Floppy mitral valve and ventricular septal defect: an anatomic study

Eighteen percent of heart specimens with isolated ventricular septal defect also had a floppy mitral valve. There was no statistical difference in the incidence of floppy mitral valve in the three age groups considered (less than 1 year, 1 to 16 years and 17 to 91 years). In no patient was a floppy mitral valve considered to be the cause of death. Complications of floppy mitral valve (ruptured chordae tendineae, bacterial endocarditis, mitral regurgitation and fibrin deposits at the mitral valve-left atrial angle) occurred at approximately the same frequency as that reported in autopsy studies of isolated floppy mitral valve. In the specimens with floppy mitral valve and ventricular septal defect, 63% also had floppiness of the tricuspid valve, 16% of the pulmonary valve and 5% of the aortic valve. The anatomic basis for floppy mitral valve was considered to be spongiosal invasion and disruption of the fibrosa of the valve leaflet. In this study, spongiosal invasion of the fibrosa was fully developed by 3 months of age and there was no evidence that the incidence or severity of spongiosal invasion increased between the ages of 3 months and 88 years. These data suggest that the floppy mitral valve is a congenital lesion that reaches full anatomic expression in infancy. No evidence was found that ventricular septal defect and floppy mitral valve share a common etiology.