Advances in Rheumatic Mitral Stenosis:

Echocardiographic, Pathophysiologic, and

Hemodynamic Considerations
Jeffrey J. Silbiger, MD, New York, New York

Echocardiography is the primary imaging modality used in patients with mitral stenosis. Doppler-derived mea-
surements of mitral pressure half-time are commonly used to calculate mitral valve area, but a number of he-
modynamic confounders associated with advanced age limit its utility. Planimetry remains the gold standard
for determining mitral valve area and may be performed using two- or three-dimensional imaging. Although the
Wilkins score has been used for >30 years to predict balloon mitral valvuloplasty outcomes, newer scoring
systems have been proposed to improve predictive accuracy. Some patients undergoing technically success-
ful balloon mitral valvuloplasty may not have satisfactory clinical outcomes. These individuals may be identi-
fied by the presence of reduced net atrioventricular compliance, which can be measured
echocardiographically. Exercise testing may be useful in patients with mitral stenosis whose symptomatic sta-
tus is incongruous their mitral valve area. Last, reduced left atrial systolic strain, an indicator of poor left atrial
compliance, has been shown to reliably predict adverse outcomes in patients with mitral stenosis. The author
discusses the hemodynamics and path ophysiology of mitral stenosis and reviews current and emerging roles
of echocardiography in its evaluation. (J Am Soc Echocardiogr 2021;-:---.)

Keywords: Rheumatic mitral stenosis, Net atrioventricular compliance, Low-flow, low-gradient mitral stenosis,
Balloon mitral valvuloplasty, Calcific mitral stenosis

The decline of acute rheumatic fever in industrialized countries has
resulted in a significant decrease in the incidence of mitral stenosis.
In underdeveloped countries, however, where rheumatic fever con-
tinues to remain a significant public health concern, its incidence re-
mains high. In the West, rheumatic heart disease generally comes to
clinical attention during middle age or later. In developing countries,
where rheumatic disease is more rapidly progressive, disease onset
typically occurs in the second and third decades of life.1 In fact,
women of childbearing age may first present with acute pulmonary
edema during pregnancy because of the rise in circulating blood vol-
ume.
The mitral valve (MV) is the most commonly affected in rheumatic
heart disease. Rheumatic valvulitis is believed to be triggered by an
autoimmune process caused by cross-reactivity between strepto-
coccal antigens and native heart valve proteins (molecular mimicry).2
Echocardiography plays a key role in the diagnosis of mitral stenosis
and, when indicated, in the selection of the most appropriate inter-
vention. In this review I discuss the hemodynamics, pathophysiology,
and echocardiographic assessment of this disorder.
NATURAL HISTORY OF MITRAL STENOSIS
Mitral stenosis restricts blood flow into the left ventricle during dias-
tole. The accompanying rise in left atrial (LA) pressure increases the
transmitral gradient (TMG), which helps maintain forward ventricular
filling. At the same time, increased LA pressure causes a passive up-
stream rise in pulmonary venous pressure. This is thought to trigger
pulmonary arteriolar vasoconstriction, which increases pulmonary ar-
tery (PA) pressure. Over time, irreversible obliterative changes may
develop in the pulmonary vasculature,3 which lead to fixed pulmo-
nary hypertension, sometimes referred to as the ‘‘second stenosis.’’
Interestingly, the second stenosis reduces congestive symptoms by
decreasing venous return, albeit at the expense of a reduction in car-
diac output. The development of pulmonary hypertension increases
right ventricular afterload, which over time results in right ventricular
hypertrophy, dilatation, and failure. Enlargement of the right ventricle
causes tricuspid annular dilatation as well as tricuspid leaflet tethering,
resulting in functional tricuspid regurgitation.4

TWO-DIMENSIONAL ECHOCARDIOGRAPHIC FINDINGS

There are a number of characteristic two-dimensional echocardio-

From Icahn School Medicine at Mount Sinai, New York, New York.
graphic findings in rheumatic mitral stenosis (Figure 1).5,6 Increased
Dr. Silbiger is a member of the speakers’ bureau of Lantheus Medical Imaging.
leaflet thickness typically begins at the free margins of the MV and
Reprint requests: Jeffrey J. Silbiger, MD, Echocardiography Laboratory, Depart- gradually extends toward its base. The distinctive diastolic doming
ment of Cardiology, Elmhurst Hospital Center, Icahn School of Medicine at Mount
(hockey-stick appearance) of the anterior mitral leaflet, caused by
Sinai, 79-01 Broadway, Room D3-24C, Elmhurst, NY 11373 (E-mail: jeffrey.
commissural fusion, is best appreciated in long-axis views. The poste-
silbiger@mssm.edu).
rior leaflet may also dome, although it is more often immobile. Fusion
0894-7317/$36.00
of the medial and lateral commissures of the MV, which progresses
Copyright 2021 by the American Society of Echocardiography.
inward, produces the characteristic fish-mouth appearance of the
https://doi.org/10.1016/j.echo.2021.02.015
1
2 Silbiger Journal of the American Society of Echocardiography
- 2021

