Myocarditis is a major cause of heart failure and death, particularly in young individuals. Current treatments are mainly symptomatic, but emerging therapies focus on targeting inflammation and fibrosis pathways. Natural bioactive compounds like flavonoids and phenolic acids show promising anti-inflammatory and antioxidant properties. Corticosteroids are frequently employed in the treatment of autoimmune myocarditis and appear to lower mortality rates compared to conventional therapies for heart failure. This study aims to explore the effects of Mangiferin on pro-inflammatory cytokine levels, nitro-oxidative stress markers, histopathological alterations, and cardiac function in experimental myosin-induced autoimmune myocarditis. The effects were compared to Prednisone, used as a reference anti-inflammatory compound, and Trolox, used as a reference antioxidant. The study involved 30 male Wistar–Bratislava rats, which were randomly divided into five groups: a negative control group (C−), a positive control group with induced myocarditis using a porcine myosin solution (C+), three groups with induced myocarditis receiving Mangiferin (M), Prednisone (P), or Trolox (T) as treatment. Cardiac function was evaluated using echocardiography. Biochemical measurements of nitro-oxidative stress and inflammatory markers were conducted. Finally, histopathological changes were assessed. At echocardiography, the evaluation of the untreated myocarditis group showed a trend toward decreased left ventricular ejection fraction (LVEF) but was not statistically significant, while all treated groups showed some improvement in LVEF and left ventricular fraction shortening (LVFS). Significant changes were seen in the Mangiferin group, with lower end-diastolic left ventricular posterior wall (LVPWd) by day 21 compared to the Trolox group (p < 0.001). In the first week of the experiment, levels of interleukins (IL)-1β, IL-6, and tumour necrosis factor (TNF)-α were significantly higher in the myosin group compared to the negative control group (p < 0.001, p < 0.001, p < 0.01), indicating the progression of inflammation in this group. Treatment with Mangiferin, Prednisone, and Trolox caused a significant reduction in IL-1β compared to the positive control group (p < 0.001). Notably, Mangiferin resulted in a superior reduction in IL-1β compared to Prednisone (p < 0.05) and Trolox (p < 0.05). Furthermore, Mangiferin treatment led to a statistically significant increase in total oxidative capacity (TAC) (p < 0.001) and a significant reduction in nitric oxide (NOx) levels (p < 0.001) compared to the negative control group. Furthermore, when compared to the Prednisone-treated group, Mangiferin significantly reduced NOx levels (p < 0.001) and increased TAC levels (p < 0.001). Mangiferin treatment significantly lowered creatine kinase (CK) and aspartate aminotransferase (AST) levels on day 7 (p < 0.001 and p < 0.01, respectively) and reduced CK levels on day 21 (p < 0.01) compared to the untreated group. In the nontreated group, the histological findings at the end of the experiment were consistent with myocarditis. In the group treated with Mangiferin, only one case exhibited mild inflammatory infiltrates, represented by mononucleated leukocytes admixed with few neutrophils, with the severity graded as mild. Statistically significant correlations between the grades (0 vs. 1–2) and the study groups have been highlighted (p < 0.005). This study demonstrated Mangiferin’s cardioprotective effects in autoimmune myocarditis, showing reduced oxidative stress and inflammation. Mangiferin appears promising as a treatment for acute myocarditis, but further research is needed to compare its efficacy with other treatments like Trolox and Prednisone.

Background: Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy currently described in humans and cats. It consists of a spongy myocardium characterized by prominent trabeculation and deep recesses involving more than 50% of the ventricular thickness. We describe the clinical and pathological features of LVNC combined with tricuspid valve dysplasia, double-orifice tricuspid valve and severe pulmonary stenosis in a puppy. In addition, we briefly review the LVNC causes, pathogenesis, forms and current diagnostic criteria. Case presentation: A seven-week-old intact German Shorthaired Pointer-cross male was presented with a poor body condition, exercise intolerance and dyspnea. Clinical exam identified a bilateral systolic murmur (grade IV/VI over the right heart base and grade III/VI over the left heart base). Echocardiography identified tricuspid valve dysplasia, mild mitral regurgitation, and severe pulmonic stenosis with a trans-valvar systolic pressure gradient of 106 mmHg. Left ventricular noncompaction was diagnosed by necropsy and further confirmed histopathologically by the presence of two distinct myocardial layers: an inner noncompacted zone covering more than 50% of ventricular thickness containing prominent trabeculation and deep recesses, and an outer zone of compact myocardium. Conclusions: This is the first case describing LVNC in a canine patient, supporting the introduction of this form of heart disease as a differential diagnosis for cardiomyopathies in juvenile and adult dogs.

