MITRAL STENOSIS

Brook A. June/2016
Braunwald 10th ed.
Updated
Braunwald 11th ed
 1720-1734
 MITRAL STENOSIS (ETIOLOGY)
 Rheumatic fever is the leading cause of mitral stenosis (MS) although only
50 to 70 percent of patients report a history of rheumatic fever

o In rheumatic MS, the valve leaflets are diffusely thickened by fibrous tissue
and/or calcific deposits. The mitral commissures fuse, the chordae tendineae
fuse and shorten, the valvular cusps become rigid, and these changes, in
turn, lead to narrowing at the apex of the funnel-shaped ("fish-mouth") valve

o Calcification of the stenotic mitral valve immobilizes the leaflets and narrows
the orifice further
 MITRAL STENOSIS (ETIOLOGY)
 Other less common causes
o Congenital mitral valve stenosis
o Cor triatriatum
o Mitral annular calcification with extension onto the leaflets
(degenerative)
o Left atrial myxoma
o Infective endocarditis with large vegetations
o Carcinoid heart disease
o Endomyocardial fibrosis
o Systemic lupus erythematosus
o Rheumatoid arthritis
Rheumatic Fever is the leading cause of mitral stenosis (MS)
Pure or predominant MS occurs in approximately 40% of all patients
with Rheumatic Heart Disease and a history of rheumatic fever

Although the initial insult to the mitral valve is Rheumatic, the

later changes may be a nonspecific process resulting from trauma
to the valve caused by altered flow patterns due to the initial
deformity.
Calcification of the stenotic mitral valve immobilizes the leaflets and
narrows the orifice further.

Thrombus Formation and Arterial Embolization may arise from the

calcific valve itself.

But in patients with Atrial Fibrillation (AF), Thrombi arise more

frequently from the Dilated Left Atrium (LA), particularly from within
the Left Atrial Appendage.
In other patients with rheumatic heart disease, lesser degrees of MS
may accompany mitral regurgitation (MR) and aortic valve disease.

With reductions in the incidence of acute rheumatic fever, particularly

in temperate climates and developed countries, the incidence of MS
has declined considerably over the past few decades.

However, it remains a major problem in developing nations, especially

in tropical and semitropical climates.
ETIOLOGY

Causes of Mitral Stenosis

Rheumatic fever (leading cause)
Congenital mitral valve stenosis,
Cor triatriatum,
Mitral annular calcification with extension onto the leaflets,
Systemic lupus erythematosus, rheumatoid arthritis,
Left atrial myxoma, and
Infective endocarditis with large vegetation
ETIOLOGY
 Pure or predominant MS occurs in
approximately 40% of all patients with
rheumatic heart disease and a history of
rheumatic fever.

 In other patients with rheumatic heart disease,

lesser degrees of MS may accompany mitral
regurgitation (MR) and aortic valve disease.
ETIOLOGY
 In rheumatic MS,
 The valve leaflets are diffusely thickened by fibrous
tissue and/or calcific deposits.
 The mitral commissures fuse,
 The chordae tendineae fuse and shorten,
 The valvular cusps (leaflets) become rigid

 These changes, in turn, lead to narrowing at

the apex of the funnel-shaped ("fish-mouth")
valve
STAGES
 Normal MV area= 4-6cm2

 LA pressure of ∼25 mmHg is required to

maintain a normal cardiac output (CO).

