(mitral regurgitation)

Mitral valve apparatus consist of mitral annulus, mitral valves, chordae tendineae, papillary musscles adjoining portions of left atrium near mitral annulus and lastly the portion of the left ventricle where thr papillary muscles are inserted. Mitral incompetence may develop due to involment of any of the components.


  1. Annulus: (1) (2)
  2. Valve : (3) (4)(5) (6) (7) (8) (9) (10) (11)
  3. Chordate tendineae : (5) (13)
  4. Left ventricle : (2)
  5. Prosthetic valve : (14)


  1. Calcification and dilatation of mitral annulus.
  2. Left ventricular dilation from any cause. e.g. hypertension, coronary vascular disease or aortic valve disease, cardiomynopathy, etc. this is sometimes termed as functional mitral incompetence.
  3. Rheumatic fever accounts for most of the cases of mitral insufficiency.
  4. Bacterial endocarditis resulting in destruction of the valve or rupture of chordate tendinae.
  5. Accidental tear during mitral valvotomy or trauma.
  6. Congenital (osteum primum type of ASD).
  7. Endomyocardial fibrosis involving mitral valve.
  8. Ebstein’s anomaly of the mitral valve.
  9. Prolapse of the mitral valve.
  10. Disorders of connective tissue, e.g. marfan’s syndrome, ehlers-danlos syndrome, morquio’s syndrome, etc.
  11. Left-side myxoma.
  12. Papillary muscle dysfunction or rupture from myocardial infarction.
  13. Idiopathic rupture of chordate tendineae.
  14. Leak from a prosthetic mitral valve.


Due to chronic inflammation (as in rheumatic cases) scarring and shortening of the valve cusps, papillary muscles and chordae tendineae occur. Therefore, the valve cisps are fixed and connot closed the orifice. That is the reason why incompetence is often associated with stenosis.



Due to incompetence of mitral valve, blood leaks from left ventricle into left atrium during systole resulting in increased pressure and volume of left atrium.During diastole entire volume of blood rapidly leaks into the left ventricle which dilates to accommodate:

  1. The blood that leaked in previous cardiac cycle, and
  2. The blood that has been accumulated during diastole of left atrium. SO , left ventricular end diastolic volume is increased and it gets hypertrophied in course of time.


Males predominate slightly more than females.


For a long time there may be no symptom till cardiac output begins to fall. When present they are similar to mitral stenosis described afterwards. In acute mitral incompetence as occurs in infarction however, severe dyspnoea due to pulmonary

oedema may develop rapidly.


Signs precede the symptoms by many years.


Usually no characteristic signs are seen. Pulse may be small or at times high in volume.

Examination of the Precordium

Inspection: Slight precordial bulging may be present. Palpation: Apex beat is more down than out, heaving or at times hyperkinetic in character. A systolic thrill may rarely be felt over the mitral area.

Auscultation: Mitral first heart sound is either normal or soft. Accentuated M, usually indicates posterior leaflet regurgitation or dominance of mitral stenosis in presence of mixed lesion i.e. MS with MR. A third heart sound may sometimes be audible. In severe mitral regurgitation S3 is very explosive; in presence of mixed lesion, presence of S3 always indicates dominance of regurgitation. S4 is never audible in ordinary mitral regurgitation but it is usually audible as a result of ruptured chordae, producing acute mitral regurgitation. Second sound is widely split. The hallmark of diagnosis of mitral incompetence is a loud blowing pansystolic murmur over the mitral area which is conducted towards the left axilla and inferior angle of the left scapula (Triangle of ausculation); in posterior leaflet regurgitation the murmur is often radiated to the base of the heart near aortic root simulating aortic stenosis.

The murmur may be of same intensity throughout the systole but often there may be a late systolic accentuation.

Sometimes a mid-diastolic flow murmur over mitral area may also be audible (due to relative mitral stenosis).


X-ray of the chest (PA) will demonstrarte enlargement of the left atrium and left ventricle, Dilated left atrium may be seen expanding with ventricular systole on screening. Calcification of the mitral valve may also be seen, but it is less common in comparison to MS. In acute mitral regurgitation X-ray shows evidences of pulmonary oedema.

  1. ECG may show evidences of left ventricular and left atrial enlargement with left axis deviation.

3 Cardiac catheterization and left ventriculography is particularly useful for assessment of left ventricular function and the degree of mitral incompetence.

  1. Echocardiogram and Doppler study may be useful for demonstrating the underlying cause and severity of MR.MRI and nuclear medicine study will estimate the severity of regurgitation and left ventricular function.


Benign systolic murmurs

They are difficult to differentiate at times. But these are usually not very loud, never pansystolic, do not radiate and show considerable variation with change of posture and respiration. Thrill is absent.


Aortic systolic murmur

It may be heard at the apex though it is best heard at the base of heart and is not conducted to axilla. It starts later and ends earlier (mid-systolic). First sound is audible and may be loud.S2 is faint.

Pansystolic murmur of VSD:

It is not conducted to the axilla, situated in the left 3rd space (Roger’s area) and first sound over mitral area is usually loud.

Tricuspid pansystolic murmur:

It is localized over the tricuspid area (LLSE), increased in intensity during inspiration and is not conducted to the left axilla.


1 Left ventricular failure.

2 Right ventricular failure

3 Infective endocarditis.

4 Angina pectoris.

5 Haemoptysis.

67 Atrial fibrillation.

Embolic phenomena.


If the rheumatic process is still active or complications are present the patient should be treated accordingly. Digitalis may De of value even when patient is in sinus rhythm. Surgical treatment of replacement of valves or annuloplasty under direct vision with cardiopulmonary by-pass is done now-a-days. This is required when left ventricular function gradually deteriorates or the patient’s activity becomes very much limited (NYHA class III). When the ejection fraction is less than 40% left ventricular function is very poor, operative risk becomes very high. In non-rheumatic cases valve repair is gradually gaining ground. When mitral incompetence is acute emergency surgery is mandatory.


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