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Mitral stenosis
Y Chandrashekhar, Stephen Westaby, Jagat Narula
Mitral stenosis is a common disease that causes substantial morbidity worldwide. The disease is most prevalent in
developing countries, but is increasingly being identied in an atypical form in developed countries. All treatments
that increase valve area improve morbidity. Mortality improves with surgery; the benet of percutaneous balloon
valvuloplasty to mortality might be similar to that of surgery but needs further study. Percutaneous balloon valvuloplasty
is the treatment of choice for patients in whom treatment is indicated, except for those with suboptimum valve
morphology, and even these patients are sometimes treated with this procedure if surgery is not feasible or if surgical
risk is prohibitive. We review the pathology, diagnosis, and treatment options for patients with mitral stenosis.
Introduction
Although mitral stenosis is now rare in developed
countries, it has been recognised for more than
300 yearsVieussens described the disease in 1705and
has provided major milestones in cardiology. It was the
rst disease to be diagnosed with echocardiography,1 and
the rst valve lesion to be successfully treated by surgery2
or percutaneous balloon valvuloplasty (PBV).3 Mitral
stenosis remains an important cause of morbidity despite
the ease with which it can be diagnosed and treated.
Mitrial stenosis is highly prevalent in developing
countries4 because of its association with the prevalence of
rheumatic fever, but is also seen in developed countries.5
Patients often have distinct social and demographic
indicators dependent on their country of residence: in
developing countries, patients tend to be young with a
pliable valve,6 whereas in developed countries patients are
of increased age with several comorbidities.7,8
Epidemiology
Two-thirds of the worlds population live in developing
countries with a high prevalence of rheumatic fever or
rheumatic heart disease (eg, 6 per 1000 schoolchildren in
India vs 05 per 1000 in developed countries4), resulting
in a large population with mitral stenosis. In a survey of
rheumatic fever in India,4 the mean age of presentation
was 151 years (SD 44), and two-thirds of the participants
had signs of mitral stenosis, of whom half had limiting
symptoms. Up to 30 million schoolchildren and young
adults have chronic rheumatic heart disease worldwide,
and nearly a third of these also have mitral stenosis.9,10
Progression of mitral stenosis in developing countries
is malignant and intervention is often necessary during
teenage years.11 In developed countries,7 prevalence
detected by echocardiography is about 00202%.12 The
natural history is distorted by a predominance of data
Aetiology
Although mitral stenosis most frequently follows
rheumatic fever, fewer than half of aected patients
remember having rheumatic fever. Persistent inammatory valve damage23 and haemodynamic injury contribute to gradual progression; the rate of progression
and time to clinical detection is strongly associated with
repeated episodes of rheumatic fever.24 This correlation
could partly explain the dierent natural history of mitral
stenosis across the world.10,24,25
Degenerative causes are common in developed
countries (eg, 125% in Euro Heart Survey7). In 68% of
patients with severe mitral annular calcication, who are
often elderly or dialysis-dependent, calcium encroaching
into the valve leaets causes mitral stenosis.26 For these
patients, physical ndings are atypical and surgical
options are often unattractive.
Other rare causes are congenital deformities, which
often present very early in infancy or childhood (eg,
parachute mitral valve, double orice mitral valve, supra
mitral ring27); inltrating diseases (eg, mucopolysaccharidosis); diseases aecting multiple systems (eg,
Fabrys disease, systemic lupus erythematosus, and
rheumatoid arthritis), but this cause is very rare; valve
stenosis after mitral valve repair; and disorders associated
with abnormal serotonin metabolism (eg, carcinoid and
methysergide treatment).
Pathology
The main features are leaet thickening, nodularity, and
commissural fusion, all of which result in narrowing of
the valve to the shape of a sh mouth (gure 1).28 The
leaets might be calcied. Chordal fusion and shortening
adds a further resistance to blood ow. Continued
inammation, injury, and repair aect the eectiveness
of treatment, and treatments are tailored to target these
features of disease.29,30
Whether left-ventricular systolic function is truly
reduced in patients with mitral stenosis and the clinical
signicance of reduction is unknown. A third of patients
1271
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Kothari et al
(1998)14
Gamra et al
(2003)15
Arora et al
(2002)16
John et al
(1983)17*
Chen et al
(1995)18
Iung et al
(2004)8
Palacios et al
(2002)19
Shaw et al
(2003)20
Country
India
Tunisia
India
India
China
France
USA
UK
Women
46%
70%
80%
82%
95%
273 (93)
368 (123)
47 (15)
55 (15)
76 (44)
555%
28%
241%
575%
388%
67%
612%
415%
56%
35%
42%
156%
68%
Age (years)
11 (12)
16 (28)
272 (112)
NYHA stage II
29%
64%
NYHA stage IV
6%
69%
875%
Previous
commissurotomy
0%
136%
Previous embolism
11%
Atrial brillation
0%
6%
31%
50%
85%
153%
31%
27%
10%
21%
063 (01)
07 (02)
05 ()
23 (8)
295 (7)
Grade 2 mitral
regurgitation
09%
189%
127%
128%
155%
95%
18%
272%
066 (004)
144%
24%
125%
Calcied valve
243 (77)
133%
145%
11 (03)
183 (51)
132%
103 (023)
103 (46)
09 (03)
14 (6)
086 (027)
114 (47)
26%
65%
13%
38%
171%
23%||
Left-atrial thrombus
18%
40%
Data are number of patients (%) or mean (SD). =data unavailable. NYHA=New York Heart Association stage of disease. *Surgical series from 1980s for comparison with more recent data. Data for NYHA stages
III and IV. Grades 34. Less than grade 3. Aortic regurgitation. ||Aortic stenosis.