 The elevated pulmonary venous and pulmonary

arterial (PA) wedge pressures reduce pulmonary
compliance, contributing to exertional dyspnea.
STAGES
 ACC guideline 2006
 Mild=MVA>1.5 cm2, mean gradient< 5 mm Hg, or
pulmonary artery systolic pressure<30 mm Hg
 Moderate= MVA=1.0 to 1.5 cm2, mean gradient 5-10
mm Hg, or pulmonary artery systolic pressure 30-50
mm Hg, and
 Severe= MVA<1.0 cm2, mean gradient>10 mm Hg, or
pulmonary artery systolic pressure>50 mm Hg
ECHOCARDIOGRAPHIC ASSESSEMENT OF
SEVERITY OF MS IN ADULTS
PATHOPHYSIOLOGY
 The LV diastolic pressure and ejection fraction
(EF) are normal in isolated MS

 In severe MS and whenever pulmonary vascular

resistance is significantly increased, the
pulmonary arterial pressure (PAP) is elevated at
rest and rises further during exercise, often
causing secondary elevations of right ventricular
(RV) end-diastolic pressure and volume.
PATHOPHYSIOLOGY
 In patients with moderate MS (area= 1–1.5cm2),
the CO is normal or almost so at rest, but rises
subnormally during exertion.

 In patients with severe MS (valve area <1 cm2),

particularly those in whom pulmonary vascular
resistance is markedly elevated, the CO is
subnormal at rest and may fail to rise or may
even decline during activity.
PATHOPHYSIOLOGY
 Pulmonary Hypertension
 The clinical and hemodynamic features of MS are
influenced importantly by the level of the PAP.

 Severe pulmonary hypertension results in RV

enlargement, secondary tricuspid regurgitation (TR)
and pulmonic regurgitation (PR), as well as right-
sided heart failure.
PATHOPHYSIOLOGY
 Mechanisms of pulmonary hypertension with MS
 Passivebackward transmission of the elevated LA
pressure;
 Pulmonary arteriolar constriction (the so-called
"second stenosis"), which presumably is triggered by
LA and pulmonary venous hypertension (reactive
pulmonary hypertension);
 Interstitial edema in the walls of the small
pulmonary vessels; and
 At end stage, organic obliterative changes in the
pulmonary vascular bed
NEW STAGING
ACC 2014
 ACC guideline 2014 stages MS ranging from
patients at risk of MS (stage A) or with
progressive hemodynamic obstruction (stage B)
to severe asymptomatic (stage C) and
symptomatic MS (stage D).

 Each of these stages is defined by valve

anatomy, valve hemodynamics, the consequences
of valve obstruction on the left atrium (LA) and
pulmonary circulation, and patient symptoms
NEW STAGING
ACC 2014
 The definition of “severe” MS is based on the
severity at which symptoms occur as well as the
severity at which intervention will improve
symptoms.

 Thus, a mitral valve area ≤1.5 cm2 is considered

severe.
 This usually corresponds to a transmitral mean
gradient of >5 mm Hg to 10 mm Hg at a normal heart
rate
 MVA<1cm2- Very Severe MS
PHYSIOLOGY AND NATURAL HISTORY
 LA pressure  PV pressure  interstitial
edema  ± alveolar flooding

 Adaptations:
1. Pulmonary Vascular Constriction, Intimal
Hyperplasia, Medial Hypertrophy  Reversible
Pulmonary Hypertension  ± Fixed Pulm HTN
2. Downregulation of Neuroreceptors, lymphatic
drainage
 Latent (subclinical) phase in RHD 20-40 yrs
 Continually progressive lifelong disease of plateaus. With RHD,
about 10 yrs after the Rheumatic fever, initial signs, then class
II symptoms after 10 yrs, AF in 10 more, and severe CHF in
another 10.
 10yrs of symptoms before disabling

 With physically limiting symptoms

 10 yr survival 0-15%
 10-20% Systemic Embolism
 30-40% develop AF

 With onset of Severe Pulm Hypertension

 Mean survival < 3 yrs
In normal adults, the area of the mitral valve orifice is 4–6 cm2.

In the presence of Significant obstruction, i.e., when the orifice area is

reduced to < ∼2 cm2, blood can flow from the LA to the left ventricle
(LV) only if propelled by an abnormally elevated left atrioventricular
pressure gradient, the hemodynamic hallmark of MS.