Abbreviations
rheumatic MV in the short-axis
view. Last, the chordae tendi-
AF = Atrial fibrillation neae shorten, thicken, and
BMV = Balloon mitral become fused together.
valvuloplasty Chordal abnormalities typically
begin at points of leaflet attach-
Cn = Net atrioventricular ment and progress toward the
compliance
papillary muscles. Importantly,
LA = Left atrial these abnormalities, which are
often underestimated echocar-
LF-LG = Low-flow, low-
gradient
diographically, can be seen to
advantage with intentional off-
LV = Left ventricular axis imaging (Figure 1C).
MR = Mitral regurgitation
MV = Mitral valve
LEFT VENTRICULAR
P½t = Pressure half-time SYSTOLIC FUNCTION
PA = Pulmonary artery
Several early studies demon-
TMG = Transmitral gradient strated abnormalities of left ven-
tricular (LV) systolic contractility
in about 25% of patients with mitral stenosis, with a predilection
for the posterior wall. LV ejection is usually mildly decreased. Early
workers suggested that this is due to chronic (‘‘smoldering’’) rheumatic
carditis,7 but this has not been borne out by histopathologic studies.8
Moreover, recent invasive hemodynamic studies have demonstrated
that end-systolic elastance, the gold standard of intrinsic LV contrac-
tility, is normal in mitral stenosis.9
Some workers have alternatively proposed that decreased LV sys-
tolic contractility is caused by reduced LV filling in accordance with
the Starling mechanism. Specifically, it has been suggested that the
scarred and foreshortened chords seen in mitral stenosis tether, and
thus prevent, the LV free wall from expanding during diastole.7
Reduced LV filling may also be caused by exaggeration of the other-
wise modest leftward motion of the interventricular septum normally
seen in early diastole (Figure 2). The resulting paradoxical (leftward
diastolic) motion of the septum has been attributed to predominance
of early diastolic right ventricular filling resulting from the marked
disparity in area between the mitral and tricuspid valves (Figure 2,
Video 1 available at www.onlinejase.com).10
Deformation studies11 performed in patients with mitral stenosis
demonstrate a significant reduction in LV global longitudinal strain
compared with normal control subjects, suggesting the presence of
intrinsic myocardial disease. However, when global longitudinal strain
is indexed to LV volume, these differences disappear, indicating that
the reduction in global longitudinal strain is related to reduced pre-
load rather than to a ‘‘myocardial factor.’’12
Figure 1 Characteristic two-dimensional echocardiographic
findings of rheumatic mitral stenosis. (A) Parasternal long-axis
view showing doming of the anterior mitral leaflet (arrow). (B)
MV AREA Parasternal short-axis view exhibiting fusion of the medial and
lateral commissures (arrows). (C) Intentional off-axis imaging
Severe mitral stenosis is defined as an MV area # 1.5 cm2 and very from the parasternal window reveals chordal thickening (arrow)
severe mitral stenosis as an MV area # 1.0 cm2.13 An MV area be- otherwise not appreciated in (A), obtained from the same pa-
tween 1.6 and 2.0 cm2 is not usually associated with symptoms and tient.
is variably referred to as ‘‘moderate’’ or ‘‘nonsevere’’ mitral stenosis.
Of note, there are no established indexed values for MV area. Last, tween 60 and 80 beats/min (assuming normal transmitral flow, i.e.,
it is important to emphasize that TMGs cannot be used as reliable sur- no anemia, hyperthyroidism, etc.) for moderate, severe, and very se-
rogates for MV area, because of their dependence upon heart rate and vere mitral stenosis are <5, 5 to 10, and >10 mm Hg, respectively.15
blood flow.14 Accordingly, expected mean TMGs, at a heart rate be- MV area is most commonly measured directly using planimetry or
Journal of the American Society of Echocardiography Silbiger 3
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surement is greatly simplified with three-dimensionally guided