Table: Range of patients with mitral stenosis treated by percutaneous balloon valvuloplasty
Pathophysiology
The normal mitral valve area is 46 cm and a gradient is
rare unless the valve is less than 2 cm. Pathophysiology is
closely related to the amount of diastolic ow across the
valve and the diastolic lling period (gures 2 and 3).
Generally, symptoms of dyspnoea correlate with increasing
www.thelancet.com Vol 374 October 10, 2009
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Clinical presentation
Patients usually present with dyspnoea, often during
exercise or in combination with disorders that increase
heart rate or ow across the mitral valve.57,58 The valve area
narrows gradually by 0103 cm per year,59 which
explains the variable onset of symptoms. The disease
course is accelerated in populations with recurrent
rheumatic fever, in which the natural history is compressed
to 510 years. Clinical presentation is aected by agerelated comorbidities such as systemic hypertension,
coronary artery disease, and diastolic dysfunction.60
Frequency of adverse events increases with the onset of
limiting symptoms or substantial pulmonary arterial
hypertension in the presence of severe mitral stenosis.
Other rare symptoms include haemoptysis, chest pain
(often due to pulmonary hypertension), and pressure
eects on adjacent structures, for example from a dilated
left atrium. Atypical presentations include fatigue
(spontaneous or with diuresis) with a low transmitral
gradient61 and a syndrome of right heart failure with
severe pulmonary arterial hypertension. Patients with
pulmonary oedema rarely have severe pulmonary
arterial hypertension, whereas those with severe hypertension (pulmonary vascular resistance >68 Wood
units) seem to present with right heart failure58 rather
than pulmonary oedema. Occasionally, patients rst
present with embolic episodes related mostly to atrial
brillation, or very rarely while in sinus rhythm. Death
is mainly due to heart failure or systemic embolism.57,58
Left-atrial myxoma, ball-valve thrombus, and cor
triatriatum can be clinically mistaken as mitral stenosis
and should be carefully excluded.
www.thelancet.com Vol 374 October 10, 2009
Diagnosis
Physical signs of mitral stenosis have been well
documented.58 Moderate-to-severe disease is easily
diagnosed by auscultation in the left-lateral position or
after mild exercise, unless the patient has unfavourable
body habitus (severe obesity or chronic obstructive
pulmonary disease), pulmonary oedema, very low cardiac
output, or rapid atrial brillation. Diagnostic sensitivity
and specicity is about 85% and accuracy is similar to
that of echocardiography (92% vs 97%).62
Clinical issues that need to be addressed include
severity of disease, pliability of the valve, extent of mitral
regurgitation and pulmonary arterial hypertension, and
presence of atrial brillation. At present, severity of
disease is assessed from symptoms (eg, shortness of
breath, exercise intolerance), presence of long murmur
(especially with presystolic accentuation in normal sinus
rhythm or during long RR intervals in atrial brillation),
short interval of A2 to opening snap (OS), and signs of
pulmonary arterial hypertension or right ventricle
overload. Pliability of the valve is assessed from loud S1
and prominent OS. Two useful assessment methods are
electrocardiography, which most commonly shows leftatrial enlargement and right-ventricle pressure overload,
often with atrial brillation, and chest radiography, which
shows left-atrial enlargement, pulmonary arterial
hypertension, and pulmonary congestion. However,
imaging is the mainstay of diagnosis and treatment
selection (gure 4).
Echocardiography is used to diagnose and judge stage of
disease, assess mitral regurgitation, exclude conditions
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K
AML
AML
PML
PML
G
E
F
LV
LV
LA
LA
LA
1274
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Severe
RR interval
Tachycardia increases the gradient,
shortens A2OS interval, and reduces
the atrial contribution to left-ventricular
lling (red); consequently severe disease
shows high-pan diastolic gradient of
mitral inow.