When the mitral valve opening is reduced to <1 cm2, often referred to
as "Severe" MS, a LA pressure of ∼25 mmHg is required to maintain
a normal cardiac output (CO).
 The elevated pulmonary venous and pulmonary arterial (PA) wedge
pressures reduce pulmonary compliance, contributing to
Exertional Dyspnea.

The first bouts of dyspnea are usually precipitated by clinical events

that increase the rate of blood flow across the mitral orifice, resulting
in further elevation of the LA pressure (see below).

To assess the severity of obstruction hemodynamically,

 Both the transvalvular pressure gradient and the flow rate must be
measured (Chap. 230).
The latter depends not only on the CO but on the heart rate, as well.

An increase in Heart Rate shortens diastole proportionately more than

systole and diminishes the time available for flow across the mitral
valve.

Therefore, at any given level of CO, tachycardia, including that

associated with rapid AF, augments the transvalvular pressure
gradient and elevates further the LA pressure.

Similar considerations apply to the pathophysiology of tricuspid

stenosis.
 The LV Diastolic Pressure and Ejection Fraction (EF) are Normal
in Isolated MS.

In MS and Sinus Rhythm, the elevated LA and PA wedge pressures

exhibit

 A Prominent Atrial Contraction Pattern (a wave) and

 A gradual pressure decline after the v wave and mitral valve opening
(y descent).
 In severe MS and whenever pulmonary vascular resistance is
significantly increased :

 The pulmonary arterial pressure (PAP) is elevated at rest and rises

further during exercise
 Often causing secondary elevations of right ventricular (RV) end-
diastolic pressure and volume.
 SYMPTOMS OF MS
 The interval between the episode of rheumatic fever and the clinical presentation of MS varies
geographically, ranging from as little as a few years in countries with a high prevalence of
rheumatic fever to 20 years in countries where rheumatic fever is rare
 Dyspnea, cough,orthopenia and PND

 Palpitation (the development of permanent AF often marks a turning point in the patient's
course and is generally associated with acceleration of the rate at which symptoms progress)
 Hemoptysis

 Hoarsness

 Thromboembolism: Systemic embolization, the incidence of which is 10–20%, occurs more

frequently in patients with AF(over 80 percent of patients with MS who have an embolism are
in AF), in older patients, and in those with a reduced CO. However, systemic embolization may
be the presenting feature in otherwise asymptomatic patients with only mild MS
 Chest pain: infrequent

 Infective endocarditis: this complication is primarily associated with mild mitral stenosis when
the valve is stiff and fibrotic. Endocarditis is uncommon once the valve becomes calcified and
very rigid
 Right sided HF
CLINICAL FEATURES
 Hemoptysis results from rupture of pulmonary-
bronchial venous connections secondary to
pulmonary venous hypertension.

 It occurs most frequently in patients who have

elevated LA pressures without markedly
elevated pulmonary vascular resistances and is
rarely fatal.
CLINICAL FEATURES
 Pulmonary Changes
 In addition to the aforementioned changes in the
pulmonary vascular bed, fibrous thickening of the
walls of the alveoli and pulmonary capillaries occurs
commonly in MS.
 The vital capacity, total lung capacity, maximal
breathing capacity, and oxygen uptake per unit of
ventilation are reduced.
 Pulmonary compliance falls further as pulmonary
capillary pressure rises during exercise
CLINICAL FEATURES
 Thrombi may form in the left atria, particularly
within the enlarged atrial appendages of patients
with MS.

 Systemic embolization, the incidence of which is

10–20%, occurs more frequently in patients with
AF, in patients >65 years of age, and in those
with a reduced CO.

