1. Rheumatic-commonest.
  2. Congenital-may be associated with ASD, cor-triatriatum and coarctation of aorta.
  3. Infective endocarditis.
  4. AEndocardial fibroelastosis.
  5. Viral and Rickettsial infection.
  6. Left atrial myxoma causing mitral obstruction.

Incidence of mitral stenosis is same as that of rheumatic fever. But it occursS cartter in tropical countrie pafticularly in TIndia In the western world, Rheumati incidence is gradually declining but it is not so in tropica and sub-tropical countries.


In active rheumatic valvulitis, the, damage of the valves mostly occurs at the line of apposition (which is slightly inside the edge of valves) due to trauma during repeated closure Fibrin and platelets are deposited in that line, ultimately fibroblastic prolifefation facilitates adhesion between the valvesThe scarring of the valves may be followed by całcification in some cases The chordae tendineae, papillary muscles and fibrous ring are also involved in the rheumatic process leading to scarring and rigidity.The mitral opening may be like a slit as in ‘button hole or may be further narrowed down to a ‘funnel shape’ due to shortening of chordae The normal mitral orifice area is 5 cm2 When it becomes 2.5 cm symptoms appear after physical exertion but symptoms appear even at rest when the orifice area becomes critical, i.e., 1 cm2, which occurs in 10%-15 % of cases. In moderate mitral stenosis the valve area is <1 cm2


The resistance of narrow lumen of mitral orifice gives rise to high left atrial pressure, more so in tachycardia when diastolic ventricular filling time becomes shorter. The high pressure in left atrium gives rise to left atrial hypertrophy and dilatation and transmitted to pulmonary veins and to pulmonary capillaries. The pulmonary arterial pressure also rises. The increased pulmonary vascular resistance is responsible for decreased pulmonary blood flow to the lung bases and redistribution of blood flow occurs in the upper lobe. With the relief of stenosis this resistance becomes reversible. In a few cases the pulmonary arterioles become narrowed which in turn leads to increased pulmonary arterial pressure. All these put great strain to right ventricle which hypertrophies and eventually dilates leading to failure. | MITRAL STENOSIS


These usually develop insidiously after 3-4 years of acute rheumatic fever but may be delayed as late as 50 years. Sex: Females usually predominate (75%)

  1. Dyspnoea is the chief symptom and may be of different grades. It is due to congêstfon anfd stiffhess of lung with high pulmonary venous pressure and interstitial oedema so that the total lung volume, vital capacity and pulmonary compliance are reduced The dyspnoea may be paroxysmal In long standing cases due to pulmonary oedema (pulmonary venous pressure >30 mm of Hg). When cardiac arrhythmia like atrial fibrillation develops dyspnoea is virtually always present.
  2. Palpitation is often distressing and is due to tachycardia because of low cardiac output and also due to atrial arrhythmias. It is rarely the chief complaint.
  3. (Haemoptysis in mitral stenosis is a fairly common symptom. It is the second important symptom of the disease It may be due to:
  4. a) rupture of a pulmonary vein,
  5. b) rupture of a bronchial vein (bronchopulmonary anastomotic link),
  6. c) sometimes due to rupture of a pulmonary arteriole,
  7. d) due to pulmonary infarction,
  8. e) blood streaked sputum with winter coughs as in chronic bronchitis,
  9. f) due to pulmonary haemosiderosis,
  10. g) pink frothy sputum of acute pulmonary oedema, and
  11. h) rarely due to pulmonary tuberculosis.
  12. Patient may also complain of cough, chest pain (due to pulmonary hypertension or myocardial ischaemia), angina pectoris, weakness, fatigue etc. | MITRAL STENOSIS


General Survey

  1. Mitral facies-due to peripheral vaso-constriction because of low output. Peripheral cyanosis is found in face and hands, and this is rarely seen. Sometimes malar flush is seen which may be due to vascular stasis and arteriovenous anastomosis.
  2. Pulse volume low, BP slightly low.

Cardiovascular System | MITRAL STENOSIS

  1. Inspection: Precordial bulging may be present due to right ventricular hypertrophy.
  3. a) Apex beat is tapping in character as left ventricular impulse is practically impalpable and only the first sound (Mi) is felt.
  4. b) A diastolic thrill is felt over the mital area, particularly on left lateral position.
  5. c) Pulmonary arterial pulsation and valve closure (diastolic shock) may be felt over the left second space when there is marked pulmonary hypertension.
  6. d) Parasternal heave and epigastric pulsation may be present which signify right ventricular hypertrophy.
  7. Auscultation: Over the mitral area first sound is short and accentuated (sudden loud) and second sound (A) is feeble; opening snap may be present which is best heard at left lower edge of sternum or just internal to the apex beat and is due to sudden bellowing down of the mitral cusps into the left yentricle at the end of isometric relaxation phase. Opening snap disappears when mitral valves become rigid or calcified. Immediately following the opening snap, a rumbling mid-diastolic murmur with presystolic accentuation is heard which ends in the accentuated first sound. The murmur is not conducted and is sharply localised there. The murmur is low pitched and is better heard with the bell of a stethoscope with the patient inclined to left lateral position. Over the pulmonary area second heart sound is closely split and pulmonary component (P2) is accentuated due to pulmonary hypertension and rarely there may be an early diastolic murmur, called Graham Steelľ’s murmur due to dilatation of the pulmonary artery.


