Mitral Valve Stenosis

Overview

Mitral Valve Stenosis occurs due to improper opening of the mitral valve thus preventing normal flow of blood from the left atrium to the left ventricle during diastole.

Etiologies

The predominant cause of mitral stenosis is Rheumatic Heart Disease and occurs in nearly 40% of those with previous history Rheumatic Fever. When caused by rheumatic heart disease the mitral valve leaflets appear fibrotically thickened and calcified. The Mitral Commissures, the regions where the leaflets meet, also become fused. Together, these changes lead to stenosis of the mitral valve which interferes with proper atrial to ventricular blood flow. In many cases the chordae tendineae are thickened and shortened which can yield mitral regurgitation along with mitral stenosis. Other uncommon etiologies include congenital stenosis of the mitral valve or age-related calcification.

Pathophysiology

Stenosis of the mitral valve considerably increases the resistance to blood flow between the left atrium and the left ventricle. To maintain a sufficient cardiac output, the blood pressure gradient between these two chambers must increase and is achieved by substantially increasing the Left Atrial Pressure (LAP). However, increased LAP results in a number of pathophysiological consequences described below. In general, increases in left atrial pressures are largely able to maintain cardiac output at rest in mild mitral stenosis although cardiac output may not rise normally with physical activity. However, as the stenosis becomes more severe, deficient cardiac output may be experienced even at rest.

Increased LAP results in passive backup of blood into the pulmonary circulation and thus pulmonary edema which can manifest clinically as dyspnea.

In most patients, pulmonary hypertension is due to passive backward transmission of the left atrial pressure. In some patients, however, there appears to be an active component to the pulmonary hypertension caused by reactive vasoconstriction of pulmonary arterioles. Whatever the case, pulmonary hypertension substantially increases the afterload on the right Heart, and often results in concentric right ventricular hypertrophy.

Chronically increased LAP will eventually result in left atrial dilation which can derange the electrophysiology of the left atrium and cause atrial fibrillation.

Stasis of blood in a dilated left atrium can increase the risk of thrombosis within this chamber. Embolization of thrombi can result in development of systemic thromboemboli.

Naturally, a deformed, fibrotic, or calcified mitral valve will increase the risk of its colonization with bacteria and thus endocarditis

Clinical Consequences

The symptomology of mitral valve stenosis is variable and largely depends on the severity of stenosis. In general, patients usually present with stenotic symptoms more than 20 years after the initial attack of rheumatic fever.

Dyspnea is the dominant symptom of mitral stenosis and manifests with varying severity depending on the degree of stenosis
With mild stenosis, Dyspnea may manifest only under conditions that require increased cardiac output such as physical activity or emotional excitement. As stenosis intensifies Dyspnea may be encountered at rest and may evolve to include orthopnea and paroxysmal nocturnal dyspnea.

Chronic pulmonary hypertension can substantially increase the demand on the right heart. Over time, this may lead to the congestive symptomology of Right Heart Failure (see page).

In certain cases, increased pulmonary venous pressures will cause opening of collateral channels between the pulmonary and bronchial circulation. Rupture of these collaterals may manifest as hemoptysis.

As mentioned above, atrial fibrillation, thromboembolism, and infective endocarditis may develop secondary to mitral valve stenosis.

Signs

Stenosis of the mitral valve results in a number of prototypical physical findings associated with changes in the valvular dynamics and hemodynamics.

S1 is normally caused by closure of the mitral valve and is often accentuated or delayed in the context of mitral stenosis. This may be because the larger pressure gradient between atria and ventricle during diastole maintains mitral leaflets wide apart even during late stages of diastole. As ventricular pressure ramps up during systole, the leaflets are slammed shut with greater force, generating a louder sound, or with a slight delay. However, S1 accentuation and delay tend to become mild or disappear all together in late stages of the disease.

Opening of the stenotic mitral valve generates an audible "Opening Snap" immediately after S2, likely due to tensing of the thickened chordae tendineae. The intensity of the Opening Snap is thought to correlate with the degree of mitral stenosis.

Diastolic passage of high pressure atrial blood into the ventricle through the stenotic mitral valve generates a low-pitched, rumbling murmur best heard at the apex. Importantly, the duration of the murmur best correlates with the degree of mitral stenosis, reflecting the length of time required to dissipate the diastolic atrial-ventricular pressure gradient. Frequently, the murmur will accentuate just before systole, termed "Pre-systolic Accentuation", reflecting atrial systolic ejection of additional blood into the ventricle.

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