 However, systemic embolization may be the

presenting feature in otherwise asymptomatic
patients with only mild MS.
CLINICAL FEATURES
 Auscultation
 S1 accentuated and slightly delayed
 P2 accentuated
 S2 splitting
 The opening snap (OS) audible in expiration at, or just
medial to, the cardiac apex.
 generally follows the sound of aortic valve closure (A2) by 0.05–
0.12 s.
 Murmur following OS: low-pitched, rumbling, diastolic
murmur, heard best at the apex with the patient in the
left lateral recumbent position
 Soft, grade I or II/VI systolic murmurs are commonly
heard at the apex or along the left sternal border in
patients with pure MS and do not necessarily signify the
presence of MR.
PHYSICAL FINDINGS (INSPECTION AND PALPATION)
 The arterial pulses are reduced in volume due to the decreased stroke volume
 When MS is severe and the cardiac output is diminished, there is
vasoconstriction, resulting in pinkish-purple patches on the cheeks (mitral facies)
 Pulmonary hypertension and right ventricular hypertrophy can lead to a
prominent "a" wave (atrial contraction or systole) in jugular venous pulsations,
reflecting elevated right atrial pressure. The "a" wave is absent in patients with
AF and only a prominent "v" wave (atrial filling during ventricular systole when
the tricuspid valve is closed) is seen. If present, tricuspid regurgitation can lead
to a prominent "c-v" wave (reflecting regurgitation of blood into the right
atrium) and the neck veins are very pulsatile
 Precordial examination reveals an apical impulse that is generally normal,
although it may be reduced in intensity, reflecting the decreased left ventricular
filling. However, if pulmonary hypertension is present, there may be a right
ventricular heave (substernal lift) and a palpable S2
 An apical diastolic thrill can be appreciated as well
 PHYSICAL FINDINGS (AUSCULTATION)
  S1 (the first heart sound (S1) is loud, reflecting the increased excursion of the
leaflets . As the leaflets become more rigid and calcified, their motion is limited and S1
becomes soft)
  P2

 Opening snap (OS): it is most prominent at the apex and is due to the abrupt halt in
leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the
leaflet tips.The time interval between A2 and OS varies inversely with the severity of
the MS
 Diastolic murmur: is a low-pitched diastolic rumble that is most prominent at the
apex. It is heard best in a quiet room with the patient lying on the left side in held
expiration and by using the bell of the stethoscope. Although the intensity of the
diastolic murmur does not correlate with the severity of the stenosis, the duration of
the murmur is helpful since it reflects the transvalvular gradient and the duration of
blood flow across the valve.When the CO is markedly reduced in MS, the typical
auscultatory findings, including the diastolic rumbling murmur, may not be detectable
(silent MS), but they may reappear as compensation is restor
CLINICAL FEATURES
 Hepatomegaly, ankle edema, ascites, and pleural
effusion, particularly in the right pleural cavity,
may occur in patients with MS and RV failure.
CLINICAL FEATURES
 Associated Lesions
 Functional Tricuspid Regurgitation
 A pansystolic murmur produced by functional TR may be
audible along the left sternal border
 This murmur is usually louder during inspiration and

diminishes during forced expiration (Carvallo's sign).

 When the COP is markedly reduced in MS, the

typical auscultatory findings, including the diastolic
rumbling murmur, may not be detectable (silent MS),
but they may reappear as compensation is restored.
CLINICAL FEATURES
 Associated Lesions
 The Graham Steell murmur of PR, a high-pitched,
diastolic, decrescendo blowing murmur along the left
sternal border, results from dilation of the
pulmonary valve ring and occurs in patients with
mitral valve disease and severe pulmonary
hypertension.

 This murmur may be indistinguishable from the more

common murmur produced by aortic regurgitation
(AR), although it may increase in intensity with
inspiration and is accompanied by a loud and often
palpable P2.
EKG
 P wave usually suggests LA enlargement

 It may become tall and peaked in lead II and

upright in lead V1 when severe pulmonary
hypertension or TS complicates MS and right
atrial (RA) enlargement occurs

