Development of an artificial intelligence-based method for the diagnosis of the severity of myxomatous mitral valve disease from canine chest radiographs.

An algorithm based on artificial intelligence (AI) was developed and tested to classify different stages of myxomatous mitral valve disease (MMVD) from canine thoracic radiographs. The radiographs were selected from the medical databases of two different institutions, considering dogs over 6 years of age that had undergone chest X-ray and echocardiographic examination. Only radiographs clearly showing the cardiac silhouette were considered. The convolutional neural network (CNN) was trained on both the right and left lateral and/or ventro-dorsal or dorso-ventral views. Each dog was classified according to the American College of Veterinary Internal Medicine (ACVIM) guidelines as stage B1, B2 or C + D. ResNet18 CNN was used as a classification network, and the results were evaluated using confusion matrices, receiver operating characteristic curves, and t-SNE and UMAP projections. The area under the curve (AUC) showed good heart-CNN performance in determining the MMVD stage from the lateral views with an AUC of 0.87, 0.77, and 0.88 for stages B1, B2, and C + D, respectively. The high accuracy of the algorithm in predicting the MMVD stage suggests that it could stand as a useful support tool in the interpretation of canine thoracic radiographs.

A Recurrent Inflammatory Myofibroblastic Tumor-like Lesion of the Splenic Capsule in a Kitten: Clinical, Microscopic and Ultrastructural Description.

OBJECTIVE: To describe the findings of an unusual splenic tumor in a kitten. METHODS: A grossly multinodular mass arising from the splenic capsule of a 7-month-old male Havana kitten was echographically detected and surgically removed by splenectomy, then analyzed microscopically and ultrastructurally. RESULTS: The mass showed features of an inflammatory myofibroblastic tumor. TREATMENT AND OUTCOME: Two months after surgical excision, the mass recurred in the same intra-abdominal area but disappeared after 2 months of anti-inflammatory therapy. Follow-up at 18 months after surgery revealed resolution of the disease. CLINICAL RELEVANCE: Inflammatory myofibroblastic tumor in cats have been rarely reported and are usually in the orbital region. In the present report, an unusual multinodular gross presentation, a recurrence over time, and a favorable clinical course, are described.

Congenital heart disease in boxer dogs: results of 6 years of breed screening.

The aim of this study was to analyse the results of 6years (1999-2004) of mandatory breed screening for congenital heart disease in Boxer dogs using physical examination and echocardiography. Records of 1283 Boxers were reviewed and 165 dogs (12.86%) were found to be affected by heart disease, with aortic and pulmonic stenosis being the most frequent cardiac lesions. Comparison of these results with those of a previous survey showed a lower overall prevalence of both outflow obstructions, particularly of the more severe forms. A male predisposition for both aortic and pulmonic stenosis was evident from the study. Consistent with reports from other countries, soft left basilar heart murmurs were detected in both healthy dogs and dogs affected with congenital heart disease.

Different cardiovascular potential of adult- and fetal-type mesenchymal stem cells in a rat model of heart cryoinjury.

