Mitral valve prolapse is the most common cause of primary MR in developed countries and is degenerative or myxomatous mitral valve disease.

Trauma can cause ruptured chordae and acute MR. Rheumatic heart disease is uncommon in developed countries but continues to constitute a significant burden in the rest of the world. Rheumatic mitral valve disease is more frequent in women than men and disease detection is higher by echocardiography compared to clinical examination.

A variety of congenital anomalies of the mitral valve can cause MR, for example, a cleft anterior or posterior mitral leaflet. Mitral annular calcification is a common finding in older adults that is often associated with mild to moderate MR.

Pathophysiology

Acute phase:

• The left atrium (LA) and left ventricle (LV) do not have the opportunity to gradually enlarge and compensate for the volume overload
  
• LA pressure rises and the patient develops congestive heart failure with diminished cardiac output and pulmonary venous congestion. Most patients with severe acute mitral regurgitation require emergency surgical intervention.

Subacute compensated phase:

• Eccentric left ventricle hypertrophy and increased-end diastole volume
  
• Normal ejection fraction (EF) allows the ejection of a sufficiently large stroke volume that makes the forward stroke volume return toward normal despite the fraction being regurgitated
  
• LA enlarges to accommodate the regurgitant volume and can maintain a lowered filling pressure.

Chronic phase:

• LV and LA enlargement
  
• End systole volume increases
  
• End diastole pressure increases
  
• Pulmonary congestion

Mechanisms of MR

• Failure to coapt (perforation, annulus dilatation, cleft)
  
• Excessive leaflet motion (prolapse, flail leaflet, chordal rupture)
  
• Restriction leaflet motion (chordal shortening and fusion, leaflet stiffness)

Determination of severity: Over 20 variables for judging the severity of MR have been described [1]. Through the employment of this approach severe lesions are readily recognized, but distinguishing among the intermediate grades of MR (mild to moderate, moderate to severe mitral regurgitation) can be more difficult.

Echocardiography is essential for establishing the etiology and hemodynamic consequences of MR. Other important echocardiographic features are LA and LV size, systolic function, and pulmonary artery pressures. LA size is usually increased. LV size and systolic function are normal early in the disease course but progressive ventricular dilation and a decline in EF occur with chronic severe regurgitation. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease, consensus statement on management of valvular heart disease [2], recommended using multiple parameters when determining the severity of mitral regurgitation. These parameters include structural, color Doppler, and quantitative Doppler parameters.

Structural parameters: Structural abnormalities associated with MR supplement the quantitation of regurgitation and include LA and LV size, and appearance of the mitral apparatus.

• Mild MR is usually associated with normal or near-normal LA and LV size, and intact mitral apparatus.
  
• Moderate MR is frequently associated with some degree of LA enlargement, normal or mildly dilated LV, and varying degrees of mitral apparatus abnormalities.
  
• Severe chronic MR is usually associated with moderate to severe LA enlargement, some degree of LV dilatation, and often associated with flail mitral leaflet, ruptured papillary muscle, or malcoaptation of the mitral leaflets.

Color flow Doppler: The features of severe mitral regurgitation seen by color flow Doppler imaging arise from the high energy transfer of a volume of blood into LA, producing the characteristic “jet” in LA (Figure 12.2). Color flow Doppler is usually considered a quantitative or semiquantitative parameter.

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