentric mitral regurgitation.
Features associated with mitral regurgitation
In addition to abnormalities of the valve itself, other echocardiographic findings are usually seen in patients with moderate or severe mitral regurgitation :
- •
LA dilatation. This is common with chronic severe regurgitation but is not a feature of acute regurgitation.
- •
Pronounced left-to-right bowing of the atrial septum due to elevated LA pressure. This is best seen in the midesophageal four-chamber or bicaval views.
- •
Spherical enlargement of the left ventricle with eccentric hypertrophy (i.e., wall thickness is increased in proportion to the increase in LV size; see Chapter 7 ). End-diastolic volume increases before end-systolic volume.
- •
Hypercontractile left ventricle. This is usual with severe mitral regurgitation. Normal or mildly reduced LV systolic contractility (ejection fraction <55% and an end-systolic short-axis diameter >4 to 4.5 cm) suggests significant LV impairment.
- •
Signs of pulmonary hypertension, consistent with LV decompensation (see Chapter 19 ). These include a tricuspid regurgitation jet velocity greater than 3 m/sec and enlargement of the right ventricle and the right atrium.
Grading mitral regurgitation
There are various ways of assessing the severity of mitral regurgitation. These need to be considered collectively and in context, as they may provide conflicting information ( Table 9-3 ). The ASE has published guidelines for grading valvular regurgitation, and these are referred to later.
| Sign | Mild (2+) | Moderate (3+) | Severe (4+) |
|---|---|---|---|
| Structural | |||
| LA size | Normal | Normal or dilated | Dilated * |
| LV size | Normal | Normal or dilated | Dilated * |
| Leaflets | Normal or abnormal | Normal or abnormal | Abnormal: cleft, perfosation, leaflet flail, ruptured papillary muscle, marked restriction |
| Color Flow Doppler | |||
| Jet area | Small central jet, usually <4 cm 2 or <20% of LA volume | Variable | Large central jet, usually >10 cm 2 or >40% of LA area, or wall-hugging jet |
| Vena contracta width (cm) | <0.3 | 0.3-0.69 | ≥0.7 |
| Flow convergence zone on LV side of MV in systole | Absent | Variable | Present, with radius >1 cm at alias velocity = 40 cm/sec |
| Spectral Doppler | |||
| Mitral inflow (PW) | A wave dominant | Variable | E wave dominant, usually >1.2 cm/sec |
| Jet density (CW) | Incomplete or faint | Dense | Dense |
| Jet contour (CW) | Parabolic | Parabolic | Early peaking with V wave cutoff sign |
| Pulmonary vein flow (PW) | Systolic dominance | Systolic blunting | Systolic reversal |
| Quantitative Parameters | |||
| EROA (PISA method; cm 2 ) | <0.2 | Mild–moderate: 0.2–0.29 Moderate–severe: 0.3–0.39 | ≥0.4 |
| Regurgitant volume (mL) | <30 | Mild–moderate: 30–44 Moderate–severe: 45–59 | ≥60 |
| Regurgitant fraction (%) | <30 | Mild–moderate: 30–39 Moderate–severe: 40–49 | ≥50 |
* Exception: Acute mitral regurgitation when LA and LV size may be normal.
Quantitative Doppler echocardiography can provide an objective assessment of the severity of regurgitation, but in the perioperative setting, the necessary measurements are relatively time consuming to make, and there is considerable potential for inaccuracy. A number of semiquantitative techniques have been well validated and are applicable to intraoperative TEE. These are discussed in the next section. Using semiquantitative techniques, mitral regurgitation may be graded as mild (2+), moderate (3+), or severe (4+) (see Table 9-3 ). Trivial mitral regurgitation is sometimes classified as trace (1+). The ASE limits the differentiation of moderate mitral regurgitation into mild-to-moderate and moderate-to-severe to assessments using quantitative measurements; thus, in the perioperative setting using semiquantitative techniques these grades should not be used.
Color flow Doppler
There are three methods of assessing the severity of mitral regurgitation using color flow Doppler mapping: jet area, width of the vena contracta, and flow convergence (PISA).
Jet area
In general, small jets (<4 cm 2 , <20% of LA area) are consistent with mild mitral regurgitation and large jets (>10 cm 2 or >40% of LA area) are severe. However, there are several problems with using jet area to grade mitral regurgitation, and the ASE does not recommend using the technique. Jet area measurements are influenced by loading conditions, ventricular function, atrial size, and Doppler gain settings. Thus, a patient with acute mitral regurgitation and ventricular decompensation will have a smaller jet area for the same degree of mitral regurgitation than a hypertensive patient with chronic mitral regurgitation and a large left atrium. In addition, because of the Coanda effect (see Chapter 21 ), jet area underdiagnoses the severity of mitral regurgitation with eccentric jets compared to central jets. Indeed, all wall-hugging jets (see Figure 9-18 ) should be considered severe until proven otherwise.
Vena contracta
The width of the vena contracta is the most useful semiquantitative method for grading the severity of mitral regurgitation, and it is recommended by the ASE. The vena contracta is the narrowest point of the jet as it passes through the valve ( Figure 9-21 ) and is in effect the diameter of the effective regurgitant orifice area (EROA) (see Figure 21-1 ). The vena contracta should only be estimated in the midesophageal long-axis view to avoid cutting the coaptation line obliquely and potentially overestimating the width of the jet. In 2-D imaging, a magnified or zoom view of the MV should be used and the focus should be adjusted to optimize the view of the mitral leaflets. The size and position of the color box should be adjusted to focus on the region of leaflet coaptation (i.e., not the entire regurgitant jet within the left atrium). The color Doppler gain and scale settings should be optimized. Doppler gain should be just below the level at which spontaneous flecks of color, unrelated to blood flow, are seen. A scale setting of 40 to 60 cm/sec is usually satisfactory. The scan plane influences the dimensions of the vena contracta. Thus, the probe should be turned to the left and to the right to identify the point along the coaptation line where the width of the vena contracta is at its maximum. A vena contracta width of less than 3 mm usually indicates mild mitral regurgitation, and a width equal to 7 mm usually indicates severe mitral regurgitation, although the cutoff has varied between 6 and 8 mm.
Vena contracta width is reliable for evaluating central and eccentric jets and is less influenced by loading conditions than jet area; however, it is not validated for multiple jets.
Proximal flow acceleration and proximal isovelocity surface area
During systole, as blood approaches the narrow regurgitant orifice on the LV side of the valve, it speeds up. With color flow Doppler imaging, the point at which the velocity exceeds the Nyquist limit is identified by color aliasing (i.e., reversal of color, from red to blue). This region of color reversal is a PISA and can be used to assess mitral regurgitation or measure the (EROA) qualitatively (see Chapter 21 ).
Qualitatively, the presence of a visible PISA at a Doppler scale of 50 to 60 cm/sec alerts the echocardiographer to the presence of significant mitral regurgitation.
The PISA method of calculating EROA is based on blood flow at the point of color aliasing being the same as flow through the regurgitant orifice (see Chapter 21 ). Flow is the product of velocity (V) and cross-sectional area (CSA); therefore:
V PISA × CSA PISA = V orifice × EROA ,
where V PISA is the velocity at the PISA (i.e., the Nyquist limit) and V orifice is the velocity at the regurgitant orifice, which is the peak regurgitant jet velocity. Assuming that the surface area of the PISA is that of a hemisphere of radius r, then CSA PISA is 2π r 2 . Thus,
EROA = 2 π r 2 × NL V MR .
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