Mitral stenosis remains the commonest stenotic valvular lesion in young people in the developing world. Most often, the etiology is rheumatic heart disease, with rare instances of congenital and acquired cases. Clinical presentation is typical with symptoms developing early in the developing countries and in later life in the Western World. Echocardiography remains the cornerstone of diagnosis and choice for therapeutic intervention. Echocardiography defines the pathological processes like leaflet thickening and calcification, commissural fusion, chordal thickening and fusion. Commissural fusion narrows the primary orifice while the interchordal fusion reduces the secondary orifice size. Of late, three-dimensional echocardiography (3DE) has contributed to the better understanding of the echocardiographic anatomy. Most guidelines allocate Class I status to echocardiography for detection of mitral stenosis, assessment of its hemodynamic severity, detection of concomitant valve lesions and for definition of valve morphology. Its use for guiding therapeutic interventions is gaining ground.
Mitral valve is a bileaflet structure housed in a fibrous ring (Fig. 3.1). It guards the inlet of the left ventricle (LV) and prevents regurgitation of blood into the left atrium (LA).
The mitral apparatus is composed of the left atrial wall, the annulus, the leaflets, the tendinous chords, the papillary muscles, and the left ventricular walls.1-3 The valve is located obliquely behind the aortic valve.
In its open state, the valvular leaflets are like a funnel extending from the hinge line at the atrioventricular junction to the free margins. Tendinous cords attach the leaflets to two closely arranged groups of papillary muscles. The interchordal spaces serve as important pathways for blood flow (Fig. 3.2). The mitral valve requires all its components, together with the adjacent atrial and ventricular musculature, to function properly.2
Components of the Valve Apparatus
• Leaflets
• Annulus
• Chordae tendineae
• Papillary muscles
• Interannular fibrosa
• Adjacent left atrial and ventricular musculature
The mitral annulus is a fibrous ring that connects with the leaflets. It is not a continuous ring around the mitral orifice and appears to be more D-shaped, rather than circular (Figs 3.3 and 3.4).
The straight border of the annulus is posterior to the aortic valve. Expansions of fibrous tissues at either extreme of the area of continuity form the right and left fibrous trigones. The aortic valve is located between the ventricular septum and the mitral valve. The annulus functions as a sphincter that contracts and reduces the surface area of the valve during systole to ensure complete closure of the leaflets.
Mitral valve consists of a continuous veil inserted around the circumference of the mitral orifice (Fig. 3.5). The free edges of the leaflets have several indentations. Two of these indentations, the anterolateral and posteromedial commissures, divide the leaflets into anterior and posterior.
These commissures can be accurately identified by the insertions of the commissural chords into the leaflets.
Normally, the valvular leaflets are thin, pliable, translucent and soft. Each leaflet has an atrial and a ventricular surface. When viewed in profile, two zones can be distinguished in the anterior leaflet and three zones in the posterior leaflet according to the insertions of the tendinous cords.3
• In both leaflets, there is a clear zone that is devoid of chordal attachments (Figs 3.6 and 3.7).
• Nearer the free edge, the atrial surface is irregular with nodular thickenings. This is also the thickest part, corresponding with the line of closure and the free margin. Tendinous chords attach to the underside of this area described as the leaflet's rough zone.
• The basal zone that is found only in the posterior leaflet is the proximal area that has insertions of basal cords to its ventricular surface. Being distant from the ventricular wall, the anterior leaflet does not have attachments to basal cords.
• In normal valve closure, the two leaflets meet each other snugly with the rough zone and free edge riding over each other.
• The anterior leaflet is located posterior to the aortic root and is also anchored to the aortic root, unlike the posterior leaflet. The anterior leaflet is large and semicircular in shape. It has a free edge with few or no indentations. The zones on the anterior leaflet are referred to as rough and clear zones, according to the chords insertion. These 2 zones are separated by a prominent ridge on the atrial surface of the leaflet, which is the line of the leaflet closure. The prominent ridge is located approximately 1 cm from the free edge of the anterior leaflet.
