Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.

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Background and Aim: Left ventricular myocardial remodeling could play an important role in the progression of chronic heart failure (CHF) syndrome in dogs with mitral valve endocardiosis. The aim of this study was to evaluate the left ventricular myocardial remodeling in dogs with mitral valve endocardiosis and to study the dependence of the incidence of this pathological phenomenon on the functional class (FC) of progression of the CHF syndrome. Materials and Methods: A total of 108 afflicted dogs and 36 clinically healthy dogs were examined using transthoracic echocardiography. The following structural and geometric parameters of the left ventricular remodeling were evaluated: Myocardial mass and its index, sphericity index at the end of systole and diastole, end-systolic and end-diastolic relative wall thickness, and integral remodeling index. Results: In all clinically healthy dogs, a normal type of the left ventricular chamber geometry was revealed, whereas, in dogs with mitral valve endocardiosis, the normal geometry of the left ventricle occurred in 56.4%, eccentric hypertrophy in 24.1%, concentric remodeling in 10.2%, and concentric hypertrophy in 9.3% of the cases. In patients with endocardiosis, there was no dilatation type of cardiac remodeling observed. Conclusion: When compared to the clinically healthy animals, the dogs with mitral valve endocardiosis presented with indicators of structural and geometric remodeling, such as increased myocardial mass, myocardial mass index, and sphericity index at the end of systole and diastole, as well as relatively reduced integral systolic index of remodeling and systolic relative thickness of the walls of the heart. The parameters of the left ventricular myocardial remodeling correlated significantly with the FC of CHF syndrome.

Background and Aim: It is known that during the early postpartum and lactation periods in dairy cows, metabolic disorders develop, that is, ketosis, which can lead to secondary damage to internal organs. Therefore, it is important to address the issues of changing the lactating cows' clinical, laboratory, and physiological parameters regarding the development of hepatocardial syndrome. This study aimed to provide clinical and diagnostic justification for developing hepatocardial syndrome in highly productive dairy cows. Materials and Methods: The study was conducted on 20 black and white cows in the early postpartum period (7–10 days after birth), with a milk production level of >4500 kg of milk during the previous lactation period, a positive result in the formol colloid sedimentary test, the presence of deafness and splitting of heart sounds, changes in the size, or increased pain sensitivity of the percussion field of the liver. Clinically healthy dairy cows in the early postpartum period were used as controls (n = 24). Clinical, electrocardiographic, echocardiographic, and biochemical parameters were also evaluated. Results: Dairy cows with hepatocardial syndrome developed arterial hypertension and sinus tachycardia, which led to a significant decrease in PQ and QT intervals at ECG. A significant increase in the diastolic size of the interventricular septum, systolic size of the free wall of the left ventricle, and diastolic and systolic sizes of the left ventricle and a significant decrease in the shortening fraction of the left ventricular myocardium were observed in the cows due to the development of hepatocardial syndrome. The affected cows demonstrated a significant increase in serum activity of gamma-glutamyl transferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, troponin, malondialdehyde, diene conjugates, and ceruloplasmin and a decrease in glucose concentration. In addition, they demonstrated decreased activity of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Conclusion: Hepatocardial syndrome in dairy cows occurs due to ketosis, characterized by arterial hypertension, sinus tachycardia, a moderate decrease in myocardial contractility, oxidative stress, and cytolysis of cardiomyocytes and hepatocytes. Therefore, the control and prevention of the development of hepatocardial syndrome will make it possible to maintain the productive health and longevity of dairy cows.

The article presents data on biocenotic diagnostics of 12 farms in the Moscow region that are endowed with endometritis and mastitis in cows, as well as gastrointestinal and respiratory diseases of newborn calves, with the aim of identifying zoo-hygienic, zootechnical and veterinary deficiencies to optimize the strategy for dealing with them. Studies on biocenoses were carried out in 12 farms unsuccessful in cows’ obstetric and gynecological diseases, gastrointestinal and respiratory diseases of newborn calves, with a total number of cattle 12 254, including 4445 cows. For this purpose, field trips were periodically carried out for epizootological examinations of farm biogeocenoses and for the selection of blood serum stabilized with heparin and samples of pathological material for bacteriological, mycological, virological, hematological and immunological studies. It was established that in experimental farms there are no proper conditions to ensure the breaking of the epizootic chain during the infectious process. So, the main factors that contribute to the development and spread of these pathologies are poor food supply, violations of elementary veterinary and sanitary rules for keeping and milking, and failure to fully implement measures to prevent these diseases. An analysis of the epizootic situation for cattle diseases caused by conditionally pathogenic bacteria indicates that farms that are unsuccessful for factor infections have all the conditions for the circulation of pathogens, repeated passage through susceptible animals, the increase in the virulence of conditionally pathogenic microorganisms, and in some cases for appearing pathogenicity in saprophytic bacteria. An effective fight against malignant microbial ecosystems requires in-depth knowledge of the parasitocenoses’ quantitative and species composition, the study of relationships between its individual representatives, the mandatory identification of pure cultures of all its members, and determination of the microbial agents marker biological properties, as well as detailed biocenotic diagnosis of the animal habitat (farm, barn, etc.).