The floppy mitral valve. Study of incidence, pathology, and complications in surgical, necropsy, and forensic material.

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Abstract
In a study of 1984 hospital necropsies the mitral valve was examined from the left atrium in the intact heart with a pressure head of water in the left ventricle. The valve was graded from grade O (normal) to grade 4:grade 1, expansion of a small part of 1 cusp only; grade 2, over 1/3 of the posterior cusp or 1/2 of the anterior cusp expanded, with intact chordae grade 3, ruptured chordae; grade 4, chordal fusion to ventricular wall. The frequency of grade 2-4 floppy valves rose with age with an overall incidence of 3.9% in men and 5.2% in women. Grade 1 floppy valves have no clinical significance. Grade 2 floppy valves were associated with auscultatory signs but often only contributed to cardiac failure or were coincidental findings. Grade 3 and 4 floppy valves were direct causes of death from bacterial endocarditis and/or severe mitral regurgitation. The surgical series of floppy valves showed that chordal rupture was the event which most commonly made operation necessary in middle age; in a minority this was caused by bacterial endocarditis. Dilatation of the annulus was an important contributory factor but can produce significant mitral regurgitation without chordal rupture, particularly in inherited connective tissue disorders such as the Marfan syndrome. Forensic necropsies confirm that sudden death occurs in patients with floppy valves. The majority have grade 3 or 4 floppy valves and presumably significant mitral regurgitation. A minority have minimal valve involvement and the mechanism of death is unexplained. The exact magnitude of the risk for any patient with a floppy valve of developing bacterial endocarditis, or chordal rupture leading to significant mitral regurgitation, or of dying suddenly, is not known but must be very low considering the frequency of the valve lesion. The essential pathology of the floppy mitral valve is weakening of the central fibrous core allowing cusp expansion and chordal elongation to occur. The weakness of the collagen is in part genetically determined, in part age related. Identical changes occur in the tricuspid valve, and in the aortic root, leading to aortic regurgitation. Similar pathological changes are well recognized in other mammals, particularly the aged dog.