• The posterior leaflet is the section of the mitral valve that is located posterior to the commissural areas. It has a wider attachment to the annulus than the anterior leaflet. It is divided into 3 scallops by 2 indentations or clefts. The middle scallop (P2) is larger than the other 2 (called medial and lateral or P3 and P1). The zones on the posterior leaflets are referred to as rough, clear, and basal zones, according to the chord insertion.
The chordae tendineae are small fibrous strings that originate either from the apical portion of the papillary muscles or directly from the ventricular wall and insert into the valve leaflets or the muscle. These 2 types are called true chordae tendineae and false chordae tendineae, respectively. The leaflet chordae are the chordae that insert into the anterior or posterior leaflets. Two types of chordae tendineae are connected to both leaflets and the third type to only the posterior leaflet.
• Primary or rough zone chords insert into the distal portion of the leaflets known as the rough zone.
• Secondary or strut chords; the chordae that branch before inserting into the leaflet.
• Basal chordae are unique to the posterior leaflet; these insert into the basal zone of the posterior leaflet, which is located between the clear zone and the mitral valve annulus.
Papillary Muscles and Left Ventricular Wall
These structures represent the muscular components of the mitral apparatus. the papillary muscles normally arise from the apex and middle third of the left ventricular wall. the anterolateral papillary muscle is normally larger than the posteromedial papillary muscle and is supplied by the left anterior descending artery or the left circumflex artery. The posteromedial papillary muscle is supplied by the right coronary artery. At their bases, the muscles sometimes fuse or have bridges of muscular or fibrous continuity before attaching to the ventricular wall. Fusion of papillary muscles results in parachute malformation with potential for valvular stenosis.
Pathoanatomy of Mitral Stenosis the following are the common etiological factors of mitral stenosis:4-8
• About 99% cases of the mitral stenosis are postinflammatory (rheumatic heart disease) as a sequelae of poststreptococcal infection (Fig. 3.8).
• Congenital (arcade type or parachute mitral valve) (Fig. 3.9).
• Infective endocarditis (due to large obstructive vegetations).
• Mitral annular calcification (Fig. 3.10).
• Systemic lupus erythematosus.
• Postmitral annuloplasty.
• Degenerated bioprosthesis with calcification (Fig. 3.11).
• Malignant carcinoid.
• Rheumatoid arthritis.
• Atrial myxoma.
• Ball thrombus (Fig. 3.12).
• Gout.
• Malignant sarcoid.
• Mucopolysacchridosis.
• Anorexiogenic drug-induced valvulopathy.
• Radiation-induced valvulopathy.
Typically, rheumatic mitral stenosis is characterized by:4
• Fibrous thickening of the leaflets with shortening and retraction (Figs 3.13 and 3.14).
• Commissural fusion, which narrows the primary orifice (Fig. 3.15).
• Thickening and fusion of the chords reduces the secondary opening, which is accentuated by papillary muscle scarring and fusion (Fig. 3.16).
• Later on, there is dystrophic calcification of the leaflets, which may extend into the commissures (Fig. 3.17).
• Occasionally, there is tunnel-like mitral orifice narrowing due to minor primary orifice narrowing and predominant narrowing at insertion of chords to papillary muscle heads (Fig. 3.18).
There is a close similarity between echocardiographic appearance and pathological pictures (Figs 3.19 to 3.21).
Hemodynamics of Mitral Stenosis
Normal mitral valve area exceeds 4 cm2 and there is almost no pressure gradient between the left atrium and the left ventricle during diastole. Blood flows without much resistance. As the valve area narrows to < 2cm2, transmitral pan-diastolic gradient develops with rise in the left atrial pressure (Fig. 3.22).
