Echocardiographic findings of tricuspid blood cyst mimicking bacterial endocarditis in a dairy cow

The most common endocardial disease in cattle is bacterial endocarditis. The diagnosis of the disease in living animals is mainly based on clinical findings and echocardiographic detection of an irregularly thickened valve. Despite its presumed good sensitivity, little is known on the specificity of transthoracic echocardiography with regards to endocarditis. This case report describes the echocardiographic findings in a dairy cow diagnosed with a chronic inflammatory process, liver and splenic abscesses and tricuspid valve blood cysts that can be mistaken for bacterial endocarditis, thus emphasizing the need to improve antemortem diagnostic tools for endocarditis in cattle.     

Pathologic and clinical features of infectious endocarditis

Infectious endocarditis is a systemic disease associated with high morbidity and mortality. Clinical recognition and effective management is challenging, but insights can be gleaned from relevant pathologic features. Risk factors include subaortic stenosis, possibly certain other congenital anomalies, and bacteremia. Auscultation can provide clues regarding valvular involvment, particularly when a diastolic left basilar murmur of aortic valve regurgitation is present. Aortic valve vegetations and insufficiency may also alter femoral arterial pulse characteristics. Echocardiography may facilitate diagnosis, particularly with aortic valve lesions, but may not be able to distinguish between small mitral valve vegetations and early chronic degenerative valve disease. Vegetative lesions develop along edges of valve closure on the ventricular aspect of the aortic valve and the atrial surface of atrioventricular valves. They may extend across valve leaflet, from valves to adjacent left atrial endocardium, interventricular or interatrial septum, or chordae tendineae. Vegetations can be friable and frequently embolize to spleen, kidney, and left ventricle — often before clinical recognition of the disease. Valvular insufficiency develops as a consequence of valvular vegetations, necrosis, perforation, or rupture of the chordae tendineae. Histopathologic appearance varies with respect to duration of disease and antimicrobial therapy. These factors influence the amount of necrotic material, blood clot, fibrin, and inflammatory cells which make up the vegetations. Bacteria are not always identified in valvular lesions, especially following antibacterial therapy, but may be detected in other organs. Common sequellae include congestive heart failure, sepsis, arrhythmias, and systemic organ infarction.     

Insights into Serotonin Signaling Mechanisms Associated with Canine Degenerative Mitral Valve Disease

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-β 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.     

Cardiac Troponin I Is Associated with Severity of Myxomatous Mitral Valve Disease, Age, and C-Reactive Protein in Dogs

Background: Concentrations of cardiac troponin I (cTnI) and C-reactive protein (CRP) might be associated with cardiac remodeling in dogs with myxomatous mitral valve disease (MMVD). Age- and sex-dependent variations in cTnI concentration have been described.
Objective: To investigate whether plasma concentrations of cTnI and CRP are associated with severity of MMVD, and investigate potential associations of dog characteristics on cTnI and CRP concentrations.
Animals: Eighty-one client-owned dogs with MMVD of varying severity.
Methods: Dogs were prospectively recruited for the study. Dogs were classified according to severity of MMVD. Plasma cTnI was analyzed by a high sensitivity cTnI assay with a lower limit of detection of 0.001 ng/mL, and plasma CRP was analyzed by a canine-specific CRP ELISA.
Results: Higher cTnI concentrations were detected in dogs with moderate (0.014 [interquartile range 0.008–0.029] ng/mL, P = .0011) and severe (0.043 [0.031–0.087] ng/mL, P < .0001) MMVD, compared with healthy dogs (0.001 [0.001–0.004] ng/mL). Dogs with severe MMVD also had higher cTnI concentrations than dogs with mild (0.003 [0.001–0.024] ng/mL, P < .0001) and moderate ( P = .0019) MMVD. There were significant associations of age, CRP, heart rate, and left ventricular end-diastolic diameter, on cTnI concentration C-reactive protein did not differ among severity groups, but was significantly associated with cTnI, breed, and systolic blood pressure on CRP concentration.
Conclusions and Clinical Importance: Analysis of cTnI concentration has potential to increase knowledge of overall cardiac remodeling in dogs with MMVD. However, effect of age on cTnI needs consideration when assessing cTnI.     

Effect of Pimobendan on Echocardiographic Values in Dogs with Asymptomatic Mitral Valve Disease

Background: Pimobendan (PIMO) is a novel inodilator that has shown promising results in the treatment of advanced mitral valve disease (MVD), but little is known about its hemodynamic effects, especially regarding the mitral regurgitant volume in naturally occurring MVD.
Hypothesis: The addition of pimobendan to treatment decreases the regurgitant fraction (RF) in dogs with asymptomatic MVD.
Animals: Twenty-four client-owned dogs affected by International Small Animal Cardiac Health Council class Ib MVD.
Methods: Prospective, blinded, and controlled clinical trial. Dogs were assigned to a PIMO treatment group (n = 19) (0.2–0.3 mg/kg q12h) or a control group (n = 5). Echocardiographic evaluations were performed over a 6-month period.
Results: The addition of PIMO to treatment did not decrease the RF of dogs affected by asymptomatic class 1b MVD over the study period ( P = .85). There was a significant increase in the ejection fraction of the PIMO treated dogs at 30 days (80.8 ± 1.42 versus 69.0 ± 2.76, corrected P = .0064), and a decrease in systolic left ventricular diameter (corrected P = .011) within the PIMO group compared with baseline. However, this improvement in systolic function was not sustained over the 6-month trial period.
Conclusion and Clinical Importance: This study did not identify beneficial long-term changes in the severity of mitral regurgitation after addition of PIMO to angiotensin converting enzyme inhibitor treatment of dogs with asymptomatic MVD.