Hypereosinophilic syndrome with cardiac infiltration and congestive heart failure in a cat.

Hypereosinophilic syndrome is an uncommon disorder in the cat. It is a heterogeneous group of conditions defined by a persistent hypereosinophilia associated with organ damage directly attributable to tissue hypereosinophilia. A seven-year-old castrated domestic shorthair cat presented to the emergency service for dyspnea. Initial physical examination identified the presence of a grade III/VI systolic left parasternal murmur with no gallop or arrhythmia. A snap N-terminal-pro hormone brain natriuretic peptide was abnormal, and a point-of-care ultrasound revealed mild pleural effusion, scant pericardial effusion, and an enlarged left atrium. There was leukemia (72.35 K/uL, reference range 4.5-15.7 K/uL) predominated by eosinophilia (33.84 K/uL; reference range 0-1.9 K/uL). On echocardiogram, there was concentric hypertrophy of the left ventricular walls with irregular endocardial borders. The left atrium was enlarged with evidence of spontaneous echogenic contrast. The mitral valve was thickened with a vegetative lesion on the anterior leaflet. Despite treatment, the patient experienced cardiopulmonary arrest, and cardiopulmonary resuscitation was unsuccessful. Complete necropsy with histopathology revealed eosinophilic infiltrates in multiple organs and the presence of a severe, acute-on-chronic, fibrinous, and eosinophilic-granulomatous endomyocarditis with mural thrombosis and marked endocardial fibrosis. This case represents an unusual presentation of the hypereosinophilic syndrome in the cat with cardiac involvement and congestive heart failure as a primary clinical sign.

Early detection of myocardial dysfunction in a cat that gradually progressed to endomyocardial form of restrictive cardiomyopathy.

BACKGROUND: Restrictive cardiomyopathy (RCM) is a common myocardial disease in cats, characterized by diastolic dysfunction and atrial enlargement without myocardial hypertrophy. Especially, endomyocardial form of RCM, one of the subtypes in RCM, is characterized by endocardial fibrosis, endocardial scar bridging the interventricular septum and left ventricular (LV) free wall, and deformation and distortion of the LV. However, it is unclear how the myocardial dysfunction and the endocardial scar contribute to the pathophysiology of RCM disease progression. CASE PRESENTATION: A 3 years and 2 months old, intact male, Domestic shorthaired cat was presented for consultation of cardiac murmur. At the first visit (day 0), the notable abnormal finding was echocardiography-derived chordae tendineae-like structure bridging the interventricular septum and the LV free wall, resulting high-speed blood flow in the left ventricle. Electrocardiography, thoracic radiography and noninvasive blood pressure measurements were normal. No left atrial enlargement was observed, and LV inflow velocity showed an abnormal relaxation pattern. Although there was no abnormality in tissue Doppler imaging-derived myocardial velocity, two-dimensional speckle tracking echocardiography (2D-STE) revealed a decrease in the LV longitudinal strain and an increase in endocardial to epicardial ratio of the LV circumferential strain on day 0. On day 468, obvious left atrium enlargement and smoke like echo in the left atrium were observed. The LV inflow velocity was fused, and the tissue Doppler imaging-derived early-diastolic myocardial velocity of the septal mitral annulus decreased. Regarding 2D-STE, LV circumferential strain was further decreased, and right ventricular strain was additionally decreased. Although the general condition was good, we made a clinical diagnosis of endomyocardial RCM based on the above findings. On day 503, the cat showed the radiographic evidence of pulmonary edema and congestive heart failure signs. CONCLUSIONS: Cats with abnormal LV structure and associated myocardial dysfunction like this case needs careful observation. Additionally, 2D-STE indices may be useful for early detection of myocardial dysfunction in feline RCM.

Accessory left ventricular chamber in a cat: multimodality imaging description by cardiac magnetic resonance imaging and echocardiography.

A left ventricular accessory chamber is a complex and uncommon phenotype consisting in a subdivision of the left ventricle by a thick-walled muscle bundle or septum into two cavities. Multiple aetiologies such as congenital double-chambered left ventricle and acquired endomyocardial form of restrictive cardiomyopathy have been reported. The endomyocardial form of restrictive cardiomyopathy, owing to its structural heterogeneity, can present a similar phenotype to the congenital abnormality with intraventricular lesions bridging the ventricular septum and left ventricular free wall. Conventional echocardiography is the first-line, accepted, non-invasive imaging modality to investigate underlying cardiac disease but presents limitations for the overall assessment of myocardial tissue. This report describes the use of cardiac magnetic resonance imaging as an additional imaging modality to provide multiplanar morphological, structural, and functional information of the myocardium. In the presented images, hyperintensities on cardiac magnetic resonance imaging within the myocardium along with hyperechoic and heterogeneous myocardial tissue on echocardiography and elevated troponin I were suggestive of a presumptive acquired pathological process such as feline endomyocarditis-left ventricular endomyocardial fibrosis complex, rather than a sole congenital anomaly. Although the diagnosis was not confirmed, this case exemplifies the advantages of using complementary multimodality imaging in a cat presented with a left ventricular accessory chamber.