Mitral stenosis becomes critical when the valve area narrows < 1 cm2 and mean gradient rapidly rises.9
Pulmonary hypertension may develop as a result of (1) retrograde transmission of left atrial pressure, (2) pulmonary arteriolar constriction, (3) interstitial edema or (4) obliterative changes in the pulmonary vascular bed (intimal hyperplasia and medial hypertrophy). As pulmonary arterial pressure increases, right ventricular dilation and tricuspid regurgitation may develop.
Source: American Society of Echocardiography and European Association of Echocardiography, 2009
Hemodynamics of mitral stenosis are determined by the following:
• Complex anatomical and pathophysiologic features of the valve apparatus (Fig. 3.23)
• Properties of the left ventricle, atrium and pulmonary vasculature (Fig. 3.24)
• the valve and the cardiac chambers have a functional reserve that becomes exhausted as the stenosis worsens and/or the compensatory mechanisms of the chambers fail.
Severity of mitral stenosis is judged by estimating transmitral gradients and mitral valve area as shown in Table 3.1.10
Assessment of Severity of Mitral Stenosis Transmitral pressure gradient:
• Estimation of the diastolic pressure gradient is derived from the transmitral velocity flow curve, using the simplified Bernoulli equation, that is, DP = 4V2 (Fig. 3.25).
• ttis estimation is reliable, as shown by the good correlation with invasive measurements.
• Use of continuous wave Doppler is preferred to ensure maximal velocities are recorded. When pulsed-wave Doppler is used, the sample volume should be placed at the level or just after leaflet tips.
• Doppler gradient is assessed using the apical window in most cases, as it allows for parallel alignment of the insonifying beam and mitral inflow.
• the ultrasound Doppler beam should be oriented to minimize the intercept angle with mitral flow to avoid underestimation of velocities.
• Color Doppler in apical view is useful to identify eccentric diastolic mitral jets that may be encountered in cases of severe deformity of valvular and subvalvular apparatus. In these cases, the Doppler beam is guided by the highest flow velocity zone identified by color Doppler.
• Optimization of gain settings, beam orientation and a good acoustic window are needed to obtain well- defined contours of the Doppler flow. Maximal and mean mitral gradients are calculated by integrated software using the current echocardiographic systems.
• Mean gradient is the valid hemodynamic data for severity. Maximal gradient is of limited value as it is derived from peak mitral velocity, which is influenced by net left-sided atrioventricular compliance (Fig. 3.26).
• Heart rate at which gradients are measured should always be reported.
• In patients with atrial fibrillation, mean gradient should be calculated as the average of five cycles, with the least variation of R-R intervals and as close as possible to normal heart rate (Fig. 3.27).
Mitral gradient, although reliably assessed by Doppler, is not the best marker of the severity of mitral stenosis. Transmitral pressure gradients are reliable but depend
upon:
• Severity of mitral stenosis
• Net left-sided atrio-ventricular compliance (mainly affects peak gradients)
• Flow (Fig. 3.28)
• Diastolic filling period and heart rate
• Associated mitral regurgitation (Fig. 3.29).
The transmitral mean pressure gradient commonly increases during exercise, regardless of the severity of stenosis, in accordance with exercise duration and exercise-induced changes in cardiac output.
Mitral valve area can be estimated by four different techniques as shown in Table 3.2.11-13
• Planimetry using two-dimensional (2D) echocardiography of the mitral orifice has the advantage of being a direct measurement of MVA and, unlike other methods, does not involve any hypothesis regarding flow conditions, cardiac chamber compliance or associated valvular lesions.
• Planimetry has been shown to have the best correlation with anatomical valve area. For these reasons, planimetry is considered as the gold standard measurement of MVA.
• Planimetry measurement is obtained by direct tracing of the mitral orifice, including opened commissures on a parasternal short-axis view (Fig. 3.30).
• Careful scanning from the apex to the base of the LV is required to ensure that the valve area is measured at the leaflet tips.
• The measurement plane should be perpendicular to the mitral orifice, which has an elliptical shape.
