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Abstract

Objective—To evaluate morphologic changes in valvular interstitial cells of dogs and to find evidence for disease-associated phenotypic changes in these cells.

Animals—5 clinically normal dogs and 5 dogs with severe mitral valve endocardiosis.

Procedure—Mitral valve leaflets were evaluated by use of transmission electron microscopy. Differences in cell type and cell location were identified.

Results—A change in cell type toward a myofibroblast or smooth muscle cell phenotype was detected, with the smooth muscle cell type being most common. These cells had long amorphous cytoplasmic extensions, fibrillar cytoplasm, incomplete basal lamina, few mitochondria, and eccentrically placed nuclei but lacked smooth endoplasmic reticulum or Golgi complexes. Remaining valvular interstitial cells had heterochromatic nuclei and produced only minimal quantities of collagen. Compared with normal valves, myxomatous valves had many interstitial-like cells located adjacent to the endothelium. Deeper within the abnormal valves, cells with a heterogenous phenotype formed groupings that appeared to be anchored to adjacent collagen.

Conclusions and Clinical Relevance—Myxomatous degeneration of the mitral valve in dogs is associated with phenotypic alteration, changing from an interstitial to a mixed myofibroblast or smooth muscle cell phenotype. A closer association between interstitial cells and the endothelium is evident in diseased valves. In response to the disease process, valvular interstitial cells of dogs appear to change toward a smooth muscle phenotype, possibly in an attempt to maintain valve tone and mechanical function. (Am J Vet Res 2005;66:1408–1414)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To map the cellular distribution and phenotypic alteration of the predominant stromal cell population throughout the entire valve length of dogs with myxomatous mitral valve disease (MMVD).

Sample Population—31 mitral valve complexes (ie, mitral valve leaflets) collected from 4 clinically normal dogs and 27 dogs with MMVD of varying severity.

Procedures—A combination of standard histologic and immunohistochemical techniques was used to identify pathologic changes, the presence of mast cells, and the density and distribution of cells expressing vimentin, desmin, A-smooth muscle actin (A-SMA), smooth muscle myosin, and the macrophage marker MAC387.

Results—Vimentin-positive cells predominated in the mitral valve leaflets from clinically normal dogs and were located throughout the leaflet, but cell density was appreciably decreased with disease progression, and minimal cell numbers were found in distinct myxomatous areas. Cells that were positive for A-SMA were uncommon in the mitral valve leaflets from clinically normal dogs and only seen in appreciable numbers in mitral valves of dogs with severe late-stage disease, in which cells were typically located close to the ventricularis valve surface. A slight increase in mast cell numbers was observed in the distal zone of affected leaflets.

Conclusions and Clinical Relevance—Activated-myofibroblasts (α-SMA–positive cells) were increased and inactive-myofibroblasts (vimentin-positive cells) were reduced in mitral valve leaflets of dogs with MMVD, compared with that of clinically normal dogs.

Impact on Human Medicine—This is the first description of spatial and temporal alterations in mitral valve cells of any species with MMVD and has clinical importance in the understanding of disease development in dogs and humans.

Full access
in American Journal of Veterinary Research

Abstract

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

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

Procedure—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.

Results—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.

Conclusions and Clinical Relevance—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. (Am J Vet Res 2004; 65:198–206)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To map aspects of the innervation of the mitral valve complex and determine any association with the development or progression of myxomatous mitral valve disease (MMVD) in dogs.

Sample Population—Septal mitral valve leaflets from 11 dogs aged 6 months to > 10 years.

Procedures—Expression of protein gene product 9.5 (general neuronal marker), tyrosine hydroxylase (adrenergic innervation marker), vasoactive intestinal peptide (parasympathetic innervation marker), and calcitonin gene–related peptide (sensory innervation marker) was assessed by use of a standard immunohistochemical technique. Innervation was assessed qualitatively and semiquantitatively. Differences between valvular zones and between groups were analyzed statistically.

Results—MMVD was present in leaflets of all dogs ≥ 5 years of age. Innervation was confirmed in all leaflets but was markedly reduced in leaflets of dogs > 10 years of age. Innervation was most dense at the base of valves and mainly associated with the epimysial, perimysial, and endomysial layers of the muscle and blood vessels within the valve. Innervation was reduced within the middle zone of the valve and lacking at the free edge. Innervation was not identified at the tip of the leaflet, the free edge, or the chordae. Nerve fibers were mostly sympathetic, with the remainder being parasympathetic or sensory. Existence of MMVD did not alter the pattern or density of innervation.

Conclusions and Clinical Relevance—Mitral valve leaflets in the study dogs were innervated, with most of the nerve fibers associated with the myocardium in the valve base. Development of MMVD appeared to precede the reduction of innervation associated with advancing age.

Full access
in American Journal of Veterinary Research