Peer-reviewed veterinary case report
Cell changes in mitral valve disease in Cavalier King Charles
By Lu, C-C et al.·Published in Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology·2016·Royal (Dick) School of Veterinary Studies and The Roslin Institute, United Kingdom·View original on PubMed →
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Original publication title: Comparison of cellular changes in Cavalier King Charles spaniel and mixed breed dogs with myxomatous mitral valve disease.
- Species:
- dog
Plain-English summary
A group of Cavalier King Charles spaniels and mixed breed dogs with severe myxomatous mitral valve disease (MMVD) were studied to see if there were differences in their heart valve cells. The researchers found that both breeds showed similar cellular changes, with increased numbers of certain cells in the valves of dogs with MMVD compared to healthy dogs. While there were no significant differences between the breeds, the Cavalier King Charles spaniels had more specific cell types present. This suggests that the disease affects both breeds similarly, which could help veterinarians in diagnosing and treating MMVD in dogs.
People also search for: Cavalier King Charles spaniel heart disease symptoms · myxomatous mitral valve disease treatment for dogs · mixed breed dog heart problems
Abstract
INTRODUCTION: The aim of this study was to determine if there are differences in cellular changes in Cavalier King Charles spaniel (CKCS) myxomatous mitral valves compared to non-CKCS dogs. ANIMALS: Cavalier King Charles spaniels (n = 6) and age-matched mixed breed (n = 6) with severe myxomatous mitral valve disease (MMVD), and normal mixed breed (n = 4) dogs. MATERIALS AND METHODS: Immunohistochemistry staining and qualitative and quantitative analysis of mitral valves sections, examining for the presence of CD11c and CD45, vimentin, alpha smooth muscle actin (α-SMA) and embryonic smooth muscle myosin heavy chain (Smemb), von Willebrand factor and CD31 and Ki-67. RESULTS: Vimentin positive cell numbers were increased in the MMVD dogs and distributed throughout the valve with greatest density close to the endothelium. There were no significant differences in cell marker expression for the two diseased groups, but cell numbers were significantly increased compared to controls for α-SMA (CKCS only) and Smemb (CKCS and mixed breed: p < 0.05). Alpha smooth muscle actin+ cells were primarily located at the valve edge, with Smemb+ cells similarly located, but also present throughout the valve stroma. A small number of cells close to the valve edge co-expressed α-SMA and Smemb. Endothelial von Willebrand factor expression was identified in all valves, with evidence of disrupted endothelium in the diseased, but was also found in diseased valve stroma. There was no staining for CD11c, CD45 or CD31 in any valve. Ki-67+ cells formed linear clusters at the leaflet tip and were sparsely distributed throughout both myxomatous valve groups. CONCLUSIONS: The cellular changes notes with advanced stage MMVD appear similar for CKCS when compared to mixed breed dogs.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/26860643/