HIGHLIGHTS
 Decreased ejection fraction in mitral stenosis is caused by
reduced preload.
 Low-flow, low-gradient mitral stenosis occurs when ventricular
compliance is low.
 Patients with Cn < 4 mm Hg/mL may remain symptomatic af-
ter successful valvuloplasty.
 Low Nunes scores correctly predict good outcomes even
when Wilkins scores are >8.
 For any given valve area, gradients are lower in calcific than
rheumatic valves.
indirectly using the pressure half-time (P½t) method. Methods
involving the continuity principle are seldom used.
Planimetry
Planimetry is considered the echocardiographic gold standard for
measuring MV area because it is not subject to the various con-
founders that influence Doppler-based methods. Because the MV
domes in diastole, it is critical that planimetry is performed at the
leaflet tips, otherwise MV area will be overestimated. MV area mea-
biplane imaging (Figure 3). When the cursor is positioned across the
tips of both leaflets in the parasternal long-axis view, the orthogonal
short-axis view is simultaneously displayed, such that the MV can
be planimetered along its free margin.16 Real-time three-dimensional
imaging permits visualization of the mitral leaflets in multiple planes
and thus facilitates accurate identification of the narrowest opening
of the MV (Figure 4). Last, cardiac computed tomography has been
successfully used to measure MV area in patients with rheumatic
mitral stenosis who have suboptimal echocardiographic images.17
Mitral P½t Method
The mitral P½t is the time it takes for the peak LA-LV pressure
gradient to fall by a factor of one half. This is determined by the
rate at which falling LA and rising LV diastolic pressures come into
equilibrium. When equilibrium is reached slowly, P½t is prolonged
and mitral stenosis is severe, and vice versa (Figure 5). Empiric obser-
vations from invasive hemodynamic studies reveal18 that when P½t is
220 msec, MV area equals 1.0 cm2. Hence, MV area can be calculated
using the formula: 220/P½t (the Hatle formula). Doppler-derived
P½t (Figure 6) can be used to calculate MV area using the same for-
mula, but it does not perform accurately unless the MV is stenotic.19
It is important to point out that P½t is influenced by a number of
factors that render calculation of MV area inaccurate.20 Among older