Efficacy of adult (bone marrow, BM) versus fetal (amniotic fluid, AF) mesenchymal stem cells (MSCs) to replenish damaged rat heart tissues with new cardiovascular cells has not yet been established. We investigated on the differentiation potential of these two rat MSC populations in vitro and in a model of acute necrotizing injury (ANI) induced by cryoinjury. Isolated BM-MSCs and AF-MSCs were characterized by flow cytometry and cytocentrifugation and their potential for osteogenic, adipogenic, and cardiovascular differentiation assayed in vitro using specific induction media. The left anterior ventricular wall of syngeneic Fisher 344 (n = 48) and athymic nude (rNu) rats (n = 6) was subjected to a limited, nontransmural epicardial ANI in the approximately one third of wall thickness without significant hemodynamic effects. The time window for in situ stem cell transplantation was established at day 7 postinjury. Fluorochrome (CMTMR)-labeled BM-MSCs (2 x 10(6)) or AF-MSCs (2 x 10(6)) were injected in syngeneic animals (n = 26) around the myocardial lesion via echocardiographic guidance. Reliability of CMTMR cell tracking in this context was ascertained by transplanting genetically labeled BM-MSCs or AF-MSCs, expressing the green fluorescent protein (GFP), in rNu rats with ANI. Comparison between the two methods of cell tracking 30 days after cell transplantation gave slightly different values (1420,58 +/- 129,65 cells/mm2 for CMTMR labeling and 1613.18 +/- 643.84 cells/mm2 for genetic labeling; p = NS). One day after transplantation about one half CMTMR-labeled AF-MSCs engrafted to the injured heart (778.61 +/- 156.28 cells/mm2) in comparison with BM-MSCs (1434.50 +/- 173.80 cells/mm2, p < 0.01). Conversely, 30 days after cell transplantation survived MSCs were similar: 1275.26 +/- 74.51/mm2 (AF-MSCs) versus 1420.58 +/- 129.65/mm2 for BM-MSCs (p = NS). Apparent survival gain of AF-MSCs between the two time periods was motivated by the cell proliferation rate calculated at day 30, which was lower for BM-MSCs (6.79 +/- 0.48) than AF-MSCs (10.83 +/- 3.50; p < 0.01), in the face of a similar apoptotic index (4.68 +/- 0.20 for BM-MSCs and 4.16 +/- 0.58 for AF-MSCs; p = NS). These cells were also studied for their expression of markers specific for endothelial cells (ECs), smooth muscle cells (SMCs), and cardiomyocytes (CMs) using von Willebrand factor (vWf), smooth muscle (SM) alpha-actin, and cardiac troponin T, respectively. Grafted BM-MSCs or AF-MSCs were found as single cell/small cell clusters or incorporated in the wall of microvessels. A larger number of ECs (227.27 +/- 18.91 vs. 150.36 +/- 24.08 cells/mm2, p < 0.01) and CMs (417.91 +/- 100.95 vs. 237.43 +/- 79.99 cells/mm2, p < 0.01) originated from AF-MSCs than from BM-MSCs. Almost no SMCs were seen with AF-MSCs, in comparison to BM-MSCs (98.03 +/- 40.84 cells/mm2), in concordance with lacking of arterioles, which, instead, were well expressed with BM-MSCs (71.30 +/- 55.66 blood vessels/mm2). The number of structurally organized capillaries was slightly different with the two MSCs (122.49 +/- 17.37/mm2 for AF-MSCs vs. 148.69 +/- 54.41/mm2 for BM-MSCs; p = NS). Collectively, these results suggest that, in the presence of the same postinjury microenvironment, the two MSC populations from different sources are able to activate distinct differentiation programs that potentially can bring about a myocardial-capillary or myocardial-capillary-arteriole reconstitution.

Prognostic indicators for dogs with dilated cardiomyopathy.

The purpose of this study was to investigate the prognostic value of various clinical, ECG, echocardiographic, and Doppler echocardiographic variables in dogs with dilated cardiomyopathy. The relationship to survival of 11 variables was evaluated in 63 dogs. Studied variables were age at time of diagnosis, class of heart failure (HF), dyspnea, ascites, atrial fibrillation (AF), ejection fraction (EF), E-point septal separation, end-diastolic volume index, end-systolic volume index (ESV-I), and restrictive or nonrestrictive transmitral flow (TMF) pattern. Median survival time was 671 days (lower 95% confidence limit, 350 days). Survival curves showed that severity of HF, ascites, ESV-I greater than 140 mL/m2, EF less than 25%, and restrictive TMF pattern had a significant negative relation to survival time. Thirty-nine dogs with both sinus rhythm and AF presented adequate TMF recordings; in these dogs, after stratification by TMF pattern, the restrictive TMF pattern was the most important negative prognostic indicator. We conclude that in dogs with dilated cardiomyopathy the restrictive TMF pattern appears to represent a useful prognostic indicator. Class of HF, ascites, ESV-I, and EF are also useful indexes if an adequate TMF pattern is not recorded.

Asymptomatic double ureteral stricture in an 8-month-old Maine Coon cat: an imaging-based case report.

Congenital ureteral strictures are rare both in human and veterinary medicine. While the diagnosis is generally made after a symptomatic or febrile urinary tract infection, we report here a case in which this condition represented an incidental finding during routine ultrasonography. To the best of the authors' knowledge imaging findings of a double monolateral ureteral stricture have not previously been reported.

Cardiac sympathetic neurons provide trophic signal to the heart via ß2-adrenoceptor-dependent regulation of proteolysis.

