MITRAL STENOSIS
&
MITRAL VALVE
APPARATUS

MITRAL VALVE
• Mitral valve connects the left atrium and left ventricle.
• The normal function of the mitral valve depends on its 6
components, MITRAL VALVE APPARATUS which are
(1) the left atrial wall,
(2) the annulus,
(3) the leaflets,
(4) the chordae tendineae,
(5) the papillary muscles, and
(6) the left ventricular wall.

Mitral Valve
apparatus :
Left Atrial wall
Annulus
Leaflets
Chordae
Tendineae
Papillary Muscles
Left ventricular
wall

Mitral Annulus: Anatomical structure that separates the LV & LA
Caption

2. MITRAL LEAFLETS
• Mitral Leaflets : Thin and pliable
leaflets that contain scallops which
represent segmental markers.
• 2 Leaflets with 3 Scallops
◦ Anterior Leaflet (AML):
larger & thicker
Dome-shaped
Scallops: A1 (lateral),
A2 (central), A3 (medial)
◦ Posterior Leaflet (PML):
thinner & more flexible
Crescent shaped
Scallops: P1 (lateral),
P2 (central), P3 (medial)
• Leaflets thin & pliable
• Scallops serve as segmental
markers of Leaflets

3. COMMISSURES
Commissures: 2 specific
sites where the leaflets
insert and join into mitral
annulus
• Anterolateral
Commissure
• Posteromedial
Commissure

4. CHORDAE TENDINAE
Chordae Tendinae: Fibrous strings
that attach specific portions of mitral
leaflets to papillary muscle tips
• Normal average length is around
20mm
• Normal average thickness is 1-
2mm
• Key items to look for: thickening,
fusion, calcification, elongation,
rupture

5. PAPILLARY MUSCLES
Papillary Muscles: Large trabeculae
muscles that branch from 1/3rd of LV,
connecting chordae to mitral leaflets
2 papillary muscles:
• Anterolateral (APM):
◦ Dual blood supply (LAD & Cx)
• Posteromedial (PPM):
◦ Single blood supply (Either
RCA or LCX)
◦ Prone to injury from MI due to
single blood supply

MITRAL STENOSIS

• In normal adults, the area of the mitral valve orifice is
4-6 cm2.
• In mitral stenosis, the area of valve orifice
decreases.
• Minimal MS - >2.5 cm2
• Mild MS - 1.6- 2.5 cm2
• Moderate MS – 1- 1.5 cm2
• Severe MS(tight/critical) - <1 cm2

• 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 <1.5 cm2,
referred to as “severe” MS, an LA pressure of ~25 mmHg
is required to maintain a normal cardiac output (CO).

Major Causes of Mitral Stenosis
•Rheumatic fever
•Congenital (parachute valve, cor triatriatum)
•Severe mitral annular calcification with leaflet involvement
•SLE, RA
•Myxoma
• IE with large vegetations

PATHOPHYSIOLOGY
• Rheumatic fever is the most common
cause of MS.
• In rheumatic MS, chronic inflammation
leads to diffuse thickening of the valve
leaflets with formation of fibrous tissue
and/or calcific deposits.
• The mitral commissures fuse, the
chordae tendineae fuse and shorten,
the valvular cusps become rigid.
• These changes, in turn, lead to
narrowing at the apex of the valve.
• Calcification of the stenotic mitral valve
immobilizes the leaflets and narrows
the orifice further.

Mitral Stenosis: Natural History
• Progressive, lifelong disease,
• Usually slow & stable in the early years.
• Progressive acceleration in the later
years
• 20-40 year latency from rheumatic fever
to symptom onset.
• Additional 10 years before disabling
symptoms

CLINICAL PRESENTATION
• Symptoms d/t pulmonary hypertension-
1. Dyspnoea, orthopnea, PND
2. Recurrent pulmonary infections, i.e., bronchitis,
bronchopneumonia and lobar pneumonia especially during the
winter months.
3. Hemoptysis results from rupture of pulmonary-
bronchial venous connections.
4. Cough
5. Fatigue
6. Lower limb swelling, pain rt hypochondrium.

• Palpitations can develop in case if A.fib develops
•Recurrent pulmonary emboli sometimes with infarction, are an
important cause of morbidity and mortality late in the course of
MS.
•Systemic embolization may be the presenting feature in
otherwise asymptomatic patients with only mild MS.

PHYSICAL EXAMINATION
MITRAL FACIES
Plethoric cheeks with bluish
patches due to
Cutaneous vasodilatation in
severe MS causing
Low CO

• Pulse - irregularly irregular if AF is present.
• JVP
• -If RV failure develops, jugular veins will be distended
• - If pulmonary hypertension develops, “a” wave will be
prominent.
• Parasternal heave can be there d/t RVH.
• Tapping type of apex beat (palpable 1st heart sound) is
there, normal in position, can go outwards if RVH present.
• A diastolic thrill may rarely be present at the cardiac
apex, with the patient in the left lateral recumbent
position.

• On auscultation
-S1 will be loud if mitral valve is pliable.
It will be muffled in calcified MS.
Due to wider excursion of the leaflets while closure,
since elevated LAP has kept the leaflets relatively wide
apart
In addition, stiff noncompliant leaflets and chordae
tendineae appear to resonate with increased amplitude

• LOUD P2 AND S2 CLOSELY SPILT
• OPENING SNAP followed by A2
• The pulmonic component of the second heart sound (P2) is often
accentuated with elevated PA pressure.(PHTN)
• -Opening snap i.e. mitral valve opens suddenly with the force of
increased left atrial pressure.
• -Low pitched rough rumbling mid diastolic murmur with pre systolic
accentuation and opening snap with bell of stethoscope at the end of
expiration best heard at the apex in left recumbent position which
increases on isometric exercises

• If the patient is in sinus rhythm, murmur becomes louder at
the end of diastole d/t atrial contraction i.e. PRESYSTOLIC
ACCENTUATION.
• Presystolic accentuation will be absent in case of AF, Left atrial
failure and big left atrial thrombus.

