International journal of cardiology · 2012
Structural analysis of chordae tendineae in degenerative disease of the mitral valve.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Icardo José M, Colvee Elvira, Revuelta José M
Аннотация
BACKGROUND: Degenerative disease of the mitral valve (DDMV) is always accompanied by lengthening and/or rupture of chordae tendineae. However, the mechanisms and the mode of chordal rupture remain controversial, and the pathologic anatomy of the apparently healthy chordae has mostly been overlooked. We analyze the structural aspects of both ruptured and intact chordae tendineae in DDMV.
METHODS AND RESULTS: Structural and ultrastructural microscopic analyses indicate that both the extracellular matrix and the interstitial cells are severely affected. Degenerative chordae show alterations in the synthesis and deposition of collagen and elastin, disorganization of collagen bundles and rupture of collagen fibres, accumulation of proteoglycans and of cellular and vesicular remnants, and cell transformation into a myofibroblast phenotype. Structural disruption makes the spongiosa and the dense collagenous core separate and break. Degeneration of the chordae is segmental, affecting both chordae that are clearly abnormal, and chordae that appear healthy on visual inspection.
CONCLUSIONS: Changes in both matrix synthesis and degradation disturb the ordered collagen arrangement and modify the structural and physical properties of the chordae. Progressive structural disruption of the diseased chordae is the cause of chordal rupture. Mitral surgery corrects the damage, but the underlying causes of DDMV are not corrected. Thus, progression of the disease and affectation of additional chordae may be at the basis of the late complications and the recurrent mitral regurgitation which occurs several years after surgery. Our results indicate that a more aggressive approach to surgery may be needed.
METHODS AND RESULTS: Structural and ultrastructural microscopic analyses indicate that both the extracellular matrix and the interstitial cells are severely affected. Degenerative chordae show alterations in the synthesis and deposition of collagen and elastin, disorganization of collagen bundles and rupture of collagen fibres, accumulation of proteoglycans and of cellular and vesicular remnants, and cell transformation into a myofibroblast phenotype. Structural disruption makes the spongiosa and the dense collagenous core separate and break. Degeneration of the chordae is segmental, affecting both chordae that are clearly abnormal, and chordae that appear healthy on visual inspection.
CONCLUSIONS: Changes in both matrix synthesis and degradation disturb the ordered collagen arrangement and modify the structural and physical properties of the chordae. Progressive structural disruption of the diseased chordae is the cause of chordal rupture. Mitral surgery corrects the damage, but the underlying causes of DDMV are not corrected. Thus, progression of the disease and affectation of additional chordae may be at the basis of the late complications and the recurrent mitral regurgitation which occurs several years after surgery. Our results indicate that a more aggressive approach to surgery may be needed.