 The QRS complex is usually normal. However,

with severe pulmonary hypertension, right-axis
deviation and RV hypertrophy are often present.
CXR
 The earliest changes are
 Straightening of the upper left border of the cardiac
silhouette,
 Prominence of the main pulmonary arteries,
 Dilation of the upper lobe pulmonary veins, and
 The left bronchus is elevated
 On the lateral projection, the left atrium is displaced posteriorly, impinging
on the esophagus .Posterior displacement of the esophagus by
an enlarged LA.
 Kerley B lines- fine, dense, opaque, horizontal lines that are
most prominent in the lower and mid-lung fields and that
result from distention of interlobular septae and lymphatics
with edema when the resting mean LA pressure exceeds
approximately 20 mmHg. interlobar effusions (Kerley C lines) .In more
severe cases, Kerley A lines (straight dense lines running toward the hilum)
BARIUM SWALLOW IN MS
ECHOCARDIOGRAPHY
 TTE- with color flow and spectral Doppler imaging
provides critical information, including
 Measurements of mitral inflow velocity during early (E
wave) and late (A wave in patients in sinus rhythm)
diastolic filling, estimates of the transvalvular peak
and mean gradients
 Mitral orifice area,
 The presence and severity of any associated MR,
 The extent of leaflet calcification and restriction,
 The degree of distortion of the subvalvular apparatus,
and
 The anatomic suitability for percutaneous mitral
balloon valvotomy [percutaneous mitral balloon
valvuloplasty (PMBV)
ECHOCARDIOGRAPHY
 TTE additional benefits: LV and RV function,
chamber sizes, Pulmonary artery pressure (PAP),
and an indication of the presence and severity of
any associated valvular lesions.

 TEE- provides superior images and should be

employed when TTE is inadequate for guiding
management decisions.
 TEE is especially indicated to exclude the presence
of left atrial thrombus prior to PMBV.
CARDIAC CATHETERIZATION
 Left and right heart catheterization is useful
when there is a discrepancy between the clinical
and TTE findings that cannot be resolved with
either TEE or cardiac magnetic resonance (CMR)
imaging

 The growing experience with CMR for the

assessment of patients with valvular heart
disease may decrease the need for invasive
catheterization.
CARDIAC CATHETERIZATION
 Catheterization is helpful in assessing associated
lesions, such as aortic stenosis (AS) and AR.

 Catheterization and coronary angiography are

not usually necessary to aid in decision-making
about surgery in patients younger than 65 years
of age, with typical findings of severe mitral
obstruction on physical examination and TTE
CARDIAC CATHETERIZATION
 Coronary angiography indicated preop in
 Men older than 40 years of age,
 Women older than 45 years of age, and
 Younger patients with coronary risk factors
 NB. Especially those with positive noninvasive stress
tests for myocardial ischemia,

 This is to identify patients with critical coronary

obstructions that should be bypassed at the
time of operation
CARDIAC CATHETERIZATION
 Computed tomographic coronary angiography
(CTCA) is now often used to screen
preoperatively for the presence of coronary
artery disease (CAD) in patients with valvular
heart disease and low pretest likelihood of CAD.

 Catheterization and left ventriculography are

indicated in most patients who have undergone
PMBV or previous mitral valve surgery, and who
have redeveloped limiting symptoms, especially if
questions regarding the severity of the valve
lesion(s) remain after echocardiography.
DIFFERENTIAL DIAGNOSIS
 Significant MR with anterograde mitral valve
flow
 Austin Flint murmur of AR

