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Scanning and transmission electron microscopic studies on isolated ruptures of chordae tendineae
Abstract:
Electron microscopic studies of chordae tendineae of the mitral valve were carried out in 17 patients who underwent mitral valve replacement due to a spontaneously isolated rupture of chordae tendineae. The normal chordae, used as the control group, were obtained at autopsy from 5 patients who died from extracardiac causes and were compared with the ruptured chordae. In all patients with chordal rupture, scanning electron microscopy showed perforations of the chordae tendineae, with extensive desquamation and disruption of the endothelial cells and wide-spread destruction of the collagen fiber bundles in the central collagenous core. These pathological findings were not observed in the normal chordae from the control group. Transmission electron microscopy showed that the ruptured chordae were characterized by heterogeneous collagen fibrils with intrinsic structural alterations and disorganization in fibril arrangement. There was a wide variation in the diameters of collagen fibrils which always showed abnormal morphology, with abnormally large, peculiarly shaped fibrils. Apparent loss and/or a disordered arrangement of the typical periodicity of the fibrils were frequently observed. In addition, various degrees of degenerative changes of collagen tissue were often present. These abnormalities were never seen in the fibrils of the normal chordae, and were observed consistently in both the fibrils of the ruptured chordae and in the macroscopically intact chordae in the group with spontaneous rupture of chordae tendineae. These results suggest that a defective organization of collagen into fibrils and fibers, associated with secondary degeneration of collagen within the central collagenous core of the chordae tendineae, are important pathogenetic mechanisms for spontaneously 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.