Figure 2 (A) M-mode echocardiogram from a patient with mild mitral stenosis and normal motion of the interventricular septum. Note
the brief early downward diastolic motion of the septum (arrow) caused by early right ventricular filling preceding LV filling. (B) M-
mode echocardiogram from a patient with hemodynamically significant mitral stenosis exhibiting abnormal interventricular septal
motion. In early diastole, the septum moves (paradoxically) toward the left ventricle (arrow) because initial filling of the right ventricle
occurs earlier through an unrestricted tricuspid valve, while LV filling is delayed by the stenotic MV. (C) Apical four-chamber view of
the patient in (B) demonstrating abnormal early diastolic motion of the base of the interventricular septum toward the left ventricle
(arrow). (D) After the initial leftward deviation of the interventricular septum in (C), filling of the left ventricle moves the septum
back to neutral position (arrow). See Video 1. Images courtesy of Dr. Michael Picard, Massachusetts General Hospital.
4 Silbiger
Figure 3 Three-dimensionally guided biplane imaging of the MV. The cursor is passed through the MV tips in the parasternal long-
axis (PLAX) view, such that the orthogonal short-axis (SAX) view simultaneously displays the free margins of the MV, which can then
be traced. LA, Left atrium; LV, left ventricle; RV, right ventricle.
patients, in whom heart failure with preserved ejection fraction (LV
diastolic dysfunction) is common, reduced ventricular compliance
may cause a steep rise in LV diastolic pressure leading to a shortened
P½t and overestimation of MV area. Significant aortic regurgitation
similarly increases the rate of diastolic LV pressure rise, thereby short-
ening the P½t.
When significant mitral regurgitation (MR) complicates mitral ste-
nosis, the marked rise in peak E-wave velocity prolongs the time
required for transmitral velocity to decrease to peak E-wave veloc-
ity/O2, thereby lengthening P½t (Figure 6). At the same time, LA vol-
ume overload from MR decreases the operational compliance of the
atrium by shifting its pressure-volume relationship onto the steep up-
per portion of its pressure-volume curve. As a result, there is a rapid
decline in LA pressure (and E-wave velocity), which shortens the
P½t. The utility of the P½t for estimating MV area rests in the fact
that peak transmitral pressure gradient (peak E-wave velocity) and
LA compliance influence the P½t in opposite directions. However,
in some patients with mixed mitral stenosis and MR, this balance be-
comes disturbed, and LA compliance change predominates,
rendering the Hatle formula (220/P½t) inaccurate.21 Volume over-
load of the left atrium during pregnancy may cause overestimation
of the MV area by the P½t method for similar reasons.22 Last, P½t
is decreased when an atrial septal defect is present because of simul-
taneous runoff into the right atrium and left ventricle.23
When MV area is measured using the Doppler P½t method, decel-
eration of the continuous-wave Doppler signal occasionally displays
Journal of the American Society of Echocardiography
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an early, steep fall in velocity followed by a more gradual fall, produc-
ing a ‘‘ski-slope’’ appearance23 (Figure 7). The mid-diastolic decrease
in slope is caused by the increase in operational compliance that takes
place as the left atrium empties (shifts onto the less steep portion of its
pressure-volume curve).24 In such instances, it is recommended that
the P½t be measured using the less steep mid-diastolic slope.25
LOW-FLOW, LOW-GRADIENT MITRAL STENOSIS
The operational compliance of the left atrium is reduced in mitral ste-
nosis because of the rise in atrial volume that attends decreased cham-
ber emptying.26 Additional perturbations common in older
individuals further decrease atrial compliance. First, comorbidities
prevalent among the elderly (diabetes mellitus, hypertension, obesity,
and coronary artery disease) reduce LA compliance by promoting
atrial fibrosis.27 In addition, reduced LV compliance, common among
older individuals, decrease operational LA compliance because of the
attendant rise in atrial volume (atrioventricular coupling).
Concomitant reduction of atrial and ventricular compliance,
commonplace among older individuals, may result in the novel clin-
ical entity low-flow, low-gradient (LF-LG) mitral stenosis. The reduced
atrial compliance seen in this disorder increases the LA V wave (and
hence mean LA pressure; Figure 8), resulting in dyspnea and effort
intolerance.28 Poor LA compliance also causes a rapid decline in
the LA y-descent (Figure 8), because the atrium is operating on the
Journal of the American Society of Echocardiography Silbiger 5
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Figure 4 Real-time three-dimensional measurement of MV area. Multiplane reconstruction allows precise identification of the nar-
rowest opening of the MV. Images courtesy of Gila Perk, MD, Mount Sinai Medical Center.
6 Silbiger
Figure 5 Simultaneous tracings of LA pressure (LAP) and LV pressure (LVP) displaying a short (left) and a long (right) P½t.
Figure 6 P½t can be ascertained using Doppler imaging by
measuring the time offset between peak E-wave transmitral ve-
locity (Vmax) and the velocity at Vmax/O2. See text.
Figure 7 ‘‘Ski-slope’’ mitral stenosis. P½t should be measured
using the mid-diastolic slope (red line). See text.
steep upper portion of its pressure-volume curve.29 This, combined
with a rapid rise in LV diastolic pressure caused by poor ventricular
compliance (Figure 8), decreases the magnitude of the TMG.
Journal of the American Society of Echocardiography
- 2021
Figure 8 Simultaneous LA and LV pressure curves in LF-LG
mitral stenosis. Note the tall LA V wave and steep y-descent
of the LA pressure curve and the steep upward trajectory of
the LV pressure curve during diastole (asterisk). See text.
Figure 9 Net atrioventricular compliance (Cn). Note that Cn is
inversely related to the mitral E-wave downslope. The latter in-
creases as LA and/or LV compliance decreases.
In practical terms, LF-LG mitral stenosis is characterized by the
