A 14-year-old 4.5-kg (9.9-lb) neutered male domestic shorthair cat was referred to a veterinary teaching hospital for evaluation of a sudden onset of dyspnea 12 hours prior to referral. The cat's dyspnea was suspected to be secondary to left-sided congestive heart failure (CHF) on the basis of the physical and radiographic examination findings reported by the referring veterinarian. The cat was treated with an IV bolus of furosemidea (1 mg/kg [0.45 mg/lb]) every 4 hours. Following improvement in its respiratory pattern, the cat was referred for further evaluation.
At the referral evaluation, the cat was bright, alert, and
Objective—To evaluate morphologic changes in
valvular interstitial cells of dogs and to find evidence
for disease-associated phenotypic changes in these
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)
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
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;
Objective—To identify the most frequent underlying diseases in dogs examined because of dyspnea and determine whether signalment, clinical signs, and duration of clinical signs might help guide assessment of the underlying condition and prognosis.
Design—Retrospective case series.
Animals—229 dogs with dyspnea.
Procedures—Case records of dogs referred for dyspnea were reviewed and grouped according to location or etiology (upper airway, lower respiratory tract, pleural space, cardiac diseases, or obesity and stress). Signalment, clinical signs at initial examination, treatment, and survival time were analyzed.
Results—Upper airway (n = 74 [32%]) and lower respiratory tract (76 [33%]) disease were the most common diagnoses, followed by pleural space (44 [19%]) and cardiac (27 [12%]) diseases. Dogs with upper airway and pleural space disease were significantly younger than dogs with lower respiratory tract and cardiac diseases. Dogs with lower respiratory tract and associated systemic diseases were significantly less likely to be discharged from the hospital. Dogs with diseases that were treated surgically had a significantly better outcome than did medically treated patients, which were significantly more likely to be examined on an emergency basis with short duration of clinical signs.
Conclusions and Clinical Relevance—In dogs examined because of dyspnea, young dogs may be examined more frequently with breed-associated upper respiratory tract obstruction or pleural space disease after trauma, whereas older dogs may be seen more commonly with progressive lower respiratory tract or acquired cardiac diseases. Nontraumatic acute onset dyspnea is often associated with a poor prognosis, but stabilization, especially in patients with cardiac disease, is possible. Obesity can be an important contributing or exacerbating factor in dyspneic dogs.
Objective—To compare myocardial cytokine expression in dogs with naturally occurring cardiac or systemic diseases and dogs without cardiac or systemic diseases (control dogs)
Sample—Myocardial tissue samples from 7 systemic disease-affected dogs (SDDs), 7 cardiac disease-affected dogs (CDDs), and 8 control dogs.
Procedures—mRNA expression of interleukin (IL)-1, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, transforming growth factor (TGF)-β1, TGF-β2, TGF-β3, and growth differentiation factor-15 in myocardial tissue samples obtained from CDDs, SDDs, and control dogs were analyzed via quantitative PCR assays.
Results—In control dogs, only mRNA for TNF-α, TGF-β1, and TGF-β3 was detected; concentrations were significantly higher in male than in female dogs. In SDDs and CDDs, all cytokines, growth factors, and growth differentiation factor-15 were expressed. Compared with findings in SDDs, IL-1, IL-6, IL-8, IL-10, TNF-α, and IFN-γ expression was significantly increased in CDDs; specifically, IL-1, IL-8, TNF-α, TGF-β1, and TGF-β3 expression was increased in the atria and IL-8, IL-10, TNF-α, and IFN-γ expression was increased in the ventricles of CDDs.
Conclusions and Clinical Relevance—Data suggested that the alterations in cytokine expression in SDDs and CDDs, compared with control dog findings, were a result of inflammatory system activation. The differences in cytokine expression in atria and ventricles between SDDs and CDDs were suggestive of different remodeling processes. A better knowledge of myocardial involvement in SDDs and of immune regulation in CDDs might beneficially affect morbidity and mortality rates and provide new treatment approaches.
Objective—To compare the degree of mRNA expression for matrix metalloproteinases (MMPs), tissue inhibitors (TIMPs), and lysyl oxidase in myocardial samples from dogs with cardiac and systemic diseases and from healthy control dogs.
Sample—Myocardial samples from the atria, ventricles, and septum of 8 control dogs, 6 dogs with systemic diseases, 4 dogs with dilated cardiomyopathy (DCM), and 5 dogs with other cardiac diseases.
Procedures—Degrees of mRNA expression for MMP-1, -2, -3, -9, and -13; TIMP-1, -2, -3, and -4; and lysyl oxidase were measured via quantitative real-time PCR assay. Histologic examination of the hearts was performed to identify pathological changes.
Results—In myocardial samples from control dogs, only TIMP-3 and TIMP-4 mRNA expression was detected, with a significantly higher degree in male versus female dogs. In dogs with systemic and cardiac diseases, all investigated markers were expressed, with a significantly higher degree of mRNA expression than in control dogs. Furthermore, the degree of expression for MMP-2, TIMP-1, and TIMP-2 was significantly higher in dogs with DCM than in dogs with systemic diseases and cardiac diseases other than DCM. Expression was generally greater in atrial than in ventricular tissue for MMP-2, MMP-13, and lysyl oxidase in samples from dogs with atrial fibrillation.
Conclusions and Clinical Relevance—Degrees of myocardial MMP, TIMP, and lysyl oxidase mRNA expression were higher in dogs with cardiac and systemic diseases than in healthy dogs, suggesting that expression of these markers is a nonspecific consequence of end-stage diseases. Selective differences in the expression of some markers may reflect specific pathogenic mechanisms and may play a role in disease progression, morbidity and mortality rates, and treatment response.