Mitral regurgitation

What it is

In mitral regurgitation the mitral valve fails to close properly, so blood goes back into the left atrium. The valve can fail because the leaflets themselves are damaged, because the chordae tendineae or a papillary muscle give way, or because the left ventricle has dilated under the valve. Reading the murmur is only half the work; the other half is asking which of those three the failure is, because that decides how fast it must be treated.

Causes and risk

The most common cause is LV dilation from CAD or HTN. Rheumatic heart disease and IE are the other main causes.

The longer list is grouped as acute and chronic.

Acute:

• Rupture chordae tendineae, which permits prolapse of a portion of a mitral valve leaflet into the left atrium.
• Papillary muscle rupture.
• Endocarditis, which may lead to valvular destruction.
• Trauma.

Chronic:

• Rheumatic heart disease, causing scarring and retraction of valve and leaflets.
• Papillary muscle dysfunction.
• Mitral valve prolapse, also called click-murmur syndrome, Barlow syndrome or floppy mitral valve.
• Endocarditis.
• Calcification of the mitral valve annulus.
• Accompanying hypertrophic obstructive cardiomyopathy.
• Congenital endocardial cushion defect, corrected transposition.
• Endocardial fibroelastosis.
• Severe left ventricular dilatation.

Two settings are worth holding apart. After myocardial infarction, papillary muscle rupture gives acute mitral regurgitation, and it is reported at 2-7 days. In acute rheumatic fever, inflammatory damage gives leaflet edema and elongation of chordae tendineae, so the valve fails to close; in chronic rheumatic heart disease, progressive fibrosis, thickening and calcification make mitral stenosis the usual long-term outcome, with or without MR. In infective endocarditis the mitral valve is the one most often hit, through leaflet destruction, perforation or chordae rupture.