 Left atrial myxoma

 ASD
 Significant MR with anterograde mitral valve flow but in patients with
isolated MR, this diastolic murmur commences slightly later than in
patients with MS, and there is often clear-cut evidence of LV
enlargement. An OS and increased P2 are absent, and S1 is soft or
absent. An apical pansystolic murmur of at least grade III/VI intensity
as well as an S3 suggest significant MR
 severe AR (Austin Flint murmur) may be mistaken for MS but can be
differentiated from it because it is not intensified in presystole and
becomes softer with administration of amyl nitrite or other arterial
vasodilators.
 TS, which occurs rarely in the absence of MS, may mask many of the
clinical features of MS or be clinically silent; when present, the diastolic
murmur of TS increases with inspiration and the y descent in the jugular
venous pulse is delayed.
 Atrial septal defect may be mistaken for MS; in both
conditions, there is often clinical, ECG, and chest x-ray evidence of RV
enlargement and accentuation of pulmonary vascularity. However, the
absence of LA enlargement and of Kerley B lines and the
demonstration of fixed splitting of S2 with a grade II or III mid-
systolic murmur at the mid to upper left sternal border all favor atrial
septal defect over MS. Atrial septal defects with large left-to-right
shunts may result in functional TS because of the enhanced diastolic
flow.
 LA myxoma often have features suggestive of a systemic disease, such
as weight loss, fever, anemia,systemic emboli, and elevated serum IgG
and interleukin 6 (IL-6) concentrations. The auscultatory findings may
change markedly with body position. The diagnosis can be established
by the demonstration of a characteristic echo-producing mass in the
LA with TTE
TREATMENT
 Penicillin prophylaxis of group A β-hemolytic
streptococcal infections for secondary
prevention of rheumatic fever
 Prophylaxis for infective endocarditis when
indicated
 Restriction of sodium intake and small doses of
oral diuretics.
 Beta blockers, nondihydropyridine calcium
channel blockers (e.g., verapamil or diltiazem),
and digitalis glycosides are useful in slowing the
ventricular rate of patients with AF.
TREATMENT
 ACC 2014 Class I
 Anticoagulation (vitamin K antagonist [VKA] or
heparin) is indicated in patients with
 MS and AF (paroxysmal, persistent, or permanent),
or
 MS and a prior embolic event, or
 MS and a left atrial thrombus

 Warfarin to an INR of 2–3 should be

administered indefinitely
TREATMENT
 The routine use of warfarin in patients in sinus
rhythm with LA enlargement (maximal dimension
>5.5 cm) with or without spontaneous echo
contrast is more controversial (ACC 2006*)

 If AF is of relatively recent onset in a patient

whose MS is not severe enough to warrant PMBV
or surgical commissurotomy, reversion to sinus
rhythm pharmacologically or by means of
electrical countershock is indicated.
TREATMENT
 Conversion to sinus rhythm is rarely successful
or sustained in patients with severe MS,
particularly those in whom the LA is especially
enlarged or in whom AF has been present for
more than 1 year.

 This difficulty is also because the rheumatic

process itself may lead to
 Fibrosis
of the internodal and interatrial tracts and
 Damage to the sinoatrial node.
TREATMENT
Heart rate control may be considered for
patients with MS in normal sinus rhythm and
symptoms associated with exercise
 (ACC 2014- Class IIb)
TREATMENT
INTERVENTIONS
Recommendations COR/LOE
PMBC is recommended for symptomatic patients with severe MS IA
(MVA <1.5 cm2, stage D) and favorable valve morphology in the
absence of contraindications
Mitral valve surgery is indicated in severely symptomatic patients IB
(NYHA class III/IV) with severe MS (MVA <1.5 cm2, stage D)
who are not high risk for surgery and who are not candidates for or
failed previous PMBC
Concomitant mitral valve surgery is indicated for patients with IC
severe MS (MVA ≤1.5 cm2, stage C or D) undergoing other
cardiac surgery
TREATMENT- MITRAL VALVULOTOMY
 Unless there is a contraindication, mitral
valvotomy is indicated in symptomatic NYHA
Class II–IV patients with isolated MS, whose
effective orifice (valve area) is < ∼1 cm2/m2
body surface area, or <1.5 cm2 in normal-sized
adults