constellation of (1) low flow (stroke volume < 35 mL/m2 by the con-
tinuity equation) due to reduced MV area and decreased LV filling
due to a stiff ventricle, (2) a low gradient (reduced out of proportion
to the planimetered MV area) due to low flow as well as rapid
Journal of the American Society of Echocardiography
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Figure 10 Note the high reflectivity of the calcified medial mitral
commissure (arrow). Compare with Figure 1B in which the com-
missures are fused by fibrosis.
Figure 11 Short-axis image of a MV following balloon valvulo-
plasty. Note dropout in the anterior leaflet, representing a tear
(arrow). Inset reveals severe MR.
equalization of LA and LV pressures, and (3) dyspnea resulting from
increased mean LA pressure (tall LA V wave).9,30
Additional factors such as right ventricular and LV systolic dysfunc-
tion may also decrease stroke volume (and transmitral flow) in LF-LG
mitral stenosis. Decreased stroke volume can also result from reduced
LV filling associated with severe subvalvular disease, LV concentric re-
modeling, loss of LA kick due to atrial fibrillation (AF), paradoxical
septal motion, and pulmonary hypertension (the second stenosis).9,30
Increased afterload associated with hypertension and aortic stiffness,
common in older individuals, can similarly reduce LV stroke vol-
ume.9,30
Given the impact that reduced LA and LV compliance have on the
hemodynamics of mitral stenosis, it would be useful to be able to mea-
sure these parameters noninvasively. Although the individual compli-
ances of the left atrium and left ventricle cannot be measured,31 net
atrioventricular compliance (Cn)32 can be measured echocardio-
graphically using the simple Doppler-based formula Cn (mL/mm
Hg) = 1,270  (planimetered MV area [cm2]/mitral E-wave deceler-
ation slope [cm/s2]) (see Appendix). It is intuitive from this formula
that Cn is reduced when LA or LV compliance is decreased, as both
prolong E-wave downslope (shorten P½t; Figure 9). In patients with
pure mitral stenosis, reduced Cn is due to decreased LA compliance.
Among older individuals with LF-LG mitral stenosis, however, Cn is
further reduced by decreased LV compliance.29
Not surprisingly, low Cn (<4 mL/mm Hg) in patients with LF-LG
mitral stenosis has been shown to worsen prognosis and has been
Silbiger 7
linked to an increased likelihood of downstream AF, heart failure,
repeat MV intervention, and death.33,34 Moreover, symptomatic
improvement may not occur in as many as 40% of such patients,
despite technically successful balloon mitral valvuloplasty (BMV).
This is thought to be due to the tall LA V wave (high mean LA pres-
sure), which remains unaffected by the procedure9 (Figure 8).
Echocardiographically, such ‘‘BMV nonresponders’’ may demonstrate
a tall mitral E wave with an E/A ratio > 1 and a short P½t. Potentially
salutary interventions in such patients include vasodilator therapy for
those with increased LV afterload (hypertension and increased aortic
stiffness) and restoration of sinus rhythm in those with AF. The utility
of these therapeutic measures, however, remains to be substantiated.9
LF-LG mitral stenosis should be distinguished from so-called
pseudosevere MS. Low flow associated with the latter is insufficient
to adequately open the MV despite the negligible resistance it of-
fers.9 Unfortunately, these two disorders cannot be readily distin-
guished.
LA STRAIN
Mitral stenosis has a number of effects on LA strain. Peak LA systolic
(reservoir) strain, a reflection of atrial compliance, has been shown to
correlate with functional capacity.35 Reduced peak LA strain predicts
symptoms, hospitalizations, AF, thromboembolic events, and the
need for valve replacement or BMV at 3 years in asymptomatic pa-
tients with moderate mitral stenosis.36 Decreased conduit strain in pa-
tients with mitral stenosis reflects the effects of concomitant LV
diastolic dysfunction.37,38 Intercession of atrial contractile dysfunction
(due to high LA afterload) decreases atrial pump strain. With the onset
of AF, pump strain is no longer evident.38
STRESS ECHOCARDIOGRAPHY
Exercise stress testing is particularly useful in mitral stenosis when
there is discordance between a patient’s symptoms and MV area
(i.e., asymptomatic patients with severe mitral stenosis [MV area #
1.5 cm2] and symptomatic patients with nonsevere mitral stenosis
[MV area > 1.5 cm2]).13
Patients who deny symptoms despite severe mitral stenosis often
do so because they limit their physical activity. Poor exercise tolerance
can nevertheless be demonstrated in almost half of such patients dur-
ing stress testing.39 Interestingly, high PA systolic pressure (>60 mm
Hg) at peak exercise correlates poorly with exercise intolerance in
these patients.39 In contrast, a rise in PA systolic pressure39 or a
decrease in Cn40 at a low workload reliably predicts dyspnea during
stress, likely representing the effects of poor LA compliance.40
Exercise testing may be helpful in guiding treatment in symptom-
atic patients with nonsevere mitral stenosis. If such patients demon-
strate increases in mean TMG during exercise to >15 mm Hg, mitral
intervention may be considered (class IIb recommendation) accord-
ing to the 2014 American Heart Association/American College of
Cardiology guidelines.13 Although dobutamine stress has also
been used in patients with mitral stenosis, exercise is preferred
because it is more physiologic.13 Indeed, the rise in PA systolic pres-
sure ordinarily seen during exercise may be blunted with dobut-
amine infusion because of its b2 effects on the pulmonary
vasculature.41
8 Silbiger Journal of the American Society of Echocardiography
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Figure 12 Two-dimensional imaging of the mitral commissures. When the commissures are partially open, the point of fusion can be
detected within a few millimeters of the leaflets’ free margins. When the commissures are fully open, there is no evidence of fusion to
the level of the annulus. (A) Both commissures are fused. (B) Partially open commissures. (C) One commissure is open (arrow). (D)
Both commissures are open (arrows). Reproduced with permission from Messika-Zeitoun et al.51

