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In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. Blood flows in the proper direction because during this phase of the cardiac cycle the pressure in the left ventricle is lower than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood the left atrium needs a higher pressure than normal to overcome the increased gradient.
Most cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Less common 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 Bacterial endocarditis where the vegetations may favor increase risk of stenosis.
The normal area of the mitral valve orifice is about 4 to 6 cm2. Under normal conditions, a normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during diastole will be equal. The result is that the left ventricle gets filled with blood during early diastole, with only a small portion of extra blood contributed by contraction of the left atrium (the "atrial kick") during late ventricular diastole.
When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
When the mitral valve area goes less than 1 cm2, there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).
Increases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.
The constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).
In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.
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 M1 component of the M1, T1 the two components of the first heart sound is accentuated.
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 maybe 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.
A mid-diastolic rumbling murmur will be heard after the opening snap. The murmur is best heard at the apical region and is not radiated. Since it is low-pitched it should be picked up by the bell of the stethoscope. Rolling the patient towards left, as well as isometric exercise will accentuate the murmur. A thrill might be present when palpating at the apical region of the praecordium.
Peripheral signs include:
In most cases, the diagnosis of mitral stenosis is most easily made by echocardiography, which shows decreased opening of the mitral valve leaflets, and increased blood flow velocity during diastole. The trans-mitral gradient as measured by Doppler echocardiography is the gold standard in the evaluation of the severity of mitral stenosis.
Another method of measuring the severity of mitral stenosis is the simultaneous left heart catheterization and right heart 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 right atrium during ventricular diastole, which is a marker for the severity of mitral stenosis. This method of evaluating mitral stenosis tend to over-estimate 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.
The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.
In individuals who were offered mitral valve surgery but refused, survival with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction.
The treatment options for mitral stenosis include medical management, surgical replacement of the valve, and percutaneous balloon valvuloplasty.
Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates.
The indication for invasive treatment with either a mitral valve replacement or valvuloplasty is NYHA functional class III or IV symptoms.
To determine which patients would benefit from percutaneous balloon mitral valvuloplasty, a scoring system has been developed.2 Scoring is based on 4 echocardiographic criteria: leaflet mobility, leaflet thickening, subvalvar thickening, and calcification. Individuals with a score of ≥ 8 tended to have suboptimal results.3 Superb results with valvotomy are seen in individuals with a crisp opening snap, score < 8, and no calcium in the commissures.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Mitral_stenosis". A list of authors is available in Wikipedia.|