 Mitral valvotomy can be carried out by two

techniques: PMBV and Surgical Valvotomy.
TREATMENT- MITRAL VALVULOTOMY
 When intervention is warranted in patients with
rheumatic MS, the 2006 ACC/AHA guidelines
recommend that PMBV is preferred to surgery if
the valve morphology is favorable and the
patient does not have left atrial thrombus or
moderate to severe (3+ to 4+) mitral
regurgitation
 Unfavourable clinical characteristics: old
age,history of commissurotomy,NYHA
class IV,atrial fibirilation,severe
pulmonary hypertension
 High risk of embolism or hemodynamic
decompensation: previous history of
embolism,dense spontaneous contrast in
the LA,recent or paroxysmal AF,PAP>50
at rest,need for non-major cardiac
surgery and desire of pregnancy
CONTRAINDICATIONS TO PERCUTANEOUS
MITRAL COMMISSUROTOMY (PMC)
TREATMENT- MITRAL VALVULOTOMY
 The ACC/AHA guidelines recommended surgery
only when one or more of the following is
present:
 PMBV is not available
 There is left atrial thrombus that persists despite
anticoagulation
 The mitral valve is nonpliable or severely calcified
 Moderate to severe coexisting mitral regurgitation is
present
TREATMENT- MITRAL VALVULOTOMY
 In PMBV, a catheter is directed into the LA
after transseptal puncture, and a single balloon
is directed across the valve and inflated in the
valvular orifice.

 Ideal patients have relatively pliable leaflets

with little or no commissural calcium.

 In addition, the subvalvular structures should

not be significantly scarred or thickened, and
there should be no left atrial thrombus.
TREATMENT- MITRAL VALVULOTOMY
 The short- and long-term results of this
procedure in appropriate patients are similar to
those of surgical valvotomy, but with less
morbidity and a lower periprocedural mortality
rate.

 Event-free survival in younger (<45 years)

patients with pliable valves is excellent, with
rates as high as 80–90% over 3–7 years.
 Therefore, PMBV has become the procedure of
choice for such patients when it can be performed
by a skilled operator in a high-volume center.
TREATMENT- MITRAL VALVULOTOMY
 TTE is helpful in identifying patients for the
percutaneous procedure,
 TEE is performed routinely to exclude left atrial
thrombus at the time of the scheduled
procedure.
 An "echo score" has been developed to help
guide decision-making.
 The score accounts for the degree of leaflet
thickening, calcification, and mobility, and for the
extent of subvalvular thickening.
 A lower score predicts a higher likelihood of
successful PMBV. (see above)
TREATMENT- MITRAL VALVULOTOMY
 In patients in whom PMBV is not possible or
unsuccessful, or in many patients with
restenosis, an "open" valvotomy using
cardiopulmonary bypass is necessary.
 In addition, it is important to
 loosen any subvalvular fusion of papillary muscles and
chordae tendineae and
 Remove large deposits of calcium, thereby improving
valvular function, as well as
 Remove atrial thrombi.

 The perioperative mortality rate is ∼2%

TREATMENT- MITRAL VALVULOTOMY
 Successful valvotomy is defined by a 50%
reduction in the mean mitral valve gradient and a
doubling of the mitral valve area.

 Successful valvotomy, whether balloon or

surgical, usually results in striking symptomatic
and hemodynamic improvement and prolongs
survival
TREATMENT- MITRAL VALVULOTOMY
 However, there is no evidence that the
procedure improves the prognosis of patients
with slight or no functional impairment

 Therefore, valvotomy is not recommended for

patients who are entirely asymptomatic and/or
who have mild stenosis (mitral valve area >1.5
cm2) unless the following are present:-
 Recurrent systemic embolization or
 Severe pulmonary hypertension has occurred (PA
systolic pressures >50 mmHg at rest or >60 mmHg
with exercise),
TREATMENT- MITRAL VALVULOTOMY
 When there is little symptomatic improvement
after valvotomy, it is likely that
 The procedure was ineffective,
 It induced MR, or
 Associated valvular or myocardial disease was
present.