Double chambered right ventricle (DCRV) is a congenital heart anomaly where the right ventricle is divided into two chambers. We describe, for the first time, an unusual combination of DCRV combined with some other congenital heart defects. A 1.2-year-old Golden Retriever was presented with lethargy, exercise intolerance and ascites. Physical examination revealed an irregularly irregular pulse and a grade V/VI, systolic, right cranial murmur. Electrocardiography revealed widened and splintered QRS complexes with a right bundle-branch block pattern. Radiography demonstrated right-sided cardiomegaly. Two-dimensional echocardiography identified a DCRV with tricuspid valve dysplasia. The patient died despite abdominocentesis and 4 days of oral pharmacotherapy, and necropsy revealed an anomalous fibromuscular structure that divided the right ventricle into two compartments. Another finding was tricuspid valve dysplasia with hypoplasia of the posterior and septal leaflets. The anterior leaflet was prominent, being part of the anomalous structure that divided the right ventricle. Necropsy also identified a perimembranous ventricular septal defect and mild subaortic stenosis. Histopathological examination of the fibromuscular band that separated the right ventricle identified longitudinally oriented layers of dense fibrous connective tissue and myocardial cells arranged in a plexiform pattern. The muscular component was well represented at the ventral area of the fibromuscular band, and was absent in the central zone. Superficially, the endocardium presented areas of nodular hyperplasia covering mainly the fibrous part of the abnormal structure. The nodules were sharply demarcated and were composed by loosely arranged connective tissue with myxoid appearance, covered by discrete hyperplastic endocardium. Concomitant cardiac malformations involving DCRV, tricuspid valve dysplasia, perimembranous ventricular septal defect and mild subaortic stenosis have not been previously described in veterinary medicine, and are reported here for the first time. Moreover, this is the first report of a canine patient with tricuspid valve dysplasia (TVD) and DCRV where the anterior leaflet is part of an anomalous structure dividing the right ventricle (RV) into two separate compartments.

Hypertrophic cardiomyopathy (HCM) is a common heart disease in cats, characterized by regional or diffuse hypertrophy of the left ventricular walls, with an uncertain etiology and heterogenous natural history. Several types of rhythm disturbances are often associated with the disease. This study conducts a comprehensive review of the current literature, in order to evaluate the diagnostic and prognostic effectiveness of electrocardiography and Holter monitoring in the management of feline hypertrophic cardiomyopathy. The main subjects of discussion will include general information about HCM and its connection to arrhythmias. We will explore the rhythm disturbances documented in the current literature on Holter monitoring, as well as the techniques used for Holter monitoring. Additionally, the review will cover classical electrocardiography (ECG) and its diagnostic utility. Prognostic indicators and anti-arrhythmic therapy will also be discussed in detail. The findings highlight the importance of understanding arrhythmias in feline HCM for accurate diagnosis, risk assessment, and therapeutic intervention. ECG and Holter monitoring may offer valuable insights into managing feline HCM.

This study aimed to describe the gross and histological features of multiple endocrine and non-endocrine neoplasia, including multiple PGLs found in two Boxer dogs. Additionally, the identified PGLs were immunohistochemically evaluated, and the subunits 2, 3, and 4 of the SDHD gene were screened for possible mutations. The tumors identified include aortic and carotid body PGLs, thyroid follicular-compact carcinoma, and subcutaneous lipomas. One case also had a Leydig cell tumor and adrenal cortex hyperplasia, while the other had H-type pancreatic carcinoma. Three out of 4 PGLs appeared benign, but one aortic body tumor showed malignant features with neoplastic emboli at its edge. Immunohistochemical analysis confirmed the neuroendocrine origin of all PGLs, with positive staining for Chromogranin A, NSE, and variable positivity for S100. No somatic mutations were found in exons 2, 3, and 4 of the SDHD gene in any of the evaluated PGLs. The absence of mutations in the evaluated SDHD gene subunits suggests the involvement of other genetic factors or pathways in the development of these tumors, warranting further investigation in this field.