• Gain setting should be just sufficient to visualize the whole contour of the mitral orifice. Excessive gain setting may cause underestimation of valve area, in particular when leaflet tips are dense or calcified.
• Image magnification, using the zoom mode, is useful to better delineate the contour of the mitral orifice (Fig. 3.30).
• The optimal timing of the cardiac cycle to measure planimetry is middiastole (some recommend early diastole). This is best performed using the cine-loop mode on a frozen image.12
• It is recommended to perform several different measurements, in particular in patients with atrial fibrillation and in those who have incomplete commissural fusion.
• Another potential limitation is that the performance of planimetry requires technical expertise. The measurement plane must be optimally positioned at the mitral orifice. ttis can be done by 3D-guided
biplane imaging, which allows the cursor to be placed at the tip of the leaflets in desired middiastole (Fig. 3.31).
• Real-time 3D echo imaging is useful in optimizing the positioning of the measurement plane and, therefore, improving reproducibility.14 It also improves the accuracy of planimetry measurement when performed by less-experienced echocardiographers (Fig. 3.32). the 3D-transthoracic echocardiography (TTE) allows a 3D acquisition of the entire mitral valve, which can be sliced along any plane as desired (Fig. 3.33).
• the 3D echo and biplane imaging both have low temporal resolution as compared to standard 2D echocardiography. If adequate time and multiple attempts are made to obtain valve area, 2D echo still remains the preferred method in experienced hands.
• Planimetry using THE (either 2D or 3D) is not feasible in 5-10% of patients and 3D-transesophageal echocardiography (TEE) may represent an interesting alternative.
• It is recommended to measure the distance between the anterior and posterior mitral leaflets in the LV parasternal long-axis view in its narrowest area. When viewing the LV short-axis, planimetry of the mitral valve
is done making sure that the level of measurement is the level that has the smallest distance between anterior and posterior leaflets, which is closest to the smallest distance obtained from the LV parasternal long-axis view, and thus serving as the narrowest area possible by planimetry of the mitral orifice (Fig. 3.34).
Pressure Half-time Method for MVA
• Pressure half-time (PHT) is the time interval in milliseconds between the maximum mitral gradient in early diastole and the time point where the gradient is half the maximum initial value.15
• the decline of the velocity of diastolic transmitral blood flow is inversely proportional to valve area (cm2), and MVA is derived using the empirical formula:15
MVA = 220/PHT
• PHT is obtained by tracing the deceleration slope of the E-wave on Doppler spectral display of transmitral flow and valve area is automatically calculated by the integrated software of currently used echo machines (Fig. 3.35).
• Quality of the contour of the Doppler flow, in particular the deceleration slope, is important. The deceleration slope is sometimes bimodal, the decline of mitral flow velocity being more rapid in early diastole than during the following part of the E-wave. In these cases, it is recommended that the deceleration slope in middiastole rather than the early deceleration slope be traced (Fig. 3.36).
• In the rare patients with a concave shape of the tracing, PHT measurement may not be feasible.
• In patients with atrial fibrillation, tracing should avoid mitral flow from short diastoles and average different cardiac cycles (Fig. 3.37).
• The PHT method is widely used because it is easy to perform, but its limitations should be kept in mind since different factors influence the relationship between PHT and MVA (Fig. 3.38). Left-sided net atrio-ventricular compliance (NAVC) is the most significant factor.16-18
PHT x effective orifice area NAVC = 11.6 x (peak transmitral gradient)
• Concomitant aortic valve disease can reduce left atrioventricular compliance and PHT becomes shorter (Fig. 3.39).
• Net atrioventricular compliance, derived by Doppler echocardiography, has been shown to be an important physiological determinant of pulmonary hypertension in patients with mitral stenosis.
• Routine measurement of net atrioventricular compliance in all patients with mitral stenosis is recommended because, in addition to clarifying the inaccuracies of PHT in calculation of area out of the 4-6 mL/mm Hg range, it is also a predictor of the left atrial and pulmonary pressures, exercise capacity and the need for mitral valve replacement.
