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Am J Vet Res. 2004 Feb;65(2):198-206.

Identification of surface morphologic changes in the mitral valve leaflets and chordae tendineae of dogs with myxomatous degeneration.

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Hospital for Small Animals, Division of Veterinary Clinical Studies, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush Veterinary Centre, Roslin, Mid Lothian, Scotland, UK EH25 9RG.



To describe structural changes in the left atrioventricular (mitral) valve complex of dogs with endocardiosis by use of scanning electron microscopy.


5 clinically normal dogs and 4 dogs with mitral valve endocardiosis.


The mitral valve complex from each dog was fixed and prepared for examination via scanning electron microscopy. Findings in valves from clinically normal and affected dogs were compared to identify surface changes associated with endocardiosis.


Compared with findings in valves from clinically normal dogs, endocardiosis-affected mitral valve complexes had several morphologic abnormalities. Tissue swelling on the edge of valve leaflets, chordae tendineae, and the chordal-papillary muscle junction was evident. Damage to the valve complex endothelium was unevenly distributed; in some areas, denudation of endothelial cells had exposed the basement membrane or subendothelial valve collagen matrix. This damage was most noticeable on the leaflet edges and extended more to the ventricular aspect of the valve than the atrial side. Cell loss also extended to the chordae tendineae but was less apparent at the chordal-papillary muscle junction. The remaining endothelial cells on affected valves were arranged in less-ordered rows and had more plasmalemmal microappendages, compared with cells on unaffected valves.


Morphologic changes associated with mitral valve endocardiosis in dogs were similar to those observed in humans with mitral valve prolapse. In dogs with mitral valve endocardiosis, gross changes in the valve complex may affect hemodynamics in the heart; alterations in the leaflet and chordal endothelium may contribute to pathogenesis of this disease.

[Indexed for MEDLINE]

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