AIMS: Increased cardiac sympathetic neuron (SN) activity has been associated with pathologies such as heart failure and hypertrophy, suggesting that cardiac innervation regulates cardiomyocyte trophism. Whether continuous input from the SNs is required for the maintenance of the cardiomyocyte size has not been determined thus far. METHODS AND RESULTS: To address the role of cardiac innervation in cardiomyocyte size regulation, we monitored the effect of pharmacological sympathetic denervation in mice on cardiac structure, function, and signalling from 24 h to 30 days in the absence of other pathological stimuli. SN ablation caused an immediate reduction in the cardiomyocyte size with minimal consequences on the resting contractile function. Atrophic remodelling was mediated by the ubiquitin-proteasome system through FOXO-dependent early induction of the muscle-specific E3 ubiquitin ligases Atrogin-1/MAFbx and MuRF1, which was followed by activation of the autophagy-lysosome system. MuRF1 was found to be determinant in denervation atrophy as remodelling did not develop in denervated MuRF1 knock-out (KO) hearts. These effects were caused by decreased basal stimulation of cardiomyocyte ß2-adrenoceptor (AR), as atrophy was prevented by treatment of denervated mice with the ß2-AR agonist clenbuterol. Consistent with these data, we also observed that ß2-AR KO mice showed cardiac atrophy at rest. CONCLUSION: Cardiac SNs are strong regulators of the cardiomyocyte size via ß2-AR-dependent repression of proteolysis, demonstrating that the neuro-cardiac axis operates constitutively for the determination of the physiological cardiomyocyte size. These results are of great clinical relevance given the role of ß-AR in cardiovascular diseases and their modulation in therapy.

Pulmonary hypertension in dogs with mitral regurgitation attributable to myxomatous valve disease.

Pulmonary hypertension has been associated with mitral insufficiency caused by chronic degenerative valve disease in dogs. Our aim was to search for associations between left atrial to aortic root ratio, end-systolic and end-diastolic volume indices, and changes in the right ventricular to right atrial pressure gradient as estimated by the peak velocity of tricuspid regurgitation in dogs with chronic degenerative valve disease and different classes of heart failure. Dogs, for which follow-up was available were evaluated for changes in the right ventricular to right atrial systolic pressure gradient over time. Three hundred and forty-four dogs were studied; 51 in the International Small Animal Cardiac Health Council class la, 75 in class 1b, 113 in class 2, 97 in class 3a, and 8 in class 3b. The mean values for right ventricular to right atrial systolic pressure gradient, end-systolic volume index, end-diastolic volume index, and left atrial to aortic ratio were 49.2 +/- 17.1 mmHg, 149.12 +/- 60.8 and 37.7 +/- 21.6 ml/m2, and 1.9 +/- 0.5, respectively. A weak positive correlation was found between the right ventricular to right atrial systolic pressure gradient and the left atrial to aorta ratio (r = 0.242, P < 0.0001), end-diastolic volume index (r = 0.242, P < 0.0001), and end-systolic volume index (r = 0.129, P < 0.001). Follow up was available for 49 dogs. Of these, 18 had an increased, 12 a decreased, and 19 a stable right ventricular to right atrial systolic pressure gradient despite therapy. The equivalence point between the sensitivity and specificity curves of about 80% in the coincident point corresponded to a right ventricular to right atrial systolic pressure gradient of 48 mmHg. Our results suggest an association between the progressive nature of chronic degenerative mitral valve disease and pulmonary hypertension. It is of clinical interest that, with a right ventricular to right atrial systolic pressure gradient pressure gradient at or above 48 mmHg, pulmonary hypertension does not appear to improve despite therapy targeted at lowering the left atrial load.

Comparison of primary mitral valve disease in German Shepherd dogs and in small breeds.

The case records of 58 German Shepherds (GS group) affected by mitral valve prolapse (MVP) and/or mitral valve regurgitation (MR), and 49 dogs weighing < 15 kg (D group), affected by chronic valvular disease (CVD) were reviewed. The dogs of the GS group were presented more often without a detectable heart murmur (p < 0.01), and less frequently with a high intensity heart murmur (p < 0.01). Atrial fibrillation (AF) was more common in the GS group (p < 0.001). MVP associated with mitral valve thickening was more common in the D group (p < 0.001). Fractional shortening (FS) was lower (p < 0.0001) and end-systolic volume index (ESV-I) was increased (p < 0.0001) in the GS group, whereas end-diastolic volume index (EDV-I) did not differ between the 2 groups. Prevalence and severity of pulmonary hypertension were similar in the 2 groups. Dogs with mitral valve disease weighing more than 20 kg had a 5.8 higher chance of developing decreased FS, increased ESV-I, AF and ventricular arrhythmias. In the GS group, the decreased FS and increased ESV-I were not associated with the presence of AF or ventricular arrhythmias (p > 0.05). It appears that GS may be affected both by mitral valve prolapse and mitral insufficiency. It also appears that a comparatively large proportion of GS shows no major mitral valve thickening or MVP, but still presents with significant mitral regurgitation, possibly suggesting a different cause for the important incompetence observed in most cases.