Development of an experimental model of mitral valve regurgitation via hypertrophic chondrocytes

Abstract

Degenerative myxomatous mitral valve disease is the most common indication for surgical valve repair in the US and Europe [1, 2]. Degenerative myxomatous mitral valve disease is associated with mitral valve prolapse and abnormal movement of the leaflets into the left atrium during systole due to inadequate chordal support (elongation or rupture) and excessive valvular tissue [3]. There is a spectrum of pathologic changes found in the development of myxomatous mitral valve disease, which range from a marked increase in valve area and length to secondary ruptured chordae. Microscopically, the valves are myxomatous, with deposition of mucopolysaccahrides in a thickened spongiosa layer encroaching on the fibrosa layer [4]. Annular myxomatous changes may lead to dilation and calcification of the annulus. Previously, our laboratory has demonstrated that human myxomat mitral valve disease is associated with a chondrogenic phenotype [5].