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.Article p 1737 Chordae tendineae are similar to tendons connecting our skeletal muscles to bones in that both structures are avascular connective tissues. Chordae tendineae are ≈80% collagen; the remaining 20% is elastic fibers and layers of endothelial cells on a basal lamina.3 A wavy arrangement of collagen surrounded by elastic fibers is well adapted for the cyclic stresses to which the chordae are continuously subjected.3 Chordal disruption can be sudden and precipitate acute heart failure, and why these avascular structures suddenly rupture is often unclear. In this issue, Kimura et al4 provide evidence that rupture of the chordae tendineae is associated with local angiogenesis accompanied by the absence of tenomodulin, a potent angiogenesis inhibitor. Their findings suggest a novel paradigm for rupture of the chordae tendineae in response to mechanical or …