SEVERITY OF MS?
• The time interval between A2 and OS varies
inversely with the severity of the MS. Normally, it is 0.05-
0.12 s. The smaller the gap, the more severe is the MS.
• Longer the duration of mid diastolic murmur, the more
severe is the MS.
• As the valve cusps become immobile,
-Loud S1 softens
-opening snap disappears
• When pulmonary hypertension appears,
-P2 gets loud

• With severe pulmonary hypertension, 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).
• 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

INVESTIGATIONS
• Chest X-ray
• Electrocardiogram
• Echocardiogram
• Cardiac MRI
• Cardiac cathetrisation

• MITRALISATION of heart straightening of the left
border of heart & is due to(from above
downwards)
1. Small aortic knuckle due to low CO
2. Convexity due to dilated pulmonary artery due
to pulmonary hypertension
3. Left atrial appendages prominence
4. Left border of LV
• Double contour of right border of heart
(shadow within shadow)

• Dilated pulmonary aretries at hilum with peripheral
pruning (pulmonary hypertension)
• Bat’s wing appearance from parahilar region to
periphery and Kerly’s B lines indicating pulmonary
edema
• Elevation of left upper lobe bronchus which becomes
horizontal due to LA enlargement
• Calcified mitral valve can be seen on lateral view.
• Chest Xray (RAO view) with barium filled
esophagus shows sickling of esophagus by
enlarged LA

ECG IN MITRAL STENOSIS
• LA enlargement – Wide i.e. >0.12s (3 small sq) and notched
P wave with the interpeak duration of >0.04s (1 small sq)
i.e. P mitrale in lead v1 & II.

• P wave may become tall and peaked (>2.5 small sq) in lead
II & V1 when severe pulmonary hypertension or TS
complicates MS and right atrial (RA) enlargement occurs i.e.
P pulmonale
• Atrial fibrillation may be present.

• RVH- RAD and tall R wave in lead V1(>7mm)

ECHO IN MITRAL STENOSIS
• To see chamber enlargement , left atrial thrombus,
valve pathology, valve movement, mitral orifice,
diameter.
• In MS there are thickened immobile cusps, reduced
valve area, LA enlargement and reduced rate of
diastolic filling of LV.
• TEE provides superior images and should be used when
TTE is inadequate for guiding management decisions.
TEE is especially indicated to exclude the presence of
LA thrombus prior to percutaneous mitral balloon
valvotomy (PMBV).

CARDIAC CATHETRIZATION IN MS
• Left and right heart catheterisation can be useful when
there is a discrepancy between the clinical and
noninvasive findings, including those from TEE and
exercise echocardiographic testing when appropriate
• CT Coronary angiography is advisable preoperatively to
identify patients with critical coronary obstructions that
should be bypassed at the time of operation.
• Catheterisation can also be helpful in assessing a/w
lesions, such as AR and AS and in patients with recurring
or worsening symptoms later after mitral valve intervention

COMPLICATIONS OF MS
• Left atrial enlargement, acute left atrial failure and acute
pulmonary edema
• Pulmonary hypertension
• Right ventricular failure
• A fib, A flutter
• Embolic manifestations
• Infective endocarditis
• Recurrent broncho-pulmonary infections
• Compression of RLN (Ortner’s syndrome)
• Dysphagia

TREATMENT OF MS
• Penicillin prophylaxis of group A β-hemolytic streptococcal
infections for secondary prevention of rheumatic fever is
important for at-risk patients with rheumatic MS.
• Recommendations for infective endocarditis prophylaxis are
similar to those for other valve lesions and are restricted to
patients at high risk for complications from infection,
including patients with a history of endocarditis.
• In symptomatic patients, some improvement usually occurs
with 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.
•

•Warfarin therapy targeted to an INR of 2–3 should
be administered indefinitely to patients with MS
who have AF or a history of thromboembolism.
•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.
• Direct oral anticoagulants (e.g., apixaban,
rivaroxaban) are not approved for use in patients
with rheumatic MS.

Mitral commissurotomy
symptomatic (New York Heart Association [NYHA] Functional Class II–IV)
patients with isolated severe MS, whose effective orifice (valve area) is < ~1 cm2/m2 body surface
area, or <1.5 cm2 in normalsized adults.
Mitral commissurotomy can be carried out either percutaneously or surgically.

After trans septal puncture，the deflated balloon
catheter is advanced across the interatrial septum，
then across the mitral valve and into the left
ventricle.

The balloon is then inflated stepwise within the mitral orifice.

Successful
commissurotomy
• 50% reduction in the mean mitral
gradient
• Doubling of the mitral valve area
• Striking symptomatic and hemodynamic
improvement

INDICATIONS OF MITRAL VALVE
REPLACEMENT
• Presence of MR
• Badly diseased or badly calcified stenotic
valve
• Severly distorted valve by previous trans catheter or
operative manipulation
• Moderate or severe MS with thrombus in LA
despite anticoagulation

Recommendations for Mitral Valve Repair for Mitral
Stenosis
– Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm 2 ),*and
valve morphology favorable for repair if percutaneous mitral
balloon valvotomy is not available
– Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm 2 ),*and
valve morphology favorable for repair if a left atrial thrombus is
present despite anticoagulation
– Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm 2 ),* and a
non-pliable or calcified valve with the decision to proceed with
either repair or replacement made at the time of the operation.