ArticleVeterinary world2019
Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy.
Article in Veterinary world, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 30 citations in OpenAlex.
- Neutrophil-to-lymphocyte ratio and red blood cell distribution width to platelet ratio and their relationships with inflammatory and antioxidant status in dogs with different stages of heart failure due to myxomatous mitral valve disease.Veterinary research communications · 2024Article
- Clinical and diagnostic characteristics of the development of hepatocardial syndrome in black and white cows in the early lactation period.Veterinary world · 2022Article
- Fecal Microbiota Analysis in Cats with Intestinal Dysbiosis of Varying Severity.Pathogens (Basel, Switzerland) · 2022Article
- The role of lipid peroxidation products and antioxidant enzymes in the pathogenesis of aseptic and purulent inflammation in cats.Journal of advanced veterinary and animal research · 2021Article
- Search for Promising Strains of Probiotic Microbiota Isolated from Different Biotopes of Healthy Cats for Use in the Control of Surgical Infections.Pathogens (Basel, Switzerland) · 2021Article
- Changes of inflammatory and oxidative stress biomarkers in dogs with different stages of heart failure.BMC veterinary research · 2020Article
- Left ventricular myocardial remodeling in dogs with mitral valve endocardiosis.Veterinary world · 2019Article
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Authors and funding
10 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundDilated 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.
aimThis study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. MATERIALS AND
methodsThe 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).
resultsIn 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.
conclusionThe 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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