 About half of all patients undergoing surgical

mitral valvotomy require reoperation by 10 years.
TREATMENT- MITRAL VALVULOTOMY
 In the pregnant patient with MS, valvotomy
should be carried out if pulmonary congestion
occurs despite intensive medical treatment.

 PMBV is the preferred strategy in this setting

and is performed with TEE and no or minimal x-
ray exposure.
TREATMENT- MITRAL VALVE
REPLACEMENT
 Mitral valve replacement (MVR) is necessary in
patients with MS
 With significant associated MR,
 In whom the valve has been severely distorted by
previous transcatheter or operative manipulation, or
 In whom the surgeon does not find it possible to
improve valve function significantly with valvotomy.

 MVR is now routinely performed with

preservation of the chordal attachments to
optimize LV functional recovery.
TREATMENT- MITRAL VALVE
REPLACEMENT
 Perioperative mortality rates with MVR vary with
age, LV function, the presence of CAD, and
associated comorbidities.

 They average 5% overall but are lower in young

patients and may be twice as high in patients >65
years of age with comorbidity rates.
TREATMENT- MITRAL VALVE
REPLACEMENT
 There are also long-term complications of valve
replacement

 Thus, patients in whom preoperative evaluation

suggests the possibility that MVR may be
required should be operated on only if
 They have severe MS—i.e., an orifice area ≤1 cm2—
AND
 They are in NYHA Class III, i.e., symptomatic with
ordinary activity despite optimal medical therapy
TREATMENT- MITRAL VALVE
REPLACEMENT
 The overall 10-year survival of surgical survivors
is ∼70%.

 Long-term prognosis is worse in patients >65

years of age and those with marked disability
and marked depression of the CO preoperatively.

 Pulmonary hypertension and RV dysfunction are

additional risk factors for poor outcome.
 ACC/AHA 2014
RECOMMENDATIONS
MONITORING
PREGNANCY IN WOMEN WITH
MITRAL STENOSIS
 INTRODUCTION — Mitral stenosis (MS)
encountered in women of childbearing age is
nearly always rheumatic in origin.
 Maternal and perinatal complications during
pregnancy in women with MS reflect the
unfavorable interaction between the normal
cardiovascular changes of pregnancy and the
stenotic mitral valve.
 Prevalence — Women with heart disease
comprise approximately 1 percent of the
obstetric population seen in large volume centers
in developed countries.
IMPACT OF CARDIOVASCULAR CHANGES IN
PREGNANCY IN WOMEN WITH MITRAL STENOSIS

 In mitral stenosis (MS), the stenotic mitral valve

restricts diastolic left ventricular filling,
resulting in an elevated transmitral gradient and
left atrial pressure that are further increased
by the physiologic hypervolemia and increased
heart rate during pregnancy, thereby increasing
the risk of pulmonary congestion or pulmonary
edema
 Pregnant women with MS are at risk for
pulmonary edema and atrial arrhythmias
RISK STRATIFICATION
 Women at highest risk of maternal cardiac
complications are those with moderate or severe
mitral stenosis (MS) (mitral valve area <1.5 cm2),
baseline maternal New York Heart Association
functional class III or IV, a history of cardiac
complications (pulmonary edema, arrhythmias
requiring treatment, transient ischemic attack,
or stroke) prior to pregnancy, central cyanosis,
and left ventricular systolic dysfunction
 Preconception counseling and management — Evaluation prior to
preconception counseling includes identification of any markers of increased
maternal cardiac risk as determined by history, examination, ECG, and
transthoracic echocardiogram as described above (see 'Risk stratification'
above):

 ●History of pulmonary edema, arrhythmias requiring treatment, transient

ischemic attack, or stroke prior to pregnancy.

 ●Functional status by subjective (ie, New York Heart Association functional

class) or objective measures (exercise testing).

 ●Central cyanosis (oxygen saturation <90 percent by oximetry).

 ●Mitral valve area, extent of mitral regurgitation, left ventricular systolic

function.

 ●Systolic pulmonary artery pressure.

THANK YOU!