The mitral valve
Application for Treatment
The mitral valve

The mitral valve (also known as the bicuspid valve or left atrioventricular valve) is a dual-flap (bi- from the Latin, meaning double, and mitral - from the Latin, meaning shaped like a mitre) valve in the heart that lies between the left atrium (LA) and the left ventricle (LV). The mitral valve (not to be confused with the congenital bicuspid aortic valve) and the tricuspid valve are known collectively as the atrioventricular valves because they lie between the atria and the ventricles of the heart and control the flow of blood.
During diastole, a normally-functioning mitral valve opens as a result of increased pressure from the left atrium as it fills with blood (preloading). As atrial pressure increases above that of the left ventricle, the mitral valve opens. Opening facilitates the passive flow of blood into the left ventricle. Diastole ends with atrial contraction, which ejects the final 20% of blood that is transferred from the left atrium to the left ventricle. This amount of blood is known as end diastolic volume (EDV), and the mitral valve closes at the end of atrial contraction to prevent a reversal of blood flow.
Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.

Signs and symptoms

Symptoms of mitral stenosis include:

  • Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)
  • Palpitations
  • Chest pain
  • Hemoptysis
  • Thromboembolism in later stages when the left atrial volume is increased (i.e. dilation). The latter leads to increase risk of atrial fibrillation of which increases the risk of blood stasis (motionless). This increases the risk of coagulation.
  • Ascites and edema and hepatomegaly (if right-sided heart failure develops)

Symptoms increase with exercise and pregnancy

  • Fatigue
  • wasting (weakness)


Rheumatic heart disease at autopsy with characteristic findings (thickened mitral valve, thickened chordae tendineae, hypertrophied left ventricular myocardium).
Almost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Uncommon causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. However, there are primary causes of mitral stenosis that emanate from a cleft mitral valve.
Other causes include infective endocarditis where the vegetations may favor increase risk of stenosis. It is the most common valvular heart disease in pregnancy


Upon auscultation of an individual with mitral stenosis, the first heart sound is unusually loud and may be palpable (tapping apex beat) because of increased force in closing the mitral valve. The first heart sound is made by the mitral and tricuspid heart valves closing. These are normally synchronous, and the sounds are termed M1 and T1 respectively. M1 becomes louder in mitral stenosis. It may be the most prominent sign.
If pulmonary hypertension secondary to mitral stenosis is severe, the P2 (pulmonic) component of the second heart sound (S2) will become loud.
An opening snap which is a high pitched additional sound may be heard after the A2 (aortic) component of the second heart sound (S2), which correlates to the forceful opening of the mitral valve. The mitral valve opens when the pressure in the left atrium is greater than the pressure in the left ventricle. This happens in ventricular diastole (after closure of the aortic valve), when the pressure in the ventricle precipitously drops. In individuals with mitral stenosis, the pressure in the left atrium correlates with the severity of the mitral stenosis. As the severity of the mitral stenosis increases, the pressure in the left atrium increases, and the mitral valve opens earlier in ventricular diastole.Almost all signs increase with exercise and pregnancy.
Other peripheral signs include:

  • Malar flush - due to back pressure and build up of carbon dioxide (CO2). CO2 is a natural vasodilator.
  • Atrial fibrillation - irregular pulse and loss of 'a' wave in jugular venous pressure
  • Left parasternal heave - presence of right ventricular hypertrophy due to pulmonary hypertension
  • Tapping apex beat which is not displaced

Medical signs of atrial fibrillation include:
Heart rate is about 100-150/min. Irregularly irregular pulse with a pulse deficit>10. varying first heart sound intensity. Opening snap is not heard sometimes. Absent a waves in the neck veins. Presystolic accentuation of diastolic murmur disappears. Embolic manifestations may appear.


Severity of mitral stenosis
Degree of mitral stenosis Mean gradient Mitral valve area
Mild mitral stenosis <5 mmHg >1.5 cm2
Moderate mitral stenosis 5 - 10 mmHg 1.0 - 1.5 cm2
Severe mitral stenosis > 10 mmHg < 1.0 cm2

Cardiac chamber catheterization

Another method of measuring the severity of mitral stenosis is the simultaneous left and right heart chamber catheterization. The right heart catheterization (commonly known as Swan-Ganz catheterization) gives the physician the mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure. The left heart catheterization, on the other hand, gives the pressure in the left ventricle. By simultaneously taking these pressures, it is possible to determine the gradient between the left atrium and left ventricle during ventricular diastole, which is a marker for the severity of mitral stenosis. This method of evaluating mitral stenosis tends to overestimate the degree of mitral stenosis, however, because of the time lag in the pressure tracings seen on the right heart catheterization and the slow Y descent seen on the wedge tracings. If a trans-septal puncture is made during right heart catheterization, however, the pressure gradient can accurately quantify the severity of mitral stenosis.

Other assisting diagnostic techniques

Chest X-ray may also assist in diagnosis, showing left atrial enlargement.[
Electrocardiography may show P mitrale, that is, broad, notched P waves in several or many leads with a prominent late negative component to the P wave in lead V1, and may also be seen in mitral regurgitation, and, potentially, any cause of overload of the left atrium.Thus, P-sinistrocardiale may be a more appropriate term.


Treatment is not necessary in asymptomatic patients.
The treatment options for mitral stenosis include medical management, mitral valve replacement by surgery, and percutaneous mitral valvuloplasty by balloon catheter.
Treatment also focuses on concomitant conditions often seen in mitral stenosis:

  • Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers
  • Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers
  • Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors

Mitral valvuloplasty

Mitral valvuloplasty is a minimally invasive therapeutic procedure to correct an uncomplicated mitral stenosis by dilating the valve using a balloon. Under local anaesthetic, a catheter with a special balloon is passed from the right femoral vein, up the inferior vena cava and into the right atrium. The interatrial septum is punctured and the catheter passed into the left atrium using a "trans-septal technique." The balloon is sub-divided into 3 segments and is dilated in 3 stages. 1st the distal portion (lying in the left ventricle) is inflated and pulled against the valve cusps. Second the proximal portion is dilated, in order to fix the centre segment at the valve orifice. Finally, the central section is inflated, this should take no longer than 30 seconds since full inflation obstructs the valve and causes congestion, leading to circulatory arrest and flash pulmonary edema.
With careful patient pre-selection, percutaneous balloon mitral valvuloplasty (PBMV) is associated with good success rates and a low rate of complications. By far the most serious adverse event is the occurrence of acute severe mitral regurgitation. Severe mitral regurgitation usually results from a tear in one of the valve leaflets or the subvalvular apparatus. It can lead to pulmonary oedema and hemodynamic compromise, necessitating urgent surgical mitral valve replacement.
Other serious complications with PBMV usually relate to the technique of trans-septal puncture (TSP). The ideal site for TSP is the region of the fossa ovalis in the inter-atrial septum. Occasionally, however, the sharp needle used for TSP may inadvertently traumatize other cardiac structures, leading to cardiac tamponade or serious blood loss.
Although the immediate results of PBMV are often quite gratifying, the procedure does not provide permanent relief from mitral stenosis. Regular follow-up is mandatory, to detect restenosis. Long-term follow up data from patients undergoing PBMV indicates that up to 70-75% individuals can be free of restenosis 10 years following the procedure. The number falls to about 40% 15 years post-PBMV

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