• Impaired left ventricular diastolic function is a likely explanation of the lower reliability of PHT to assess mitral valve area in the elderly.
continuity Equation for calculation of Mitral Valve Area
Continuity equation is not recommended for routine practice in obtaining mitral valve area. It has many assumptions, which make it error prone.12 It is also not reliable in presence of atrial fibrillation, mitral or aortic regurgitation. Mitral valve area by the continuity equation can be obtained by dividing the Doppler stroke volume (from either outflow tract) with the mitral velocity-time integral (Fig. 3.40).
Proximal Isovelocity Surface Area Method (PISA)
the proximal isovelocity surface area (PISA) method is based on the continuity principle and assumes that blood flow converging toward a flat orifice forms hemispheric isovelocity shells. It has been shown that the PISA method is accurate and reproducible. ttis method is useful in mitral stenosis since the proximal convergence method can be easily visualized and it may be the only method available in certain situations (Fig. 3.41).
• Measure the radius (R) of the hemisphere from the first aliasing velocity in the left atrium up to the beginning of narrowest portion of the color jet within the valve in zoomed mode.
• Use an appropriate aliasing velocity (by baseline shift), which clearly shows hemispheric shape of the PISA.
• Estimate the mitral volume flow rate by multiplying the area of the hemisphere (6.28 x R2) with aliasing velocity. ttis further needs to be corrected for mitral leaflet angles/180°.
• Divide the mitral flow rate thus obtained by the continuous wave (CW) Doppler peak transmitral velocity to obtain mitral valve area.
• Most systems have in-built capability to obtain these data.
• the PISA method provides an assessment of the physiologic or effective orifice area at the vena cont- racta, as opposed to the anatomic orifice area measured by planimetry, which is generally somewhat larger.
• Use of lower aliasing velocity results in inadequate flow convergence shape, ambiguous surface contour and therefore difficulty in getting a reliable radius (Fig. 3.42).
• One limitation for a wider use of the proximal isovelocity surface area method (PISA) for the evaluation of the mitral valve area (MVA) in patients with mitral stenosis (MS) is the requirement of an angle correction factor (angle a between the mitral leaflets), which cannot be obtained using the machine's built-in software and requires a manual measurement.19
• The angle formed by the mitral leaflet only slightly changes in between patients and use of a fixed angle value of 100° provides an accurate estimation of the valve area by the PISA method in patients with mitral stenosis.19 This simplification would facilitate and extend the use of the PISA as an additional method for the assessment of mitral stenosis severity in routine practice.
• The use of color M-mode improves its accuracy, enabling simultaneous measurement of flow and velocity.
• PISA method has the advantage of being applicable even in presence of mitral regurgitation.
Miscellaneous Parameters of Severity of Mitral Stenosis
• Mitral valve resistance (ratio of mean gradient/ diastolic flow rate) has been proposed as a flow-independent method of assessing severity. It correlates with the degree of pulmonary hypertension. However it has limitations of assessing stroke volume and is not routinely used in clinical practice.
• Estimation of pulmonary pressures (from tricuspid and pulmonary regurgitation jets) is an indirect clue of severity or rather the consequence of mitral stenosis.
• Shortest distance between the tips of the mitral leaflets in early diastole in parasternal long-axis view has been found to correlate with severity of mitral stenosis. A distance < 10 mm indicates severe stenosis.
• Width of vena contracta in two planes, if < 11 mm, suggests severe mitral stenosis. From the vena contracta A (width) and vena contracta B, effective orifice area can be estimated as p/4 x A x B (Fig. 3.43).
Morphology of the Mitral Valve Apparatus in Mitral Stenosis
Evaluation of morphology is a major component of echocardiographic assessment of mitral stenosis because of its implications for the type of therapeutic intervention.
