Home About us Contact
|
Home About us Contact | ||
|
|
||
Degenerative Mitral Valve Disease (degenerative + mitral_valve_disease)
Kinds of Degenerative Mitral Valve Disease Selected AbstractsInsights into Serotonin Signaling Mechanisms Associated with Canine Degenerative Mitral Valve DiseaseJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010M.A. Oyama Little is known about the molecular abnormalities associated with canine degenerative mitral valve disease (DMVD). The pathology of DMVD involves the differentiation and activation of the normally quiescent mitral valvular interstitial cell (VIC) into a more active myofibroblast phenotype, which mediates many of the histological and molecular changes in affected the valve tissue. In both humans and experimental animal models, increased serotonin (5-hydroxytryptamine, 5HT) signaling can induce VIC differentiation and myxomatous valve damage. In canine DMVD, numerous lines of evidence suggest that 5HT and related molecules such as transforming growth factor-, play a critical role in the pathogenesis of this disease. A variety of investigative techniques, including gene expression, immunohistochemistry, protein blotting, and cell culture, shed light on the potential role of 5HT in the differentiation of VIC, elaboration of myxomatous extracellular matrix components, and activation of mitogen-activated protein kinase pathways. These studies help support a hypothesis that 5HT and its related pathways serve as an important stimulus in canine DMVD. This review describes the pathological characteristics of canine DMVD, the organization and role of the 5HT pathway in valve tissue, involvement of 5HT in human and experimental models of valve disease, avenues of evidence that suggest a role for 5HT in naturally occurring DMVD, and finally, a overarching hypothesis describing a potential role for 5HT in canine DMVD. [source] Evaluation of Pimobendan and N-Terminal Probrain Natriuretic Peptide in the Treatment of Pulmonary Hypertension Secondary to Degenerative Mitral Valve Disease in DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2009K.J. Atkinson Background: Pimobendan is a positive inotrope and vasodilator that may be useful in the treatment of pulmonary hypertension (PHT) secondary to degenerative mitral valve disease. Hypothesis: Pimobendan decreases the severity of PHT measured echocardiographically and improves quality-of-life scores. Changes in N-terminal probrain natriuretic peptide (NT-proBNP) concentrations will reflect improvement in severity of PHT. Animals: Ten client-owned dogs with peak tricuspid regurgitant flow velocity (TRFV) ,3.5 m/s. Methods: Prospective short-term, double-blinded, crossover design, with a long-term, open-label component. Short term, dogs were randomly allocated to receive either placebo or pimobendan (0.18,0.3 mg/kg PO q12 h) for 14 days. After a 1-week washout, they received the alternative treatment for 14 days, followed by pimobendan open-label for 8 weeks. Results: Short-term comparison: peak TRFV decreased in all dogs on pimobendan compared with placebo from a median of 4.40 (range, 3.2,5.6) to 3.75 (range, 2.4,4.8) m/s (P < .0001). NT-proBNP concentration decreased after treatment with pimobendan from a median of 2,143 (range, 450,3,981) to 1,329 (range, 123,2,411) pmol/L (P= .0009). All dogs improved their quality-of-life score (P= .006). In the long-term comparisons, peak TRFV decreased in all dogs from a median of 4.28 (range, 3.5,5.7) to 3.52 (range, 2.4,5.0) m/s (P < .0001). No significant changes in NT-proBNP or quality-of-life scores were detected. Conclusions and Clinical Importance: Pimobendan lowered severity of measurable PHT, improved quality-of-life scores, and decreased NT-proBNP concentrations short-term. Long term, only the reduction in TRFV was maintained. [source] N-terminal pro B-type natriuretic peptide and left ventricular diameter independently predict mortality in dogs with mitral valve diseaseJOURNAL OF SMALL ANIMAL PRACTICE, Issue 2 2010W. Moonarmart Objectives: To determine whether natriuretic peptide concentrations would predict all cause mortality in dogs with degenerative mitral valve disease. Methods: One hundred dogs with naturally occurring degenerative mitral valve disease were prospectively recruited for this longitudinal study. Analysis of outcome was undertaken for 73 dogs for which the outcome was known. Dogs underwent physical examination, electrocardiography and echocardiography. Natriuretic peptide concentrations were measured by Enzyme-linked immunosorbent assay. The ability of natriuretic peptide concentrations, clinical, electrocardiographic and echocardiographic data, to predict all cause mortality was determined using univariable and multivariable Cox proportional hazards analyses. Results: Thirty dogs died during the period of follow-up. Two variables were independently predictive of all cause mortality; these were the normalised left ventricular end-diastolic diameter and the N-terminal pro B-type natriuretic