Mitral stenosis is a narrowing of the mitral valve that occurs most commonly as a result of rheumatic fever. It is characterized by thickening and scarring of the mitral valve leaflets that causes the opening to narrow over time. The narrowing obstructs blood flow from the left atrium to the left ventricle, causing elevated pressures in the left atrium and lungs. Common symptoms include shortness of breath, cough, hemoptysis, and right-sided heart failure. Diagnosis is made through echocardiogram and treatment involves medications, balloon valvuloplasty, or valve replacement surgery depending on severity.

1. MITRAL STENOSIS
Dr.Manoj Aryal
MBBS,MD(KU)
Consultant Physician/Internist
Department of Internal medicine
LMCTH Palpa

2. CONTENT
• ANATOMY
• INTRODUCTION
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOLOGY
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• MANAGEMENT

3. ANATOMY
• Mitral valve apparatus consist of:
a. Valve :
- Leaflet
- Commissure
- Body of valve
b. Mitral Annulus
c. Chordae Tendineae
d. Papillary Muscle

4. • Normal valve has an orifice of 4 to 6 square cms.
• Valve functions as a door allowing entry of blood into the left ventricle during diastole and closing
appropriately during systole to prevent the back flow of blood.

5. INTRODUCTION
• Mitral stenosis is a valvular heart disease which is characterized by narrowing of the mitral valve.
• The most common cause of mitral stenosis is rheumatic fever, but the stenosis usually appears
clinically relevant only after several decades.
• With each episode of rheumatic fever, residual damage of the endocardium( as endocardium is the
one which has rheumatic sequel) increases.
• Mitral stenosis occurs approx. 20 to 30 years after the first episode of rheumatic fever.

6. EPIDIOMOLOGY
• The prevalence of rheumatic disease in developed countries is declining with an estimated
incidence of 1 in 100,000.
• The prevalence is higher in developing nations than in the United States.
• Rheumatic mitral stenosis is more common in females.
• The onset is usually between the third and fourth decade of life

7. ETIOLOGY
• Major causes of mitral stenosis are :
A. Rheumatic fever
B. Congenital ( parachute valve)
C. Severe mitral annular calcification with leaflet involvement
D. SLE, RA
E. Myxoma
F. Infective endocarditis with large vegetations

8. CLASSIFICATION OF MITRAL
STENSOIS
• Severe mitral stenosis ( ≤1.5cm2)
• Progressive mitral stenosis (>1.5 cm2)

9. PATHOLOGY
• In rheumatic MS, chronic inflammation leads to diffuse thickening of the valve leaflets with formation of
fibrous tissue often with calcific deposits.
• The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid, and the
pathologic process eventually leads to narrowing at the apex of the funnel-shaped (“fish-mouth”) valve.
• Although the initial insult to the mitral valve is rheumatic, later changes may be exacerbated by inflammation,
fibrosis, and trauma to the valve due to altered flow patterns.
• Calcification of the stenotic mitral valve immobilizes the leaflets and narrows the orifice further.

10. PATHOPHYSIOLOGY
• Under normal physiologic conditions, the mitral valve opens during left ventricular diastole to allow blood to
flow from the left atrium to the left ventricle.
• The pressure in the left atrium and the left ventricle during diastole are equal.
• The left ventricle gets filled with blood during early ventricular diastole.
• There is only a small amount of blood that remains in the left atrium. With the contraction of the left atrium
(the "atrial kick") during late ventricular diastole, this small amount of blood fills the left ventricle.

11. • Mitral valve areas less than 2 square centimeters causes an impediment to the blood flow from the left atrium into
the left ventricle.
• This creates a pressure gradient across the mitral valve. As the gradient across the mitral valve increases, the left
ventricle requires the atrial kick to fill with blood.
• 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).
• The elevated pulmonary venous and pulmonary arterial wedge pressures reduce pulmonary compliance,
contributing to exertional dyspnea.

13. PULMONARY HYPERTENSION IN MS
• Pulmonary hypertension results from :
1) Passive backward transmission of the elevated LA pressure.
2) Pulmonary arteriolar constriction (the so-called “second stenosis”), which presumably is
triggered by LA and pulmonary venous hypertension (reactive pulmonary hypertension).
3) Interstitial edema in the walls of the small pulmonary vessels.
4) At end stage, organic obliterative changes in the pulmonary vascular bed.
• Severe pulmonary hypertension results in RV enlargement, secondary tricuspid regurgitation (TR),
and pulmonic regurgitation (PR), as well as right-sided heart failure.

14. • Pulmonary Changes:
- Fibrous thickening of the walls of the alveoli and pulmonary capillaries.
- 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.

15. CLINICAL FEATURES: SYMPTOMS
• Mild MS: Exertional dyspnea and cough
• As mitral stenosis progresses lesser degree of stress causes cough and shortness of breath and eventually PND
and orthopnea occurs.
• Hemoptysis results from rupture of pulmonary-bronchial venous connections secondary to pulmonary venous
hypertension.
• Thromboembolism due to thrombus formed in the stenotic calcified valve and the atrial appendages.
• Fatigue, palpitation
• Ascities, bipedal edema and hepatomegaly if right heart failure.

16. • Hoarseness of voice:
- Due to recurrent laryngeal nerve palsy due to compression by
dilated pulmonary artery.
• Compression of the esophagus causes dysphagia.

17. VITAL SIGN
• BLOOD PRESSURE: low blood pressure due to decrease in cardiac
output.
• PULSE: Irregularly irregular pulse in case of atrial fibrillation.
Narrow pulse pressure.
• If BP is high coexisting mitral regurgitation , aortic regurgitation and
hypertension should be suspected.