ECHOCARDIOGRAPHIC ASSESSMENT IN BMV
BMV is most commonly performed with an Inoue balloon using a
transseptal approach. The design of the balloon facilitates self-
positioning and reduces the likelihood of device migration.
Balloon inflation increases MV area by splitting the medial and/
or lateral commissures. Transthoracic echocardiography is routinely
performed before undertaking BMV to determine whether MV
anatomy is suitable for commissural splitting and will increase
MV area to >1.5 cm2 without producing significant MR. A number
of scoring systems, described below, have been developed for this
purpose. Transesophageal imaging is routinely performed before
BMV to exclude the presence of an LA thrombus, which can be
dislodged during wire manipulation.42 Echocardiography during
BMV is used to assess MV area, the mechanism and severity of
MR, and the degree of commissural opening. Recommended pro-
cedural end points include complete opening of at least one
commissure, an increase in MV area to >1 cm/m2, and an increase
in MR by more than one grade on a scale of 1 to 4+.43 TMGs
should not be used to gauge BMV success, because they are influ-
enced by changes in heart rate and by the increased transmitral
flow that attends MR.
The mitral P½t is inaccurate for determining valve area for approx-
imately 24 to 48 hours after BMV.44 When BMV is performed, the
reduction in LA volume produces an immediate decrease in TMG
(and peak E-wave velocity), which shortens mitral P½t. Despite the
decrease in atrial volume, LA operational compliance remains
reduced for 24 to 48 hours, further shortening the P½t. Because
the accuracy of the P½t depends upon TMG and LA compliance
changing in opposite directions, P½t may remain inaccurate during
this time period. It is therefore recommended that MV area be
measured using planimetry following BMV.20 It is useful to note
that when planimetry cannot be accurately performed, a
P½t < 130 msec reliably predicts a post-BMV MV area $ 1.5 cm2
with high specificity but low sensitivity.45
It is recommended that BMV not be undertaken when more
than mild MR is present.42 Minor increases in MR (typically
commissural) are quite common after BMV43; severe MR occurs
in 2% to 10% of patients.46 The mitral commissures can usually
be safely split when they are fused by fibrotic tissue, but calcific
fusion (Figure 10) resists splitting and causes the force of the
expanded balloon to be transferred to more pliable leaflet tissue,
which may rupture resulting in significant MR.47 BMV is therefore
contraindicated when massive or bicommissural calcification is pre-
sent.42 Leaflet calcification, particularly when it is not uniformly
distributed, represents an additional cause of leaflet tears.48 Leaflet
tears can be recognized echocardiographically as regions of leaflet
‘‘dropout’’ (Figure 11). When assessing commissural and leaflet cal-
cium, it is important to appreciate that echocardiographic reflec-
tance does not reliably distinguish between fibrosis and
calcification. The latter is suggested by a signal intensity that exceeds
that of the adjacent aortic root and by the presence of acoustic shad-
owing.49 Fluoroscopic imaging and cardiac computed tomography
are also useful for detecting calcification.50 Acute severe MR due
to leaflet rupture is variably tolerated depending upon the compli-
ance of the left atrium. Patients with significantly reduced atrial
compliance may develop acute pulmonary edema necessitating ur-
gent MV replacement.43
Journal of the American Society of Echocardiography
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Figure 13 Three-dimensional echocardiographic images of the
MV before, during, and after BMV. Images were obtained from
the LA perspective. (A) Bilateral commissural fusion is present
(arrows). (B) Balloon (arrow) is inflated across the MV. (C) The
lateral commissure has been opened (arrow). Images courtesy
of Dr. Gila Perk, Mount Sinai Medical Center.
Evaluation of the MV commissures is important in determining the
adequacy of BMV. With two-dimensional imaging, the extent to
which the commissures are open requires careful scanning from the
annulus to the free margins of the mitral leaflets to determine where
within the mitral funnel commissural fusion extends (Figure 12).
Three-dimensional echocardiography facilitates this process, permit-
Silbiger 9
ting imaging from atrial and ventricular perspectives as well as rota-
tionally (Figure 13). Not surprisingly, one study showed that
two-dimensional imaging underestimates the extent of commissural
opening in one third of patients.51 Three-dimensional imaging is
also useful for determining whether mitral stenosis is due to commis-
sural fusion or is the result of valvular or subvalvular rigidity with open
commissures, which is not likely to benefit from BMV. The use of sur-
face rendering software with three-dimensional imaging unfortu-
nately precludes distinguishing commissural fibrosis from
calcification.
Atrial septal defects created at the time of transseptal puncture are
usually small and can be found in <10% of patients after 1 year.52
Hemodynamically significant shunts (shunt ratio $ 1.5:1) are rare,
however.53
Wilkins Score
The Wilkins score was developed >30 years ago and is still the most
commonly used.54 This score assesses the calcification, thickness, and
mobility of the anterior mitral leaflet and the thickness of the chordal
apparatus. Each of these four variables is assigned a score from 1 to 4,
and these scores are summed (Table 1). A total score # 8 predicts
favorable immediate and long-term outcomes, whereas a score > 8
portends less impressive results (Figure 14).54 Several authors have
suggested that the Wilkins score has a number of shortcomings.43,55
First, each of its echocardiographic variables is assessed semiquantita-
tively and therefore subject to interobserver variability. Moreover, all
four variables are assigned equal weighting, which is probably not
reflective of their true prognostic significance. Last, the score does
not evaluate the anatomy of the commissures and therefore fails to
predict the risk for developing MR.
Nunes Score
The Nunes score was developed in 2014 in an attempt to address the
shortcomings of the Wilkins score, although no studies comparing
them have been performed.56 In contrast to the Wilkins score, the var-
iables used in the Nunes score are dichotomous and unequally
weighted (Figure 15A). The variables assessed include (1) MV area,
(2) the extent of subvalvular disease, (3) anterior mitral leaflet
displacement into the LV cavity (Figure 15B), and (4) the commissural
area ratio, a measure of the asymmetry of commissural disease
(Figure 15C). It is important to note that the Nunes score, unlike
the Wilkins score, predicts the risk for MR. In fact, a commissural
area ratio > 1.25 independently predicts a more than one-grade in-
crease in MR severity following BMV. A combined Nunes score #
3 predicts satisfactory BMV outcomes, whereas a score between 6
and 11 predicts suboptimal results; scores of 4 and 5 are considered
intermediate. It is interesting to note that the Nunes score may
correctly predict favorable outcomes in patients with borderline
Wilkins scores (between 9 and 11), who might otherwise be deemed
suboptimal candidates for BMV.56
Sutaria (Commissural Calcification) Score
In contrast to other scoring systems that include anatomic assessment
of the mitral leaflets and chords, the Sutaria score48 evaluates only the
extent of commissural calcification (Figure 16). Satisfactory BMV out-
comes, defined as MV area > 1.5 cm2 and an increase in MR of no
more than one grade, are usually seen in patients with no (score = 0)
10 Silbiger Journal of the American Society of Echocardiography
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Table 1 Wilkins score54

