Vascularization as a potential enemy in valvular heart disease.

Valvular heart disease remains a major problem worldwide and is responsible for 20 000 deaths each year in the United States, with an estimated 99 000 inpatient valve procedures performed annually.1 The mitral and tricuspid valve complexes comprise the valve leaflets, valvular annulus, papillary muscles, and chordae tendineae, which anchor the leaflets to the papillary muscles. As papillary muscles contract, chordae tendineae transmit tension to the valves, directing the valve leaflets to their correct position during the cardiac cycle. Rupture of the chordae tendineae occurs as a consequence of infective endocarditis, myxomatous degeneration, rheumatic fever, or rarely, osteogenesis imperfecta or relapsing polychondritis.2 In addition, ischemia-induced dysfunction of papillary muscles can cause stretching and ultimately rupture of the chordae tendineae, as well as release of chordal attachment at sites of papillary muscle necrosis.