18. EXAMINATION:
• Inspection:
- Mitral facies: Rosey cheek with bluish tinged in other
part of face.
• Prominent a wave in JVP if associated with sever pulmonary hypertension

19. PALPATION
• Tapping apex beat (palpable S1): also called as closing snap,
remains in contact for less than one third of the
systole.
• If apex beat is shifted MS might be associated with MR/AR, hypertension.
• Pulmonary hypertension/ right ventricular hypertrophy:
- Palpable p2( diastolic shock)
- Left parasternal heave.
- Epigastric pulsation.
• Diastolic thrill present over the cardiac apex.

20. AUSCULTATION
• Loud S1 short sharp and snapping
• Opening snap
• Low pitched mid diastolic rumbling murmur with presystolic accentuation at the
apex with the patient present in the left lateral recombinant position at the height
of expiration best heard with bell.
• If first heart sound is not loud
- Suspect other coexisting valve.
- Calcified valve.

21. OPENING SNAP
• Pathognomonic of mitral stenosis.
• High frequency
• Early diastolic
• Just after S2
• Due to dooming of the mitral valve cusps at the onset of ventricular
diastole ( as mitral valve is near to open but has not yet open).
• Heard medial to the mitral area by the diaphragm of the stethoscope.

22. Opening snap indicates:
• MS is organic.
• Valve cusps are not calcified.
• Significant MS
• Less S2-OS time interval indicates the increase severity of stenosis.

23. LABORATORY EXAMINATION
• ECG : P Wave becomes tall and peaked in lead II , and upright in lead V1.
• ECHO:
Transthoracic echocardiography
- Estimates of the transvalvular peak and mean gradients and mitral orifice area.
- The presence and severity of any associated MR.
- The extent of leaflet calcification and restriction.
- The degree of distortion of the sub valvular apparatus.
- Measurements of mitral inflow velocity during early (E wave) and late (A wave in patients in
sinus rhythm) diastolic filling.

24. Transesophageal echocardiography :
- TEE is especially indicated to exclude the presence of LA thrombus prior to PMBC.
- The performance of TTE with exercise to evaluate the mean mitral diastolic gradient and
Pulmonary artery pressure.
Chest x- ray:
- The earliest changes are straightening of the upper left border prominence of the main Pulmonary
artery.
- Dilation of the upper lobe pulmonary veins
- Posterior displacement of the esophagus by an enlarged LA.
- Kerley B lines

25. • Cardiac catheterization:
- Left and right heart catheterization can be useful when there is a discrepancy
between the clinical and noninvasive findings.
- Catheterization can also be helpful in assessing associated lesions, such as AS and
AR, and in patients with recurring worsening symptoms later after mitral valve
intervention

26. STAGES OF MITRAL STENOSIS

27. Treatment
• Medical management
Secondary prevention of rheumatic fever

31. • In symptomatic patients, some improvement usually occurs with restriction of sodium intake and small doses
of oral diuretics.
ATRIAL FIBRILLATION WITH FAST VENTRICULAR RATE
• Beta blockers
• Nondihydropyridine calcium channel blockers (e.g., verapamil or diltiazem)
• Digitalis glycosides

32. VITAMIN K ANTAGONIST
• MS who have AF, a history of thromboembolism, or demonstrated LA thrombus.
• Target INR 2 - 3
• If AF is of relatively recent onset in MS not severe enough to warrant PMBC or surgical intervention,
reversion to sinus rhythm pharmacologically or by means of electrical countershock is indicated.
• Usually, cardioversion should be undertaken after the patient has had at least 3 consecutive weeks of
anticoagulant treatment to a therapeutic INR.
• If cardioversion is indicated more urgently, then intravenous heparin should be provided and TEE performed
to exclude the presence of LA thrombus before the procedure.

33. SURGICAL INTERVENTIONS

34. PERCUTANEOUS MITRAL BALLON
COMMISSUROTOMY
• Mitral commissurotomy is indicated in 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 normal-sized adults.
• Mitral commissurotomy can be carried out either percutaneously or surgically.
Indication
• Pliable leaflets with little or no commissural calcium.
• The sub valvular structures should not be significantly scarred or thickened.
• There should be no LA thrombus.
• Any associated MR should be of ≤2+/4+ severity.

35. • Event free surviaval rate of 80 to 90% over 3 to 7 years have been seen in younger patient <45
years.
• In patients in whom PMBC is not possible or unsuccessful, or in many patients with restenosis
after previous surgery, an “open” surgical commissurotomy using cardiopulmonary bypass is
necessary.
• Successful commissurotomy is defined by a 50% reduction in the mean mitral valve gradient
and a doubling of the mitral valve area.

36. Routine follow up
• Once mild stenosis has developed, further narrowing is slow (decrease in valve area of 0.1 cm2 per year on
average), although the rate of progression is highly variable.

37. COMPLICATIONS OF MITRAL
STENOSIS
• Left atrial enlargement: dysphagia, recurrent laryngeal nerve palsy,
acute left atrial failure , acute pulmonary edema.
• Pulmonary hypertension
• Right ventricular failure
• Atrial fibrillation
• Cardioembolic stroke
• Haemoptysis
• Recurrent chest infection
• Jaundice, cardiac cirrhosis

38. REFRENCES
• HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 21ST EDITION.
• https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000923#T4
• Shah SN, Sharma S. Mitral Stenosis. InStatPearls [Internet] 2021 Aug 11. StatPearls Publishing.

39. Thank you