Clinical, epidemiological and echocardiographic features and prognostic factors in cats with restrictive cardiomyopathy: A retrospective study of 92 cases (2001-2015).

BACKGROUND: Restrictive cardiomyopathy (RCM) is a common primary cardiomyopathy of cats. However, little information is available regarding prognostic variables in large populations of cats with RCM. OBJECTIVES: To characterize the epidemiological, clinical, and echocardiographic features of cats with RCM and to document their survival times and risk factors for cardiac death (CD). ANIMALS: Ninety-two cats with RCM. METHODS: Retrospective study. Diagnosis of RCM was based on echocardiographic and Doppler criteria. Median survival time to CD and adjusted hazard ratios (HR) were estimated by the Kaplan-Meier method and multivariate Cox models, respectively. RESULTS: The feline population (median age [interquartile range], 8.6 years [4.1-12.4]; body weight, 4.0 kg [3.3-4.7]) included 83 cats (90%) with the myocardial RCM form and 9 (10%) with the endomyocardial fibrosis RCM form. Most RCM cats (64/92, 70%) were symptomatic at the time of diagnosis, with dyspnea related to congestive heart failure in 57 of 64 cats (89%). The median survival time of the 69 cats with the myocardial RCM form and available follow-up was 667 days (range, 2-3710 days) considering CD. Independent of age, biatrial enlargement, and arrhythmias, increase of the left atrium (LA)-to-aorta (Ao) ratio (hazard ration [HR], 2.5 per 0.5-unit increase; 95% confidence interval [CI], 1.5-4.2; P < .001) and presence of severe LA enlargement (end-diastolic LA : Ao ≥2; HR, 3.4; 95% CI, 1.3-8.7; P = .01) were significantly associated with shorter time to CD. CONCLUSIONS AND CLINICAL IMPORTANCE: Cardiac death is common in RCM cats, and LA enlargement seems independently associated with decreased survival time in these cats.

The impact of obesity in the cardiac lipidome and its consequences in the cardiac damage observed in obese rats / El impacto de la obesidad sobre el lipidoma cardiaco y sus consecuencias en el daño cardiaco en ratas obesas

Aims: To explore the impact of obesity on the cardiac lipid profile in rats with diet-induced obesity, as well as to evaluate whether or not the specific changes in lipid species are associated with cardiac fibrosis. Methods: Male Wistar rats were fed either a high-fat diet (HFD, 35% fat) or standard diet (3.5% fat) for 6 weeks. Cardiac lipids were analyzed using by liquid chromatography-tandem mass spectrometry. Results: HFD rats showed cardiac fibrosis and enhanced levels of cardiac superoxide anion (O2), HOMA index, adiposity, and plasma leptin, as well as a reduction in those of cardiac glucose transporter (GLUT 4), compared with control animals. Cardiac lipid profile analysis showed a significant increase in triglycerides, especially those enriched with palmitic, stearic, and arachidonic acid. An increase in levels of diacylglycerol (DAG) was also observed. No changes in cardiac levels of diacyl phosphatidylcholine, or even a reduction in total levels of diacyl phosphatidylethanolamine, diacyl phosphatidylinositol, and sphingomyelins (SM) was observed in HFD, as compared with control animals. After adjustment for other variables (oxidative stress, HOMA, cardiac hypertrophy), total levels of DAG were independent predictors of cardiac fibrosis while the levels of total SM were independent predictors of the cardiac levels of GLUT 4. Conclusions: These data suggest that obesity has a significant impact on cardiac lipid composition, although it does not modulate the different species in a similar manner. Nonetheless, these changes are likely to participate in the cardiac damage in the context of obesity, since total DAG levels can facilitate the development of cardiac fibrosis, and SM levels predict GLUT4 levels (AU)

