The architecture of the mitral valve is complex and includes the mitral leaflets, chordae tendineae which support the leaflets, the papillary muscles which support the chordae, the mitral valve annulus, and the left ventricular chamber itself. Abnormalities of all or any one of these structures can result in significant mitral regurgitation.
Involvement of the leaflets is seen in disorders such as rheumatic heart disease, systemic lupus erythematosus, infective endocarditis, and mitral valve prolapse syndrome. Regurgitation due to the chordae tendineae most often results from spontaneous rupture of the chordae tendineae. Papillary muscles can also rupture secondary to myocardial infarction. Any disease which results in enlargement of the left ventricle can produce abnormal papillary muscle function and dilation of the annulus, both of which can result in mitral regurgitation.
What is the most common physical finding of mitral regurgitation?
The most characteristic feature of mitral regurgitation is the loud systolic murmur heard over the apex of the heart. This murmur is holosystolic and commences with the first heart sound and ends with a second heart sound. The murmur generally radiates into the axilla but can often be heard along the spine or, in severe cases, on top of the head. Patients with severe regurgitation, chronic mitral regurgitation, or severely decreased left ventricular function may have a soft murmur.
Which maneuvers can be used to change the intensity of the murmur?
Sudden standing or the use of amyl nitrate will decrease afterload and result in the decrease of the murmur.