Scanning and transmission electron microscopic studies on isolated ruptures of chordae tendineae

Insights

Spontaneous mitral valve chordae tendineae rupture is linked to defective collagen organization and degeneration. These collagen abnormalities, observed in ruptured and intact tissues, suggest a key role in the condition's pathogenesis.

Area of Science:

  • Cardiovascular Pathology
  • Biomaterials Science
  • Electron Microscopy

Background:

  • Spontaneous rupture of mitral valve chordae tendineae is a significant cause of mitral regurgitation.
  • The underlying pathogenetic mechanisms, particularly at the ultrastructural level, remain incompletely understood.

Purpose of the Study:

  • To investigate the ultrastructural changes in chordae tendineae associated with spontaneous rupture using electron microscopy.
  • To identify potential pathogenetic mechanisms contributing to isolated chordal rupture.

Main Methods:

  • Scanning and transmission electron microscopy were used to examine chordae tendineae from 17 patients with ruptured chordae and 5 control subjects.
  • Comparative analysis of morphological and structural features of collagen fibrils and endothelial cells.

Main Results:

  • Ruptured chordae exhibited perforations, endothelial cell disruption, and destruction of collagen fiber bundles.
  • Abnormal collagen fibrils with heterogeneous diameters, altered morphology, and disordered periodicity were observed in ruptured and intact chordae from affected patients.
  • Degenerative changes in collagen tissue were prevalent in the ruptured group.

Conclusions:

  • Defective collagen organization and secondary degeneration are implicated as primary pathogenetic mechanisms in spontaneous chordae tendineae rupture.
  • Ultrastructural abnormalities in collagen are present even in macroscopically intact chordae within affected individuals.
  • These findings highlight collagen defects as a critical factor in the etiology of isolated chordal rupture.

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