Objetivos: Explorar el impacto de la obesidad sobre el perfil lipídico cardiaco en ratas con obesidad inducida por dieta. Se evaluó, además, si estos cambios se asocian con fibrosis cardiaca. Métodos: Ratas macho Wistar fueron alimentadas con una dieta con alto contenido en grasa (HFD; 35% grasa) o con una dieta estándar (3,5% grasa) durante 6 semanas. El análisis del lipidoma cardiaco se realizó mediante cromatografía líquida en tándem con espectrofotometría de masas. Resultados: Las ratas HFD presentaron fibrosis cardiaca, estrés oxidativo y un aumento en el índice HOMA, adiposidad y los niveles circulantes de leptina así como una reducción en los niveles cardiacos del transportador de glucosa (GLUT 4) en comparación con las ratas controles. El análisis del lipidoma cardiaco mostró un aumento de los niveles de triglicéridos especialmente los que contenían ácido palmítico, esteárico o araquidónico, un incremento en los de diacilglicerol (DAG) aunque no cambios en los de diacilfosfatidilcolina y una reducción en los de diacilfosofatidiletanolamina, diacilfosfatidilinositol o de esfingomielinas (SM) en las ratas HFD en comparación con las control. Después del ajuste por otras variables (estrés oxidativo, hipertrofia cardiaca, índice HOMA), los niveles de DAG fueron predictores independientes de fibrosis cardiaca mientras que los de SM fueron de los de niveles de GLUT4. Conclusiones: La obesidad ejerce un impacto importante sobre el lipidoma cardiaco. Estos cambios parecen participar en el daño cardiaco en el contexto de la obesidad ya que los niveles de DAG podrían facilitar el desarrollo de fibrosis miocárdica y los de SM los de GLUT 4 (AU)

Myocardial fibrosis in a horse with polymorphic ventricular tachycardia observed during general anesthesia.

Ventricular dysrhythmias are more commonly associated with myocardial disease than are supraventricular dysrhythmias. Management of arrhythmias under general anesthesia is difficult because of the dysrhythmogenic effects of the anesthetic drugs. This report describes a severe ventricular dysrhythmia observed in a pony under general anesthesia, with a severe and old myocardial fibrosis found on postmortem examination.

Effect of Angiotensin II Type 1 receptor blocker on cardiac angiotensin-converting enzyme and chymase-like activities, and cardiac fibrosis in cardiomyopathic hamsters.

It has been reported that cardiac chymase has an effect on cardiac fibrosis through the Angiotensin (Ang) II formation and an Ang II-independent mechanism. In the present study, Ang II type 1 (AT1) receptor blocker (candesartan cilexetil) was administered to dilated cardiomyopathic (DCM; Bio TO2) hamsters for 4 weeks to study the effect of AT1 receptor blocker on cardiac chymase-like activity and cardiac fibrosis. Echocardiography, histological examination, and assessment of cardiac angiotensin-converting enzyme (ACE)/chymase-like activities were conducted. Hamsters showed cardiac dysfunction due to increased left ventricular dimensions and decreased ventricular wall thickness, significant increase in cardiac chymase-like activity, and fibrosis. This result indicates that the cardiac chymase-like activity is responsible for cardiac fibrosis. When candesartan cilexetil was administered to Bio TO2 hamsters, cardiac chymase-like activity increased significantly, whereas cardiac fibrosis decreased significantly. Cardiac ACE and chymase-like activities were unchanged in non-DCM hamsters with candesartan cilexetil. This suggests that the cardiac Ang II formation mechanism was stimulated by suppressing the effect of cardiac Ang II, and cardiac chymase-like activity could be increased. Moreover, this mechanism may be more highly activated if cardiac Ang II is activated in the heart. In conclusion, we demonstrated that AT1 receptor blocker reduced cardiac fibrosis, although cardiac chymase-like activity increased. Because the Ang II-forming pathway and the effect of chymase in hamsters is similar to that in dogs, the results of the present study may supplement the available information for dogs.

Myocardial necrosis in a captive binturong (Arctictis binturong).

An adult male binturong, Arctictis binturong, which had been anorexic and lethargic for seven days became acutely dyspnoeic and died under anaesthesia. A postmortem examination revealed left ventricular hypertrophy with a thrombus occluding the left ventricular chamber. Histological findings included moderate to severe multifocal, vasculocentric myocardial degeneration and necrosis with fibrosis replacing myocardiocytes. Escherichia coli and Proteus mirabilis were grown on cultures. The animal's serum vitamin E and selenium levels were considered adequate. The aetiology of the chronic myocardial changes could not be determined.

Feline endomyocarditis and left ventricular endocardial fibrosis.