  1. X-ray of chest (PA) will show mitralisation of the heart which includes enlargement of cardiac shadow, less prominent aortic knuckle, prominence of pulmonary artery (full pulmonary bay), prominence of left atrial shadow between pulmonary artery and left ventricular segment, straightening of the left border of the heart, right border shows double contour, one is due to right atrium and the other is due to enlarged left atrium. Splaying of left bronchus with increased carinal angle is seen. Lung fields may be congested with prominent upper lobe veins, there may be Kerley’s B lines and rarely haemosiderosis. X-ray of chest in RAO position with barium swallow will show displacement of the shadow of the oesophagus due to enlarged left atrium.
  2. ECG shows P-mitrale pattern with right ventricular enlargement and sometimes different types of cardiac afrhythmias.
  3. Echocardiogram: Echocardiography is diagnostic of mitral stenosis. This characteristically shows a decreased E-F slope of the anterior leaflet. Multi- layered echoes or thickening of echo patterns are due to calcification or thickening of the mitral valve. Characteristic doming of valve is diagnostic under cross-sectional echocardiography. CW Doppler is useful for peak mitral transventricular gradient and mitral valve area. Left atrial size is also determined by echocardiography. When the size of left atrium is increased there is fair chance of development of atrial fibrillation or systemic embolization.
  4. Left ventricular angiocardiography, dye dilution and pressure curves from left atrium and ventricle during catheterization may be helpful for diagnosis in difficult cases.


  1. Auricular fibrillation is almost an invariable complication (50%-80% cases).
  2. Congestive cardiac failure which starts as left atrial failure and then right heart failure develops.
  3. Haemoptysis due to the causes mentioned above.
  4. Embolic manifestations of which cerebral embolism is commonest. Small thrombi will cause systemic embolisation but ball thrombi will cause cardiac embolism and sudden death.
  5. Recurrent bronchitis-so called “Winter Bronchitis”.
  6. Infective endocarditis.
  7. Pressure symptoms by the giant left atrium giving rise to:
  8. a) Dysphagia as a result of pressure over the oesophagus.
  9. b) Dyspnoea as a result of collapse of lung due to pressure over the left bronchus.
  10. c) Hoarseness of voice due to pressure over the recurrent laryngeal nerve (Oartner’s syndrome).
  11. d) Deep boring pain over the thoracic vertelbrae due to erosion.


Though mitral stenosis is a progressive disease in absence of mitral valvotomy its prognosis is unpredictable. Disorganisation and calcification of the mitral valve, progressive increased pulmonary resistance, chronic right-sided heart failure with cardiac cirrhosis are ominous signs. In carefully selected cases mitral valvotomy influences the prognostic outcome.



Functional mitral mid-diastolic murmur:

OS, presystolic accentuation of the diastolic murmur and diastolic thrill are absent. Features of original disease will also be present.

Austin-Flint’s murmur

Opening snap, palpable first heart sound and diastolic thrill are absent over the mitral area. Echocardiography is very much helpful. Aortic regurgitation murmur is present over aortic area.

Conducted murmur of aortic incompetence:

This is not rumbling but blowing in character, occupies early part of diastole, not associated with opening snap or diastolic thrill.


Absence of opening snap, diastolic thrill, palpable first heart sound over the mitral area.Wide and fixed splitting of the S2 over pulmonary area, no evidence of enlargement of left atrium in the X-ray and ECG. But later may show incomplete or complete RBBB.

Left atrial myxoma

Constitutional symptoms like fever, weight loss, weakness together with high ESR, anemia, hypergamma-globulinemia may be present. Systemic embolisation, opening snap (false opening snap-tumour plop may be present), palpable first heart sound, diastolic thrill over, the mitral area are absent. Evidence of rheumatic valve disease is lacking. Murmur changes with change of posture. Left atrial angiography (which may precipitate embolisation) may show a lobulated filling defect and echocardiogram characteristically shows diastolic mass of echoes behind the mitral valve.

. Cor-triatriatum

Echocardiogram is most helpful in the diagnosis

Primary pulmonary hypertension:

This is seen in young females. Opening snap, mitral diastolic thrill and typical mitral stenotic murmur or left atrial enlargement in X-ray are absent. Normal left atrial and pulmonary wedge pressure are seen.


In age groups below 20 years or with mild mitral stenosis or where surgery is contraindicated conservative medical treatment is advised. This includes treatment of complications like chest infection, bacterial endocarditis by antibiotics; cardiac arrhythmia by antiarrhythmic drugs, embolisation by anticoagulants and heart failure by diuretics and digitalis. If the rheumatic process is persistent it should be treated in the usnal way. Prophylactic chemotherapy should also be continued both for rheumatic fever and bacterial endocarditis. The surgical treatment is indicated in the following conditions:

  1. Typical signs of mitral stenosis with a pliable mitral valve indicated by OS and loud S1
  2. Recurrent uncontrolled pulmonary oedema.
  3. Recurrent left atrial failure.
  4. Pulmonary hypertension with right ventricular hypertrophy with CCF.
  5. Increased pulmonary arteriolar resistance.
  6. Right heart failure with tricuspid incompetence.
  7. Recurrent haemoptysis.
  8. Limitation of activity in spite of medical treatment.
  9. Recurrent systemic embolisation.

There are four operative procedures:

  1. Trans-septal balloon valvotomy or balloon valvuloplasty.
  2. Closed valvotomy.
  3. Open valvotomy.
  4. Mitral valve replacement.

Though closed mitral valvotomy can be performed yet many surgeons prefer open valvotomy. In cases of combined stenosis with regurgitation in presence of grossly distorted and calcified valves, prosthetic valve replacement is indicated. Artificial valves may work efticiently for more than 20 years. Anticoagulants are to be continued for prevention of thrombus formation.

Although long-term data are not yet available, balloon valvuloplasty will be as effective as heart surgery.


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