peptide concentration. An increase of the left ventricular end-diastolic diameter by 0.1 increased the hazard of all cause mortality by 20% (95% confidence interval: 4 to 37%, P=0.01) and a 100 pmol/l increase in N-terminal pro B-type natriuretic peptide increased the hazard by 7% (95 confidence interval: 2 to 11%, P=0.003). Clinical Significance: N-terminal pro B-type natriuretic peptide concentration and left ventricular end-diastolic diameter are significantly and independently predictive of all cause mortality in dogs with degenerative mitral valve disease. [source] Neurohormonal activation in canine degenerative mitral valve disease: implications on pathophysiology and treatmentJOURNAL OF SMALL ANIMAL PRACTICE, Issue 2009M. A. Oyama Neurohormonal systems play a critical role in canine degenerative mitral valve disease (DMVD). DMVD results in mitral regurgitation, which reduces forward cardiac output and increases intracardiac pressures. These changes trigger neurohormonal responses that ultimately result in maladaptive cardiac remodelling, congestion and heightened morbidity and mortality. Medical therapies such as ACE inhibitors and spironolactone derive their benefit by interrupting or suppressing these neurohormonal responses. Thus, knowledge of neurohormonal mechanisms can lead to a better understanding of how to treat DMVD. [source] Insights into Serotonin Signaling Mechanisms Associated with Canine Degenerative Mitral Valve DiseaseJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010M.A. Oyama Little is known about the molecular abnormalities associated with canine degenerative mitral valve disease (DMVD). The pathology of DMVD involves the differentiation and activation of the normally quiescent mitral valvular interstitial cell (VIC) into a more active myofibroblast phenotype, which mediates many of the histological and molecular changes in affected the valve tissue. In both humans and experimental animal models, increased serotonin (5-hydroxytryptamine, 5HT) signaling can induce VIC differentiation and myxomatous valve damage. In canine DMVD, numerous lines of evidence suggest that 5HT and related molecules such as transforming growth factor-, play a critical role in the pathogenesis of this disease. A variety of investigative techniques, including gene expression, immunohistochemistry, protein blotting, and cell culture, shed light on the potential role of 5HT in the differentiation of VIC, elaboration of myxomatous extracellular matrix components, and activation of mitogen-activated protein kinase pathways. These studies help support a hypothesis that 5HT and its related pathways serve as an important stimulus in canine DMVD. This review describes the pathological characteristics of canine DMVD, the organization and role of the 5HT pathway in valve tissue, involvement of 5HT in human and experimental models of valve disease, avenues of evidence that suggest a role for 5HT in naturally occurring DMVD, and finally, a overarching hypothesis describing a potential role for 5HT in canine DMVD. [source] Evaluation of Pimobendan and N-Terminal Probrain Natriuretic Peptide in the Treatment of Pulmonary Hypertension Secondary to Degenerative Mitral Valve Disease in DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2009K.J. Atkinson Background: Pimobendan is a positive inotrope and vasodilator that may be useful in the treatment of pulmonary hypertension (PHT) secondary to degenerative mitral valve disease. Hypothesis: Pimobendan decreases the severity of PHT measured echocardiographically and improves quality-of-life scores. Changes in N-terminal probrain natriuretic peptide (NT-proBNP) concentrations will reflect improvement in severity of PHT. Animals: Ten client-owned dogs with peak tricuspid regurgitant flow velocity (TRFV) ,3.5 m/s. Methods: Prospective short-term, double-blinded, crossover design, with a long-term, open-label component. Short term, dogs were randomly allocated to receive either placebo or pimobendan (0.18,0.3 mg/kg PO q12 h) for 14 days. After a 1-week washout, they received the alternative treatment for 14 days, followed by pimobendan open-label for 8 weeks. Results: Short-term comparison: peak TRFV decreased in all dogs on pimobendan compared with placebo from a median of 4.40 (range, 3.2,5.6) to 3.75 (range, 2.4,4.8) m/s (P < .0001). NT-proBNP concentration decreased after treatment with pimobendan from a median of 2,143 (range, 450,3,981) to 1,329 (range, 123,2,411) pmol/L (P= .0009). All dogs improved their quality-of-life score (P= .006). In the long-term comparisons, peak TRFV decreased in all dogs from a median of 4.28 (range, 3.5,5.7) to 3.52 (range, 2.4,5.0) m/s (P < .0001). No significant changes in NT-proBNP or quality-of-life scores were detected. Conclusions and Clinical Importance: Pimobendan lowered severity of measurable PHT, improved quality-of-life scores, and decreased NT-proBNP concentrations short-term. Long term, only the reduction in TRFV was maintained. [source] | ||||||||||