Commissural fusion is assessed from the short-axis parasternal view used for planimetry (Fig. 3.44). Commissural anatomy may be difficult to assess, in particular in patients with severe valve deformity. Commissures are better visualized using real-time 3DE 20 (Fig. 3.45).
Commissural fusion is an important feature to distinguish rheumatic from degenerative MS, to check the consistency of severity measurements and to study the effects of therapeutic interventions (Fig. 3.46).
Complete fusion of both commissures generally indicates severe stenosis. However, the lack of commiss- uralfusion does not exclude significant stenosis in degenerative aetiology or even rheumatic one, where restenosis after previous valvotomy may be due to valve rigidity despite persistent commissural opening.
Echocardiographic examination is used to assess leaflet thickening and mobility in long-axis parasternal view (Figs 3.47 to 3.49).
Chordal shortening and thickening are assessed using long-axis parasternal and apical views (Figs 3.50 and 3.51).
Increased echo brightness suggests calcification. The examination should mention the homogeneity of thickening or calcification in short axis (Fig. 3.52).
Extent of mitral valve deformity is expressed in scores combining different components of mitral apparatus or using an overall assessment of valve morphology.21-22 Scores have been developed, in particular taking into account the location of valve thickening or calcification in relation to commissures (Fig. 3.53). No score has been definitely proven to be superior to another and all have a limited predictive value with regard to prognosis.
concomitant Pathology in Mitral Stenosis
• The quantitation of left atrial enlargement helps in prognostication and deciding therapeutic options.
• Left atrial spontaneous contrast, as assessed by TEE, is a predictor of the thromboembolic risk (Fig. 3.54). Spontaneous contrast can be graded and may help in deciding need for anticoagulation.
• Transoesophageal echocardiography has a much higher sensitivity than the transthoracic approach to diagnose left atrial thrombus, in particular when
Fig. 3.55: Transthoracic short-axis view demonstrating thrombus in the left atrial appendage (arrow).
located in the left atrial appendage (Figs 3.55 and 3.56). Associated mitral regurgitation has important implications for the choice of therapy. Quantitation should combine semiquantitative and quantitative measurements. More than mild regurgitation is a relative contraindication for mitral commissurotomy (Figs 3.56A and B).
The mechanism of rheumatic mitral regurgitation is restricted leaflet mobility and retraction. After balloon mitral commissurotomy, leaflet tear is a frequent cause of regurgitation (Fig. 3.57).
Mechanism of mitral regurgitation is important in patients presenting with moderate-to-severe regurgitation after balloon mitral commissurotomy. A traumatic mechanism is an indication to consider surgery more frequently than in case of central and/or commissural regurgitation due to valve stiffness without leaflet tear.
• the presence of mitral regurgitation does not alter the validity of the quantitation of mitral stenosis, except for the continuity equation valve area.
• Other valve diseases are frequently associated with rheumatic mitral stenosis. The severity of aortic stenosis may be underestimated because of low flow (decreased stroke volume). In cases of severe aortic regurgitation, PHT method underestimates severity of mitral stenosis.
• the analysis of the tricuspid valve should look for signs of involvement of the rheumatic process. More frequently, associated tricuspid disease is functional tricuspid regurgitation although occasionally dominant tricuspid valve stenosis may be seen (Fig. 3.58).
A diameter of the tricuspid annulus > 40 mm seems to be more reliable than quantitation of regurgitation to predict the risk of severe tricuspid regurgitation and need for tricuspid annuloplasty.
In summary, mitral stenosis is studied by analysis of its morphology and commissural calcification, valve area planimetry and pressure half-time. Transesophageal echocardiography is employed to rule out left atrial thrombi before balloon mitral commissurotomy. the 3DE bridges the gap between novice and expert with regard to accurately assessing severity. From a standpoint of therapeutic intervention, mitral valve morphology can be classified into three groups: flexible valve and mild subvalvular disease (chordae >10 mm long; Group I), flexible valve and extensive subvalvular disease (chordae < 10 mm long; Group II) and calcified valves (Group III).
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