A retrospective study was conducted of all feline necropsies over a 7-year period. Of a total of 1,472 necropsies, 37 cases of endomyocarditis (EMC) and 25 cases of left ventricular endocardial fibrosis (LVEF) (previously called restrictive or intermediate cardiomyopathy) were identified. There was a subset of four cats with EMC that had histologic features of both diseases. Interstitial pneumonia was seen in 25 of 35 cats (71%) with EMC but in only seven of 25 cats (28%) with LVEF. Thrombi or thromboemboli were seen in 14 of 25 cats (56%) with LVEF but in only six of 37 of cats (16%) with EMC. In both LVEF and EMC, thromboemboli were located in the abdominal aorta, left atrium and ventricle of the heart, femoral artery, cranial mesenteric artery, liver, pulmonary artery, jugular vein, or a meningeal vessel. Each cat had a single thrombus/thromboembolus, except for four cats with LVEF that had more than one. The histologic and clinical findings suggest that EMC and LVEF represent temporally different manifestations of a single disease entity.

Comparison of morphologic findings in spontaneously occurring hypertrophic cardiomyopathy in humans, cats and dogs.

Morphologic features of spontaneously occurring hypertrophic cardiomyopathy (HC) were compared in 38 humans, 51 cats and 10 dogs. Asymmetric hypertrophy of the ventricular septum, marked disorganization of cardiac muscle cells, abnormal intramural coronary arteries and myocardial fibrosis were each present in the ventricular septum of human, feline, and canine forms of HC; these abnormalities were generally more severe and most frequently identified in humans. Asymmetric left ventricular hypertrophy (based on the calculated septal-to-free wall thickness ratio) was most common in humans (31 of 38 [81%]) and dogs (8 of 10 [80%]), as compared with cats (16 of 51 [31%]; p < 0.001) with HC; in all 3 species, hypertrophy was often diffuse, involving substantial portions of the anterolateral and posterior free walls, and the ventricular septum. Marked septal disorganization (> or = 5% of the tissue section) was present in 35 patients (92%), but in only 14 cats (27%) and 2 dogs (20%) (p < 0.001). Abnormal intramural coronary arteries occurred with similar frequency in the ventricular septum of patients (n = 25; 66%), cats (n = 38; 74%) and dogs (n = 6; 60%) (p < NS). Moderate-to-severe septal fibrosis was identified more commonly in humans (15 of 38 [39%]) than in animals (13 of 61 [21%]; p < 0.001). In all 3 species, abnormal intramural coronary arteries were most commonly observed within or at the margins of areas of fibrous tissue. These morphologic findings describe spontaneously occurring models of HC in cats and dogs with substantial structural similarities to the well-recognized disease entity in humans.

[Myocardial fibrosis and degeneration with heart failure (cardiomyopathy) in two goats]. / Myokardiale Fibrose und Degeneration mit Herzinsuffizienz (Kardiomyopathie) bei zwei Ziegen.

Myocardial fibrosis and degeneration of unknown etiology is described in two adult, female goats of the Saanen and Pfauen breeds. Both animals presented with clinical signs of cardiac failure with subcutaneous edema, hydrothorax and ascites. The pathological lesions were characterized by cardiomegaly with ventricular and auricular dilatation and hypertrophy, massive subcutaneous edema and body cavity edema. The first goat additionally showed chronic liver congestion due to cardiac failure. Histologically, the most prominent changes were focally extensive cardiomyocyte degeneration and cardiac fibrosis. The clinical history and pathologic lesions are comparable to those of dilatative cardiomyopathy in SixRH cattle.

Myocarditis and cardiomyopathy in the dog and cat.

Myocarditis and cardiomyopathy were diagnosed in 36 dogs from 11 litters, and myoendocarditis and restrictive cardiomyopathy were diagnosed in 51 cats. Most of the dogs and cats died unexpectedly. Spontaneous parvoviral infection in the dogs caused acute (myocytolysis with presence of intranuclear inclusion bodies in the myocytes), subacute (inflammatory reaction and myocytolysis), and chronic (fibrosis and myocytolysis) myocarditis, which led to extensive myocardial fibrosis and abnormality of the myocytes, similar to dilated cardiomyopathy in man. Spontaneous acute, subacute, and chronic myoendocarditis in the cats led to granulation, extensive fibrosis, and necrosis of the myoendocardium, i.e., like restrictive cardiomyopathy which occurs in man without eosinophilia. Thus, the dog and cat are important animal models of primary myocardial disease.