A2
OS
Normal
Moderate
Left-atrial pressure
Left-ventricle pressure
800
700
Diastole ow (mL/s)
600
500
400
300
200
100
0
05
10
15
20
25
30
40
Seminar
300
Peak A
LA
LV
15 mm
Peak E
100
LA
100
0
20
40
60
Time (% RR)
80
100
Pulmonary hypertension
Pulmonary arterial hypertension is often found in
symptomatic patients with mitral stenosis; it could have
prognostic implications and trigger need for therapeutic
interventions.29 Mechanical factors, vascular remodelling,
and endothelial changes mediate such hypertension,83 and
neurohormones might aect the course.84,85 Moderate
pulmonary arterial hypertension is often a passive
response to left-sided obstruction, and is readily reversed
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Pregnancy
Mitral stenosis is one of the most common lesions found
during pregnancy93,94 and the diagnosis is usually made
when symptoms are precipitated by blood volume
changes, often in the second trimester.95 Mitral stenosis in
pregnancy is associated with substantial morbidity
(including pulmonary oedema), even in asymptomatic or
minimally symptomatic patients with mild-to-moderate
disease (mitral valve area 115 cm in 36% of patients;
>15 cm in 53%), and despite adequate medical
treatment. Cardiac complication rates in women with
mild, moderate, and severe disease are 26%, 38%, and
67%, respectively.96 Many patients with New York Heart
Association (NYHA) class I or II symptoms also show
worsening during pregnancy,97 which suggests that early
aggressive management could be preferable to continuing
prolonged medical management. In India, researchers
found improved outcomes with complications in less
than a quarter of patients, and only 20% of patients
needed caesarean section.98
Complications strongly correlate with NYHA class and
age.96,98 Maternal death is rare, even in developing
countries. Echocardiographic valve area is a more
constant value than, and should be used in preference to
gradient for quantication of disease. Fetal complications
include premature delivery and intrauterine growth
retardation, and occur in 20% of pregnancies. Although
haemodynamics improve post partum, complications
such as pulmonary oedema are highly likely in the early
period after delivery,99 and are probably related to
increased venous return after relief of inferior vena cava
compression.
PBV and surgical valvotomy (closed mitral valvotomy in
preference to methods needing cardiopulmonary bypass)
seem to improve outcome,100,101 but surgical series have
been associated with greater maternal and fetal morbidity
and mortality.102 The usual indication that intervention is
needed is the occurrence of severe symptoms (NYHA class
III/IV or pulmonary oedema) that are refractory to medical
treatment. Results of PBV are largely similar between
pregnant and non-pregnant patients, although re-stenosis
has been recorded in some subsequent pregnancies.98 The
eect of PBV on the fetus is controversialevidence
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100
80
60
40
20
0
0
5
Follow-up (years)
10
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100
90
80
70
60
50
40
30
20
10
0
0
10
15
Follow-up (years)
Treatment
Treatment by drugs or techniques other than surgery or
PBV for mitral stenosis is not very eective and therefore
interventional treatment is preferred except in cases of a
strong contraindication. Drugs can be used to slow heart
rate, deal with atrial brillation, do gentle diuresis, and
correct secondary conditions such as anaemia, fever,
infection, and volume overload. blockers or calcium
channel blockers (eg, diltiazem) are the mainstay for
control of heart rate; but blockers might worsen leftatrial appendage function (clinical signicance unclear),
and drugs that cross the placental barrier (eg, atenolol)
during pregnancy have been associated with fetal growth
retardation. ACE inhibitors have been tried in patients
with mitral stenosis and heart failure with some,131 but
unproven, benet. In view of the high occurrence of
embolic episodes, suggesting use of prophylactic warfarin
in patients with mitral stenosis and normal sinus rhythm
is tempting but not a proven treatment. Hypercoagulable
patients with mitral stenosis, patients with mitral stenosis
and very large atria containing severe smoke or sludge in
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High-risk indicators
Severe pulmonary arterial
hypertension at rest or
with exercise
Clinically signicant increase
in PAWP with exercise
History of thromboemboli
Very large left atrium or new
onset atrial brillation
Evidence for right-heart dysfunction
NYHA class II
PBV
Surgery
Palliative PBV
Surgery
Surgical options include closed or open valvotomy, and
mitral valve replacement. Closed valvotomy is mostly
done in developing countries when PBV is not an option;
It is eective but less so than other methods. Open
valvotomy allows controlled reconstruction of the valves,
and simultaneous tricuspid valve repair or mitral valve
replacement to be done if necessary. In fact data suggest
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