Grade Mobility Subvalvular thickening Leaflet thickening Calcification

1 Highly mobile with only
leaflet tips restricted
2 Leaflet mid and base
portions have normal
mobility
3 Valve continues to move
forward in diastole,
mainly from the base
4 No or minimal forward
movement of the leaflets
in diastole
Minimal thickening just
below the mitral leaflets
Thickening of chordal
structures extending up
to 1/3 of the chordal
length
Thickening extending to
the distal third of the
chords
Extensive thickening and
shortening of all chordal
structures extending
down to the papillary
muscles
Leaflets near normal in
thickness (4–5 mm)
Mid leaflets normal,
considerable thickening
of margins (5–8 mm)
Thickening extending
through the entire leaflet
(5–8 mm)
Considerable thickening of
all leaflet tissue ($8–
10 mm)
A single area of increased
echo brightness
Scattered areas of
brightness confined to
leaflet margins
Brightness extending into
the midportion of the
leaflets
Extensive brightness
throughout much of the
leaflet tissue

Figure 14 (A) Parasternal long-axis view from a patient with mitral stenosis and a Wilkins score of 5. Leaflet mobility is restricted at the
tips only, leaflet thickening is mild and there is minimal calcification. (B) Apical four-chamber view from the same patient. (C) Para-
sternal long-axis view from a patient with mitral stenosis and a Wilkins score of 14. Leaflet mobility is restricted in all portions of the
leaflets, leaflet thickening is marked, and there is a high degree of calcification. (D) Apical four-chamber view from the same patient.
Images courtesy of Dr. Michael Picard, Massachusetts General Hospital.
Journal of the American Society of Echocardiography Silbiger 11
Volume - Number -

Figure 15 Nunes scoring system. (A) Variables measured by the Nunes score and their point values. Because all four variables are
dichotomous, if any of the criteria listed in the table are not met (e.g., extensive subvalvular involvement), a score of zero is assigned.
(B) Leaflet displacement is measured from the mitral annular plane to the point of maximal excursion. (C) The commissural area ratio
(CAR) is obtained by first measuring the area between the inner and outer aspects of the mitral leaflets (shaded regions). The inter-
commissural length is then bisected. The CAR is the ratio of the larger to the smaller shaded region on either side of the bisector.

or mild (score = 1) commissural calcification. More extensive calcifi-
cation of the commissures (score = 2 or 3), however, is associated
with suboptimal outcomes because calcific fusion resists splitting.
BMV is contraindicated with a commissural calcium score of 4 (exten-
sive bilateral calcification).
developing significant MR after BMV. Specifically, it has been pro-
posed that patients with Sutaria scores of 2 to 4 and commissural
area ratios > 1.25 might be better suited for surgical valve replace-
ment, but this will require further validation (59).

Multifactorial Score THROMBOEMBOLISM

Most scoring systems used to predict BMVoutcomes rely solely upon
echocardiographic assessment of valvular anatomy. It has been
shown, however, that a number of clinical and hemodynamic (‘‘multi-
factorial’’) factors, including New York Heart Association functional
class I or II, pre-BMV MV area $ 1.0 cm2, pre-BMV MR < 2+,
age < 55 years, and male sex, independently predict satisfactory
BMV outcomes (i.e., MV area > 1.5 cm2 and MR < 3+). When these
variables are considered in patients with Wilkins scores > 8, who may
be excluded from BMV on this basis, their arithmetic sum predicts an
incremental increase in the likelihood of a favorable outcome. It is
thought that the nonanatomic variables assessed by the multifactorial
score serve as surrogates for various pathophysiologic abnormalities
that are not reflected echocardiographically.57
Stasis created by mitral stenosis and by the superimposition of AF may
result in LA spontaneous echocardiographic contrast (smoke) and
thrombus formation. Atrial thrombi can in fact be detected by trans-
esophageal echocardiography in about 7% of patients who are in
normal sinus rhythm60 and in 25% of those with AF.61 Of note,
thrombi are sometimes not found in the appendage but are instead
confined to the body of the left atrium.62 Interestingly, thromboem-
bolic risk is significantly greater with spherical as opposed to elliptical
LA remodeling.63
CALCIFIC MITRAL STENOSIS

Combined Scores As the population ages, mitral annular calcification has become
increasingly recognized as an important cause of mitral stenosis.
All MV scoring systems have limitations, prompting an integrated
The mechanism of valve narrowing differs in calcific and rheumatic
approach combining different systems.58,59 Some have suggested
mitral stenosis. In rheumatic disease, valve narrowing results from
that the Sutaria score and the commissural area ratio be used in pa-
commissural fusion, whereas that associated with calcific mitral
tients with Wilkins scores < 8 to identify those at increased risk for
12 Silbiger Journal of the American Society of Echocardiography
- 2021

Figure 16 Sutaria scoring system for commissural calcification.

Small black regions indicate partial commissural calcification.
Large black regions indicate extensive commissural calcifica-
tion. MVO see text.

stenosis is caused by extension of calcium from the annulus into the

base of the mitral leaflet(s). This results in the formation of a horizontal
‘‘calcium shelf’’ (Figure 17) that displaces the MV hinge point into the
LV inlet.64
Commissural fusion in the rheumatic MV is responsible for its char-
acteristic funnel shape. In contrast, the open commissures in calcific
mitral stenosis render the MV more tubular in shape, such that the
area measured at the annulus and at the valve orifice are approxi-
mately equal.65 These differences in valve geometry have important
hemodynamic consequences. Compared with the tunnel-shaped
calcific valve, the funnel-shaped rheumatic valve has a lower contrac-
tion coefficient and a larger drop in pressure as blood proceeds from
annulus to orifice. Hence, for any given valve area, the TMG will be
greater in rheumatic than calcific mitral stenosis.66
Measuring MV area can be challenging with calcific MS. Accurate
planimetry is hindered by acoustic shadowing due to calcium.67
Comorbidities commonly associated with mitral annular calcifica-
tion (e.g., hypertension, diabetes mellitus, and coronary artery dis-
ease) decrease LV compliance and therefore shorten the mitral
P½t, which precludes using the Hatle formula to calculate MV
area.67 The continuity equation is the preferred method for
measuring MV area in calcific mitral stenosis.68 However, inaccura-
Figure 17 (A) Calcium encroaching upon the posterior mitral
leaflet forms a shelf that displaces its hinge point into the LV
inlet. Note that calcium may also accumulate within the base
of the LV free wall (asterisk). (B) Extensive calcification of the
anterior (blue asterisk) and posterior (red asterisk) mitral leaflets.
Note the marked inward displacement of both leaflets’ hinge
points (arrows). AML, Anterior mitral leaflet; Ao, aorta; MAC,
mitral annular calcification; PML, posterior mitral leaflet.
cies in MV area calculation may result from underestimating the
diameter of the LV outflow tract, particularly when the aortomitral
curtain is heavily calcified.
CONCLUSION
Ongoing research will undoubtedly improve our understanding of the
complex pathophysiology and hemodynamics of mitral stenosis and
will likely lead to improved patient outcomes.
Journal of the American Society of Echocardiography
Volume - Number -
ACKNOWLEDGMENT
Special thanks to David Minsky, RDCS, for his technical expertise in
obtaining a number of the echocardiographic images used in this
article.
SUPPLEMENTARY DATA
Supplementary data related to this article can be found at https://doi.
org/10.1016/j.echo.2021.02.015.
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Journal of the American Society of Echocardiography Silbiger 14.e1
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APPENDIX

On the basis of hydrodynamic principles, the net compliance of the

left atrium and left ventricle (Cn) can be expressed as
Cn (cm3 O dynes/cm2 ) = MVA (cm2)/r (1.05 g/cm3)  dv/dt
(cm/sec2),
where MVA is MV area, r is the density of blood (1.05 g/cm3), and
dv/dt is the deceleration rate of the mitral E wave.
Because 1 mm Hg = 1,333 dynes/cm2, if the right side of the equa-
tion is multiplied by 1,333 and r (which is a constant) is incorporated,
we obtain31
Cn (cm3/mm Hg) = 1,270  MVA (cm2)/mitral E-wave downslope
(cm/sec2).